The Hummingbirds' Foundation for M.E.

The Hummingbirds' Foundation for M.E. (HFME) is fighting for the recognition of M.E.,
and for patients to be accorded the same basic human rights as those with similar
disabling and potentially fatal neurological diseases such as M.S.

An important note

Before reading the research/advocacy information given in the links below, please be aware of the following facts:

1. Myalgic Encephalomyelitis and ‘Chronic Fatigue Syndrome’ are not synonymous terms. The overwhelming majority of research on ‘CFS’ or ‘CFIDS’ or ‘ME/CFS’ or ‘CFS/ME’ or ‘ICD-CFS’ does not involve M.E. patients and is not relevant in any way to M.E. patients. If the M.E. community were to reject all ‘CFS’ labelled research as ‘only relating to ‘CFS’ patients’ (including research which describes those abnormalities/characteristics unique to M.E. patients), however, this would seem to support the myth that ‘CFS’ is just a ‘watered down’ definition of M.E. and that M.E. and ‘CFS’ are virtually the same thing and share many characteristics.

A very small number of ‘CFS’ studies refer in part to people with M.E. but it may not always be clear which parts refer to M.E. The
A warning on ‘CFS’ and ‘ME/CFS’ research and advocacy paper is recommended reading and includes a checklist to help readers assess the relevance of individual ‘CFS’ studies to M.E. (if any) and explains some of the problems with this heterogeneous and skewed research.

In future, it is essential that M.E. research again be conducted using only M.E. defined patients and using only the term M.E. The bogus, financially-motivated disease category of ‘CFS’ must be abandoned.

2. The research referred to on this website varies considerably in quality. Some is of a high scientific standard and relates wholly to M.E. and uses the correct terminology. Other studies are included which may only have partial or minor possible relevance to M.E., use unscientific terms/concepts such as ‘CFS,’ ‘ME/CFS,’ ‘CFS/ME,’ ‘CFIDS’ or Myalgic ‘Encephalopathy’ and also include a significant amount of misinformation. Before reading this research it is also essential that the reader be aware of the most commonly used ‘CFS’ propaganda, as explained in A warning on ‘CFS’ and ‘ME/CFS’ research and advocacy and in more detail in Putting research and articles on Myalgic Encephalomyelitis into context.

M.E. and other illnesses

*O* Myalgic Encephalomyelitis vs Fibromyalgia by Jodi Bassett

Introduction: Despite the fact that severe pain is a well known and very common symptom of M.E. many M.E. sufferers who have pain are told that they now also supposedly have ‘Fibromyalgia.' But if pain is a recognised symptom of M.E. then how does an additional Fibromyalgia diagnosis made purely on the presence of pain make sense?

Patients who have Fibromyalgia and patients with primary M.E. can be easily distinguished from each other with various tests (and other means including an evaluation purely based on symptomatology), so what do tests show in patients who supposedly have both? Interestingly, when patients (supposedly) have both illnesses the test results given are the ones for M.E. only. So do these M.E. patients really also have Fibromyalgia, or do they just have severe pain as part of their M.E.? As you might expect, these test results strongly suggest the latter.

The same is true of multiple chemical sensitivity syndrome (MCSS); symptoms of chemical sensitivity are part of the core symptoms of M.E. and have long been associated with M.E.(as well as with several other autoimmune illnesses such as multiple sclerosis and Lupus) and so there is no need for an additional diagnosis of MCSS to be made. This additional diagnosis is incorrect. Just because you may fit a definition of Fibromyalgia, or MCSS, or irritable bowel syndrome (IBS) this does not mean that your symptoms are caused by the same etiological or pathological process, or will respond to various treatments the same way, or will have the same prognosis as those people who have primary Fibromyalgia, MCSS or IBS, or anything else.

All of these symptoms from pain to chemical sensitivities to constipation or diarrhoea are all very common symptoms of M.E. making additional diagnoses inappropriate.

See M.E. and other illnesses and ME vs Fibromyalgia for more information.

An excerpt:

Myalgic Encephalomyelitis and Fibromyalgia: are they really similar illnesses?

In short, no they are not. The claimed similarity between M.E. and Fibromyalgia arises purely because of the mistaken belief that M.E. is the same thing as ‘Chronic Fatigue Syndrome.’ But M.E. and ‘CFS’ are anything but synonymous terms.

Differences between M.E. and Fibromyalgia include the following:

One of the most fundamental facts about M.E. throughout its history is that it occurs in epidemics. There is a history of over sixty recorded outbreaks of the illness going back to 1934 when an epidemic of what seemed at first to be poliomyelitis was reported in Los Angeles. As with many of the other M.E. outbreaks the Los Angeles outbreak occurred during a local polio epidemic. There have been zero Fibromyalgia outbreaks. Fibromyalgia does not occur in epidemics.

M.E. is an infectious neurological disease and represents a major attack on the central nervous system (CNS) by the chronic effects of a viral infection. Many symptoms of M.E. are indicative of a viral infection. The world’s leading M.E. experts, namely Ramsay, Richardson, Dowsett and Hyde, (and others) have all indicated that M.E. is caused by an enterovirus. The evidence which exists to support the concept of M.E. as an enteroviral disease is compelling. Fibromyalgia, however, has never been associated with a viral prodromic illness and does not have viral-type symptoms and is instead far more likely to be triggered by head and neck trauma, car accidents etc.

The two illness not only do not share a World Health Organisation International Classification of Diseases (ICD) listing, but are not even in the same section. Fibromyalgia is classified in ICD-10 at section M79.0 under Soft Tissue Disorders; M.E. however, is classified as an organic neurological disorder with the code G93.3. It is also not permitted for the same condition to be classified to more than one rubric, since ICD categories are mutually exclusive.

There is a much higher prevalence of Fibromyalgia compared to M.E. M.E. has a similar strike rate to multiple sclerosis and affects less than 0.5% of the population, whereas 3 - 10 % (depending on the study) of the adult population qualify for a diagnosis of Fibromyalgia.

Many people with severe M.E. (25 – 30%) are housebound and bedbound by the illness, some for many years or even decades. Many M.E. patients need part-time or full-time carers to manage the tasks of daily living; they cannot feed themselves, prepare their own food, do any of their own cleaning or manage their own personal care. Being unable to work full time or even part time is very common - even moderate M.E. is extremely disabling. This level of incapacity simply does not occur in Fibromyalgia (there is not anywhere near the same severity and level of disability in Fibromyalgia as there is in ME).

Deaths from M.E. from organ failure (most commonly pancreatic or heart failure) are well documented (one specialist puts the rate of death from M.E. at 3%). Fibromyalgia has never been documented as being fatal, and heart failure or pancreatic failure are never seen in Fibromyalgia.

Fibromyalgia is well known to commonly co-exist with a variety of illnesses such as Lyme disease, Lupus and various other autoimmune diseases. M.E. does not share this characteristic. M.E. no more occurs with other immune diseases than does M.S. or Parkinson’s disease.

Some make the statement that: ‘M.E. and Fibromyalgia are basically the same illness, how you can tell which one you have is that if fatigue is your worst symptom you have M.E., if pain is your worst symptom you have Fibromyalgia.’ This statement or ‘theory’ is utterly absurd and again, arises due to the confusion between M.E. and ‘CFS.’

M.E. is similar in a number of significant ways to multiple sclerosis, Lupus and poliomyelitis (polio). M.E. is characterised primarily by damage to the central nervous system (the brain) which results in dysfunctions and damage to many of the body’s vital systems and a loss of normal internal homeostasis. Therefore, although Myalgic Encephalomyelitis is primarily neurological, symptoms may be manifested by: cognitive, cardiac, cardiovascular, immunological, endocrinological, respiratory, hormonal, gastrointestinal and musculo-skeletal dysfunctions and damage. Symptoms are also caused by a loss of normal internal homeostasis; The body/brain no longer responds appropriately to homeostatic pressures, including (to varying extents): physical activity, cognitive exertion, sensory input and orthostatic stress. (See The M.E. Symptom List for more information.)

The hallmark feature of Fibromyalgia is severe widespread pain.

Fatigue is not the main symptom of M.E. or even an essential symptom of M.E. Severe pain however, is a very common symptom of M.E. It is entirely possible (and likely) that someone could have M.E. and no fatigue at all and for someone with Fibromyalgia to have considerable fatigue and for both patients to have the exact same level of severe pain. This ridiculous myth has to be stopped as it is entirely baseless and can only cause confusion and harm to both patient groups. (The use of terms such as ‘FM/ME/CFIDS/CFS’ etc. is equally absurd.)

How this myth may have got started is through patients with Fibromyalgia identifying with some of the features listed in the definitions of ‘CFS’ (which many studies have shown selects a very diverse patient group and in fact rates very poorly at actually identifying M.E. patients. Legitimate descriptions of the illness such as the The Nightingale Definition of M.E. and the descriptions by Ramsay tell an entirely different story however. Legitimate description of M.E. describe an illness that is entirely dissimilar to Fibromyalgia (or to the various definitions of ‘CFS’ for that matter.)

The two groups may also be distinguished from each other by various tests. Brain lesions, extremely low blood volume, low natural killer cell counts, cardiac insufficiency and mitochondrial defects (for example) are all seen in M.E. but never in Fibromyalgia, just as high levels of substance P are common in FMS patients but are not seen in those with M.E. Interestingly, when patients have both illnesses the test results given are the ones for M.E. only. The question needs to be asked; do these ME patients really have Fibromyalgia too, or do they just have severe pain as part of their M.E.? (Which has been misdiagnosed as Fibromyalgia) These test results (and other facts) strongly suggest the latter.

Because of the different symptomatology and pathology, treatments which help people with Fibromyalgia are inappropriate for ME patients and vice versa; treatments may be useless or even extremely harmful when used on the wrong illness (although there may possibly be some overlap in treatments for pain).

The symptoms of M.E. and Fibromyalgia are also completely different. People with Fibromyalgia also do not have the heart problems and orthostatic problems which are so characteristic of M.E., nor do they have the extreme exercise intolerance that all people with M.E. have. Fibromyalgia patients also do not have the cardiac and cardiovascular symptoms seen in M.E., or the problems maintaining homeostasis, or the autonomic symptoms, or the gastrointestinal symptoms, or the immune system dysfunctions, or the muscular weakness and paralysis, or any of the neurological dysfunctions.

The profound cognitive deficits seen in M.E. are never seen in Fibromyalgia. People with severe Fibromyalgia do not lose the power of speech or the ability to read or write as people with severe M.E. do. They do not become unable to recognise family members or have any other severe problems with memory. They do not have seizures. The brain lesions seen in the brain scans of M.E. patients who have such cognitive problems (and damage to the brain) are never seen in Fibromyalgia. There is not the same level or type of damage to the brain in Fibromyalgia as there is in M.E. As these are all the things which make up ME, it is fairly obvious the two illness have little in common with each other; indeed the only thing they do have in common is severe pain (which is seen in both illnesses). One symptom.

The similarities between the two illnesses are minimal and superficial at best but their differences are truly profound. Even if they do share one or two symptoms is this really significant when in so many much more important ways they are so VERY different and have so very little in common? The idea of these two very different patient groups being mixed up and treated as if they represented the exact same patient group is distressing to say the least, as the results could only be disastrous for all concerned.

(It is particularly important to note that one of the main features of ME is exercise intolerance. (See The ME Symptom List for details), overexertion is the single most common cause of relapses in M.E. Overexertion may also lead to disease progression for M.E. patients and sudden deaths have also been reported after exercise in these patients. In contrast, exercise has repeatedly been shown to greatly improve Fibromyalgia symptoms. Fibromyalgia patients react in an entirely different way to exercise than M.E. patients.) See Treating M.E. for more information.

There is a very real risk that if the illnesses were seen as ‘basically the same’ that patients would be given very inappropriate and harmful medical advice. People with M.E. may be yet again given inappropriate advice to exercise: 'people with Fibromyalgia exercise and they get better, Fibromyalgia and M.E. are the same illness basically so why don't you want to exercise? How can it be making you sicker? Maybe you want to stay ill.' It might also lead to comparisons between the very different severity levels of the illnesses. A person with very severe M.E. might unfairly be told: ‘Most people with Fibromyalgia are able to keep working full-time, you have M.E. which is basically the same illness, so why can’t you? You mustn’t be trying hard enough.’ People with Fibromyalgia may also be unfairly and inappropriately advised not to exercise (a treatment which is often very beneficial for Fibromyalgia sufferers).

If that weren’t bad enough, if the two illnesses were seen as representing the same patient group, medical understanding of both illnesses would not advance from its present level. You could say goodbye to any type of useful new research that may lead to real treatments or cures for M.E. or Fibromyalgia. Mixed Fibromyalgia and M.E. patient groups would make discovering any of these things absolutely impossible.

There is nothing to be gained by joining these two illnesses as if they were exactly the same when in reality they have almost nothing in common. All that can result from such a decision is huge disadvantages and setbacks for both groups medically, socially and politically.

Fibromyalgia and Myalgic Encephalomyelitis are distinct and unique illnesses and it is vitally important that they are always seen that way for the benefit of all patients involved.

Note: Similar lists could also be created to show the differences between Myalgic Encephalomyelitis and; Lupus, Lyme disease, multiple sclerosis or Gulf War Syndrome. Although M.E. does have far more in common with all of these illnesses than with Fibromyalgia, these illness are all (more significantly) unique and distinct illnesses with different symptoms, core characteristics, aetiology’s, and pathologies which it would be equally unwise (and unscientific) to treat as if they represented the same illness. 


M.E. vs MS:  Similarities and differneces, by Jodi Bassett

M.E. and MS are very similar diseases medically in many ways. However, for reasons that have nothing to do with science, the two diseases are treated very differently politically and socially. The contrast could not be more stark.

M.E. patients are treated terribly (and often abused terribly, even unto death in some cases), yet there is no public outcry as there would be if MS patients were treated in this same way. Thus people with M.E. find themselves in the terrible position of actually ENVYING people who have MS.

An excerpt: 

Table 1. Medical similarities between MS and M.E.

 

Multiple Sclerosis

Myalgic Encephalomyelitis

MS is primarily a neurological disease, i.e. a disease of the central nervous system (CNS).

 

M.E. is primarily a neurological disease, i.e. a disease of the central nervous system (CNS).

 

Demyelination (damage to the myelin sheath surrounding nerves) has been documented in MS.

 

Demyelination (damage to the myelin sheath surrounding nerves) has been documented in M.E.

 

Evidence of oligoclonal bands in the cerebrospinal fluid has been documented in MS.

 

Evidence of oligoclonal bands in the cerebrospinal fluid has been documented in M.E.

 

No single definitive laboratory test is yet available for MS but a series of tests are available which can objectively confirm the diagnosis with some certainty.

 

No single definitive laboratory test is yet available for M.E. but a series of tests are available which can objectively confirm the diagnosis with a high degree of certainty.

 

MS can be severely disabling and cause significant numbers of patients to be bedbound or wheelchair-reliant.

 

M.E. can be severely disabling and cause significant numbers of patients to be bedbound, wheelchair-reliant or housebound.

 

MS can be fatal (either from the disease itself or from complications arising from the disease)

 

M.E. can be fatal (either from the disease itself or from complications arising from the disease)

 

MS significantly reduces life expectancy.

 

M.E. significantly reduces life expectancy. (M.E. reduces life expectancy by a greater period than MS: see Table 3.)

 

Symptoms/problems which occur in MS include: impaired vision, nystagmus, afferent pupillary defect, loss of balance and muscle coordination, cogwheel movement of the legs, slurred speech, difficulty speaking (scanning speech and slow hesitant speech), difficulty writing, difficulty swallowing, proprioceptive dysfunction, abnormal sensations (numbness, pins and needles), shortness of breath, headaches, itching, rashes, hair loss, seizures, tremors, muscular twitching or fasciculation, abnormal gait, stiffness, subnormal temperature, sensitivities to common chemicals, sleeping disorders, facial pallor, bladder and bowel problems, difficulty walking, pain, tachycardia, stroke-like episodes, food intolerances and alcohol intolerance, and partial or complete paralysis.

 

Symptoms/problems which occur in M.E. include: impaired vision, nystagmus, afferent pupillary defect, loss of balance and muscle coordination, cogwheel movement of the legs, slurred speech, difficulty speaking (scanning speech and slow hesitant speech), difficulty writing, difficulty swallowing, proprioceptive dysfunction, abnormal sensations (numbness, pins and needles), shortness of breath, headaches, itching, rashes, hair loss, seizures, tremors, muscular twitching or fasciculation, abnormal gait, stiffness, subnormal temperature, sensitivities to common chemicals, sleeping disorders, facial pallor, bladder and bowel problems, difficulty walking, pain, tachycardia, stroke-like episodes, food intolerances and alcohol intolerance, and partial or complete paralysis.

 

MS can cause orthostatic intolerance (dizziness or faintness on standing).

M.E. commonly causes severe orthostatic intolerance (which often worsens to become severe POTS and/or NMH).

 

Short-term memory loss, word finding difficulty, difficulty with concentration and reasoning and other forms of cognitive impairment occur in 50% of MS patients. 10% of MS patients have cognitive impairments severe enough to significantly affect daily life.

 

Short-term memory loss, word finding difficulty, difficulty with concentration and reasoning and other forms of cognitive impairment occur in 100% of M.E. patients. Almost all M.E. patients have cognitive impairments severe enough to significantly affect daily life.

 

MS patients often become severely more ill in even mildly warm weather. Cold weather can also cause significant problems.

 

M.E. patients often become severely more ill in even mildly warm weather. Cold weather can also cause significant problems.

 

MS can affect autonomic nervous system function (including involuntary functions such as digestion and heart rhythms).

 

M.E. can affect autonomic nervous system function (including involuntary functions such as digestion and heart rhythms).

MS is thought to cause a breakdown of the blood brain barrier.

 

M.E. is thought to cause a breakdown of the blood brain barrier.

 

A positive Babinski's reflex is consistent with several neurological conditions, including MS. (Babinski's reflex or extensor plantar reflex is a test for dysfunction of the corticospinal tract.)

 

A positive Babinski's reflex (or extensor plantar reflex) is consistent with M.E.

 

The Romberg test will often be abnormal in MS. (This test measures neurological or inner ear dysfunction.)

The Romberg test will be abnormal in 95% or more of M.E. patients.

An abnormal neurological exam is usual in MS. Abnormalities are also commonly seen in neuropsychological testing in MS.

 

An abnormal neurological exam is usual in M.E. Abnormalities are also commonly seen in neuropsychological testing in M.E.

 

MS causes a certain type of brain lesion detectable in MRI brain scans. Abnormalities are also seen in EEG and QEEG brain maps and SPECT brain scans in MS.

 

M.E. causes a certain type of brain lesion detectable in MRI brain scans. Abnormalities are also seen in EEG and QEEG brain maps and SPECT brain scans in M.E.

 

Hypothyroidism is found in many MS patients.

 

Hypothyroidism is found in almost all M.E. patients.

 

The glucose tolerance test is often abnormal in MS.

 

The glucose tolerance test is often abnormal in M.E.

 

Low blood pressure readings (usually low-normal) are common in MS.

Low blood pressure readings are extremely common in M.E. Severely low blood pressure readings as low as, or lower than, 84/48 (or 75/35 according to many anecdotal accounts) are common in severe M.E. or those having severe relapses. This can occur at rest or as a result of orthostatic or physical overexertion. At times BP readings can be so low that they cannot be measured by the machine and error messages appear. Circulating blood volume measurements of only 50% to 75% of expected are also commonly seen in M.E.

 

Some MS patients experience a partial remission during pregnancy.

 

Some M.E. patients experience a partial remission during pregnancy.

 

Patients with MS have an increased risk of dying from heart disease or vascular diseases.

 

Deaths from cardiac problems are one of the most common causes of death in M.E.

 

Although MS is primarily neurological, it also has aspects of autoimmune disease.

 

Although M.E. is primarily neurological, it also has aspects of autoimmune disease.

 

MS usually affects people between the ages of 20 and 40 years, and the average age of onset is approximately 34 years. Onset occurs between the ages of 20 to 40 years in 70% of patients.

 

The average ages affected by M.E. are similar to those seen in MS. However, the average age of onset may be significantly younger in M.E.

 

MS was once thought to be rare in children, but we know that around 5% of MS sufferers are under 18.

 

Around 10% of M.E. sufferers are under 18.

 

MS affects more than a million adults and children worldwide.

M.E. affects more than a million adults and children worldwide. (M.E. is at least as common as MS, and may be up to twice or three-times as common.)

 

 

As well as there being many similarities in symptoms, the brain scans from M.E. and MS patients are often very similar, as this chart illustrates. MS and M.E. both cause a certain type of brain lesion detectable in brain scans. Those with MS tend to have fewer brain lesions of a larger size, while M.E. is associated with a greater number of these lesions of a somewhat smaller size.

 

M.E. and MS are so similar medically that they are sometimes misdiagnosed as one another. The names used for M.E. and MS also indicate the similarities between the two diseases. MS was first described in 1868, and MS has also been known as ‘disseminated sclerosis’ or ‘encephalomyelitis disseminate.’ Myalgic Encephalomyelitis has existed for centuries but was first comprehensively scientifically documented in 1934, when an outbreak of what at first seemed to be poliomyelitis (polio) occurred in Los Angeles (M.E. occurs in outbreaks as well as sporadically). The term Myalgic Encephalomyelitis was coined in 1956. Earlier names for M.E. include ‘atypical polio’ and atypical multiple sclerosis.’


B
oth MS and M.E. have been correctly classified as organic diseases of the central nervous system in the World Health Organization’s International Classification of Diseases for many decades. MS is classified at G 35 and M.E. at G 93.3.

 


 

The misdiagnosis of CFS by Jodi Bassett

 

An excerpt: The fact that a person qualifies for a diagnosis of Oxford Chronic Fatigue Syndrome (CFS), Fukuda (CDC) CFS, or either of the Australian CFS definitions (a) does not mean that the patient has Myalgic Encephalomyelitis (M.E.), and (b) does not mean that the patient has any other distinct and specific illness named ‘CFS.’ A diagnosis of CFS – based on these or any of the other CFS definitions – can only ever be a misdiagnosis.

The reason for this is that despite the fact that the new name and definition of CFS were created in a response to an outbreak of what was unmistakably M.E., this new name and definition did not describe the known signs, symptoms, history and pathology of M.E. It described a disease process which did not, and could not exist. (Hooper et al. 2001, [Online]) (Dowsett n.d.a. [Online]) (Hyde 2006, [Online]) As M.E. expert Dr Byron Hyde explains:

Do not for one minute believe that CFS is simply another name for Myalgic Encephalomyelitis. It is not. The CDC 1988 definition of CFS describes a non-existing chimera based upon inexperienced individuals who lack any historical knowledge of this disease process. The CDC definition is not a disease process. It is (a) a partial mix of infectious mononucleosis /glandular fever, (b) a mix of some of the least important aspects of M.E. and (c) what amounts to a possibly unintended psychiatric slant to an epidemic and endemic disease process of major importance. Any disease process that has major criteria, of excluding all other disease processes, is simply not a disease at all; it doesn't exist. The CFS definitions were written in such a manner that CFS becomes like a desert mirage: The closer you approach, the faster it disappears and the more problematic it becomes (2006, [Online]).

As Professor Malcolm Hooper explains, ‘As a basis for sound scientific research, [CFS] has been a disaster.’ (2001, [Online]) Today there are more than nine different CFS definitions. Just like the original definition of CFS produced in 1988 however, none of these definitions defines any distinct illness, including Myalgic Encephalomyelitis. (Hyde 2006, [Online]) All each of these flawed definitions ‘define’ is a heterogeneous (mixed) population of people with various misdiagnosed psychiatric and miscellaneous non-psychiatric states which have little in common but the symptom of fatigue. (Hooper et al 2001, [Online]) (Dowsett 2001b, [Online]) This is why being diagnosed with any of the definitions of CFS is not a useful or meaningful diagnosis and why a diagnosis of CFS should never be accepted – by doctor or by patient – as an end point of the process of diagnosis.

The creation of the flawed disease category of ‘CFS’ (and the equally flawed government policies that have gone along with it) have had a devastating effect on hundreds of thousands of M.E. sufferers around the world, including young children. These very ill patients are often denied appropriate medical treatment and care, denied appropriate insurance entitlements and other medical benefits and are often accused of malingering by doctors, welfare agencies and the media (and in turn even their own friends and family). M.E. patients are also routinely recommended or forced to participate in inappropriate or harmful psychologically based interventions while basic appropriate medical care is withheld. These harmful interventions (and the lack of basic medical care) have had disastrous and long-term physical effects on many sufferers. In some cases this has resulted in death. (Hooper et al. 2001, [Online]) (Hyde 2003, [Online])

Patients with M.E. are not the only patient group to be negatively affected however. Other patient groups misdiagnosed as CFS are also denied appropriate diagnosis and treatment. They may also be subjected to inappropriate psychological interventions. Doctors, researchers and the general public are also negatively affected in various ways by this subterfuge (As explained previously in Smoke and Mirrors). The only groups which gain from the ‘CFS’ confusion are insurance companies and various other organisations and corporations which have a vested financial interest in how these patients are treated, including the government.

The only way forward for every group involved is that the disease category of ‘CFS’ must be abandoned. (Hooper 2006, [Online]) Each of the patient groups involved must be correctly diagnosed and then treated as appropriate based on legitimate and unbiased science involving the SAME patient group. People with M.E. must be diagnosed and treated for M.E. Patients with depression should be diagnosed and treated for depression. Patients with cancer should be treated for cancer, and so on. Lumping these disparate patient groups together under a vague and meaningless category of ‘fatiguing illnesses’ (or CFS) only hinders each of the patient groups involved in their battle to regain their health. (Dowsett 2001b, [Online]) (Hooper 2006, [Online]) (Hyde 2003, [Online])

What a diagnosis of ‘CFS’ actually means is that the patient has a gradual onset fatigue syndrome which is usually due to a missed major disease. i.e. the patient has:

a. Missed cardiac disease, b. Missed malignancy, c. Missed vascular disease, d. Missed brain lesion either of a vascular or space occupying lesion, e. Missed test positive rheumatologic disease, f. Missed test negative rheumatologic disease, g. Missed endocrine disease, h. Missed physiological disease, i. Missed genetic disease, j. Missed chronic infectious disease, k. Missed pharmacological or immunization induced disease, l. Missed social disease, m. Missed drug use disease or habituation, n. Missed dietary dysfunction diseases, o. Missed psychiatric disease. (Hyde 2006, [Online])

Some of the illnesses commonly misdiagnosed as ‘CFS’ include:

  • Various post-viral fatigue states/post-viral fatigue syndromes (eg. following glandular fever/mononucleosis, hepatitis, Ross river virus, Q fever, flu, measles, chickenpox, herpes and many other infections)
  • Fibromyalgia
  • Candida
  • Athlete over-training syndrome
  • ‘Burnout’
  • Multiple chemical sensitivity syndrome (MCSS)
  • Multiple sclerosis
  • Thyroid illness
  • Adrenal insufficiency
  • Localised and Metastatic malignancies
  • Brain tumours, including astrocytomas, gliomas
  • Transverse Myelitis
  • Myopathic illnesses including: Myasthenia gravis, Mitochondrial myopathies, Post-infectious polymyositis
  • Vitamin B12 deficiency disorders: Pernicious anaemia, Intentional dietary deprivation, Intestinal disease associated with or independent of M.E.
  • Rheumatoid illness or lupus (SLE)
  • Sarcoma
  • Renal or liver disease
  • Infectious illnesses including: Toxoplasmosis, AIDS, Lyme disease (Borrelia burgdorferi), Tuberculosis, Brucellosis
  • Various psychiatric and social psychiatric states including: Anxiety neurosis, Uncomplicated endogenous or reactive depression, Clinical depression, Psychopathic personality disorder, Post-traumatic stress disorder (PTSD), Schizophrenia and other psychiatric disease (Ramsay 1986, [Online]) (Ramsay 1988) (Hyde 1992, p 22) (Dowsett n.d.a. [Online]) (Hooper et al. 2001, [Online]) (Hyde 2003, [Online]) (Hyde 2006, [Online])

This is of course not a comprehensive list. M.E. expert Dr. Elizabeth Dowsett explains that, ‘There are actually 30 well documented causes of ‘chronic fatigue.’’ (n.d.a. [Online]) It should also be remembered that although none of the CFS definitions define M.E., the majority of those with M.E. will be given a CFS diagnosis by default (due to the ignorance surrounding M.E., and the confusion with ‘CFS’). Therefore the possibility that a patient misdiagnosed with CFS has authentic Myalgic Encephalomyelitis should also be investigated, along with these myriad other possibilities.

Today patients with all sorts of different illnesses are commonly misdiagnosed as having ‘CFS.’ Under cover of the bogus disease category of CFS, this diverse mix of patients are treated as if they each suffered the exact same specific illness. This is clearly unscientific, and unethical. These patients must be given the opportunity to be diagnosed correctly if they are to have any chance of appropriate treatment or recovery, not given a meaningless ‘CFS’ misdiagnosis. Patients with M.E. need this same opportunity.

Treating this diverse and heterogenous patient group as if their illnesses each shared the same symptoms, aetiology, pathology and response to treatment is inappropriate and highly unlikely to benefit the health and wellbeing of any of the patient groups involved. Treating this ‘CFS’ group as if they each shared a specific psychological or behavioural illness is also clearly inappropriate. Aside from representing a heterogenous patient group, many (likely the vast majority) of those with the diagnosis are not mentally ill, and do not suffer from behavioural problems. (This includes of course, those patients with authentic M.E.) (Hooper 2006, [Online]) (Hyde 2006, [Online]) (Hooper et al. 2001, [Online])


Smoke and Mirrors by Jodi Bassett

This paper looks at the lack of evidence (and financial and political motivations) behind the 'behavioural' model of M.E. and outlines a strategy for the resolution of the confusion caused by the 'CFS' disease category

'The disease category ‘CFS’ must be abandoned completely

Patients with fatigue (and other symptoms) caused by a variety of different illnesses need to be diagnosed correctly with these illnesses if they are to have any chance of recovery; not given a meaningless Oxford or Fukuda ‘CFS’ misdiagnosis. (Some of the conditions commonly misdiagnosed as ‘CFS’ are very well defined and well-known illnesses and very treatable – but ONLY once they have been correctly diagnosed). Patients with M.E. need this same opportunity. Each of the patient groups involved must be correctly diagnosed and then treated as appropriate based on legitimate and unbiased science involving the SAME patient group. Dr Byron Hyde explains that doctors must return to the age-old medical principals of correct diagnosis (a) careful history, (b) detailed physical examination and (c) appropriate investigation. (2006, [Online])

The name Myalgic Encephalomyelitis must be fully restored (to the exclusion of all others) and the WHO classification of M.E. must be accepted and adhered to in all official documentations and government policy. There were sound medical reasons for the creation of the name in 1956, and for the classification of the illness by the WHO in 1969; neither of which has changed in the interim. Professor Malcolm Hooper explains: The term myalgic encephalomyelitis (means muscle pain, my-algic, with inflammation of the brain and spinal cord, encephalo-myel-itis, brain spinal cord inflammation) was first coined by Ramsay and Richardson and has been included by the World Health Organisation (WHO) in their International Classification of Diseases (ICD), since 1969. The currently version ICD-10 lists ME under G.93.3 - neurological conditions. It cannot be emphasised too strongly that this recognition emerged from meticulous clinical observation and examination. (Hooper 2006, [online])'


The effects of CBT and GET on patients with Myalgic Encephalomyelitis by Jodi Bassett

'As (bad) luck would have it, graded exercise programs are probably the single most inappropriate treatment that a M.E. sufferer could be recommended to undertake. This is because one of the unique features of authentic M.E. is exercise intolerance – that patients worsen with even trivial levels of activity or exercise.

Exercise or exertion intolerance is one of the many things which separates Myalgic Encephalomyelitis so distinctly from various post-viral fatigue states or other illnesses involving 'chronic fatigue' as the defining or primary feature. People with M.E. do not improve with exercise. They cannot; exercise intolerance is a large and essential part of what M.E. is. Veteran M.E. expert Dr Ramsay explained that this unique characteristic: ‘is virtually a sheet-anchor in the diagnosis of Myalgic Encephalomyelitis and without it a diagnosis should not be made.’ (1986, [Online]).

This essential feature of M.E. is characterised by a unique form of paralytic muscle weakness whereby muscles perform normally to begin with but after even a minor degree of physical effort; three, four or five days, or longer, elapse before full muscle power is restored. This is quite distinct from the ‘chronic fatigue’ seen in many other illnesses. This paralytic muscle weakness in M.E. affects all muscles including the heart and causes what is commonly known as exercise intolerance; that patients relapse with physical and mental exertion. These features are a core part of what M.E. is as they are responsible for causing much of the symptomatology and disability associated with the illness. (Ramsay 1986, [Online]) (Hyde 2003, [Online]) (Hyde 1992 p. xi) (Hyde & Jain 1992 pp. 38 - 43) (Dowsett 2001, 2000, 1999.b, b [Online])

Doctors who have experience with M.E. (and can tell the difference between authentic M.E. and various unrelated fatigue states) and the leading M.E. experts all concur; exercise can have many harmful effects on patients both in the short- and long-term.'

This unique symptom is ONLY seen in M.E. patients.


*O*O* A New and Simple Definition of Myalgic Encephalomyelitis and a New Simple Definition of Chronic Fatigue Syndrome & A Brief History of Myalgic Encephalomyelitis & An Irreverent History of Chronic Fatigue Syndrome by Dr Byron Hyde

‘Do not for one minute believe that CFS is simply another name for Myalgic Encephalomyelitis (M.E.). It is not. Though CFS is based upon a typical M.E. epidemic, in my opinion it has always been a confused and distorted view of reality. The invention of Chronic Fatigue Syndrome has to be one of the most curious cases of inventive American scientific imperialism that one could imagine. It is my opinion that the CDC 1988 definition of CFS describes a non-existing chimera based upon inexperienced individuals who lack any historical knowledge of this disease process. The CDC definition is not a disease process.’

*HIGHLY RECOMMENDED*


*O* Information on Myalgic Encephalomyelitis (M.E.)/Chronic Fatigue Syndrome (CFS) by Jill McLaughlin

ME/CFS is similar to other illnesses such as multiple sclerosis, lupus, Lyme disease, mononucleosis, Gulf War Syndrome. CFS may overlap or co-exist with fibromyalgia, multiple chemical sensitivities, irritable bowel syndrome.

However, these may co-exist with other conditions as well and are viewed as separate entities which stand on their own, regardless of whether a person has other medical problems. Even though there are similarities or overlap does not mean that they represent the same etiological or pathobiological process.


*O* SCIENCE or SEMANTICS? By Margaret Williams

"In spite of some overlap, FM and ME/CFS do not represent the same syndrome."


*O* Dr Paul Cheney on heart issues

'Next, the NJ team looked to see if there were any symptoms that were 100% observable in the group of disabled cases, but not in the others. They found that there was only one symptom (among the loooong list of CFIDS symptoms) that was seen in 100% of the patients with the Q problem. Only one. Post-exertional [illness exacerbation and realpse]. That is, when you push yourself physically, you get worse.

What distinguishes CFIDS from FM? Post-exertional  [illness exacerbation and realpse]. Patients who have FM, but not CFIDS, can exercise—it helps them. FM patients do not have a Q problem. MCS patients do not have a Q problem. They do have other issues that overlap with CFIDS. However, Q is what separates them. CFIDS patients have a big Q problem, and post-exertional [illness exacerbation and realpse] is the one symptom that correlates with Q.  


ME/CFS can be distinguished from FMS patients by the confirmed breakdown of one of the body's antiviral defense pathways.  It is interesting that if a patient meets both the criteria for ME/CFS and FMS, her/his test results will be that of  an ME/CFS patient.

While approximately 75% of ME/CFS patients also meet the criteria for FMS, only a relatively small number of FMS patient meet the criteria for ME/CFS.  This is reflected in the much higher prevelance of FMS.  Appoximately 422 per 100,000 or 0.42% of adults meet the criteria for ME/CFS,  whereas 3 - 10 % (depending on the study)  of the adult population have FMS.


Dr Darrel Ho-Yen of Scotland, (a well respected M.E. researcher and virologist) was published in the British Medical Journal in 1994:

The distribution and number of tender points in fibromyalgia are different from the chronic fatigue syndrome, and the management of the two conditions is different.  Patients with (ME/CFS) should be advised not to increase their activities gradually until they feel 80% of normal, whereas patients with fibromyalgia may benefit from a regime of increasing activity.  (BMJ 1994:309:1515).


Myalgic Encephalomyelitis / Chronic Fatigue Syndrome and Fibromyalgia:additional considerations for the MRC in relation to the PACE trials by Margaret Williams, 5th January 2005

Of foremost significance is the fact that fibromyalgia is classified as a distinct entity in ICD-10 at section M79.0 under Soft Tissue Disorders and it is not permitted for the same condition to be classified to more than one rubric, since ICD categories are mutually exclusive. The literature itself is quite clear about this distinction, stating that up to 70% of those with ME/CFS have concurrent FM, and those who have both FM and ME/CFS have worse physical functioning than those who have ME/CFS alone.

Some illustrations from the literature make these distinctions clear:

1991:  in spite of some overlap, FM and ME/CFS do not represent the same syndrome.  (Primary fibromyalgia and the chronic fatigue syndrome.  AJ Wysenbeek et al   Rheumatology Int 1991:10:227-229)

1996:  “fibromyalgia appears to represent an additional burden of suffering amongst those with (ME)CFS”   (Fibromyalgia and Chronic Fatigue Syndrome – similarities and differences.  Dedra Buchwald and Deborah Garrity.  Rheum Dis Clin N Am 1996:22:2:219-243)

1997:   levels of somatomedin C are lower in FM patients but higher in ME/CFS patients  (Somatomedin C (insulin-like growth factor) levels in patients with CFS.  AL Bennett, AL Komaroff et al. J psychiat Res 1997:31:1:91-96)

1998:   “recent studies suggest that (co-existent FM and (ME)CFS) may bode much more poorly for clinical outcome than CFS alone.  In contrast to (significantly) elevated CBG (cortisol binding globulin) levels in patients with CFS, no differences were observed in FM patients. Differences in secretion of AVP may explain the divergence of HPA axis function in FM and (ME)CFS”  (Evidence for and Pathophysiologic Implications of HPA Axis Dysregulation in FM and CFS.  Mark A Demitrack and Leslie J Crofford.  Ann New York Acad Sci 1998:840:684-697)

1998:  there is no evidence for elevated Substance P in patients with ME/CFS, whereas levels are elevated in patients with FM   (CFS differs from FM.  No evidence for altered Substance P in cerebrospinal fluid of patients with CFS.  Evengaard B et al  Pain 1998:78:2:153-155)

2001:  patients with FM are *NOT* acetylcholine sensitive (Investigation of cutaneous microvascular activity and flare response in patients with fibromyalgia.   AW Al-Allaf, F Khan, J Moreland, JJF Belch.  Rheumatology 2001:40:1097-1101)

2004: patients with ME/CFS *ARE* acetylcholine sensitive  (Acetlycholine mediated vasodilatation in the microcirculation of patients with chronic fatigue syndrome.  VA Spence, F Khan, G Kennedy, NC Abbot, JJF Belch   Prostaglandins, Leukotrienes and Essential Fatty Acids 2004:70:403-407)

2003:  endothelin-1 is *RAISED* in fibromyalgia  (Increased plasma endothelin-1 in fibromyalgia syndrome.  Pache M,  Ochs J et al  Rheumatology 2003:42:493-494)

2004:   endothelin-1 is *NORMAL* in ME/CFS  (Plasma endothelin-1 levels in chronic fatigue syndrome.   Kennedy G, Spence V, Khan F, Belch JJF   Rheumatology 2004:43:252-253)

Consultant rheumatologists who have sufficient experience with both syndromes have observed clinically that in FM, the muscle pain is helped by gentle stretching and exercise, whereas in ME/CFS, exercise makes muscle pain worse.


No evidence for elevated Substance P levels in cerebrospinal fluid of patients with CFS

Background: Substance P (SP) is a neuropeptide involved in the neurotransmission of pain from periphery to the central nervous system. It has been reported that SP in the cerebrospinal fluid is markedly elevated in patients with Fibromyalgia. As Fibromyalgia and CFS are conditions which share some symptoms, we wanted to investigate the levels of SP in the cerebrospinal fluid of CFS patients. Methods: Cerebrospinal fluid was obtained from 15 patients (9 women, average age 39.3 years) fulfilling CDC-criteria for CFS but not for Fibromyalgia. The sample was immediately centrifuged at +4°C for 10 min. at 1000g to remove cells. Rapid cooling was performed. The sample was stored in plastic cryogenic tubes and stored frozen at -70°C. An radioimmunoassay was used to analyze the sample. For comparison, cerebrospinal fluid drawn from 13 patients with cerebrovascular disease (7 women, average age 65 years) was treated and analyzed in the same manner. All samples were analyzed blindly. Results: All values of SP of the CFS patients were within previously reported normal range of SP in cerebrospinal fluid. In the control group, 2 patients had slightly increased values. Conclusion: The results support the notion that FM and CFS are different disorders in spite of overlapping symptomatology.


Specific oxidative alterations in vastus lateralis muscle of CFS patients Fulle S, Mecocci P, Fano G, Vecchiet I, Vecchini A, Racciotti D, Cherubini A, Pizzigallo E, Vecchiet L, Senin U, Beal MF Free Radic Biol Med 2000 Dec 15;29(12):1252-1259 Lab. Interuniversitario di Miologia, Dip. Biologia Cellulare e Molecolare, Universita di Perugia, Perugia, Italy

Although a specific defect in muscle metabolism has not been clearly defined, yet several studies report altered oxidative metabolism. In this study, we detected oxidative damage to DNA and lipids in muscle specimens of CFS patients as compared to age-matched controls, as well as increased activity of the antioxidant enzymes catalase, glutathione peroxidase, and transferase, and increases in total glutathione plasma levels.

From these results we hypothesize that in CFS there is oxidative stress in muscle, which results in an increase in antioxidant defenses. Furthermore, in muscle membranes, fluidity and fatty acid composition are significantly different in specimens from CFS patients as compared to controls and to patients suffering from fibromyalgia.

These data support an organic origin of CFS, in which muscle suffers oxidative damage.


Peripheral cholinergic function in humans with chronic fatigue syndrome, Gulf War syndrome and with illness following organophosphate exposure Khan F, Kennedy G, Spence VA, Newton DJ and Belch JJF Vascular Diseases Research Unit, The Institute of Cardiovascular Research, University of Dundee

Aims: In the present study, we have investigated whether the peripheral cholinergic abnormalities that we have reported previously [Spence et al. Am J Med 2000; 108: 736–9] in patients with chronic fatigue syndrome (CFS) are also present in those with Gulf War syndrome (GWS) and agricultural workers exposed to organophosphate pesticides, where cholinesterase inhibition is specifically implicated. We also looked at whether these abnormalities might be due to a reduction in the activity of cholinesterase expressed on the vascular endothelium. Methods and Results: We used laser Doppler imaging to measure the forearm skin blood flow responses to iontophoresis of acetylcholine and of methacholine (which is resistant to breakdown by cholinesterase) in patients with CFS, GWS and those with a history of ill health after definite organophosphate exposure, as well as in matched healthy controls. The response to acetylcholine was significantly higher in patients with CFS than in controls (P=0.029, repeated-measures ANOVA), but was normal in those with GWS and those exposed to organophosphates. The methacholine response was higher than the acetylcholine response in all patient groups except for those with CFS, where there was no difference between the responses. Conclusions: Although there are many clinical similarities between these three illnesses, our results indicate peripheral cholinergic abnormalities in the vascular endothelium of only patients with CFS, suggesting that this syndrome has a different aetiology, which might involve inhibition of vascular cholinesterase.


Cardiovascular response to upright tilt in fibromyalgia differs from that in chronic fatigue syndrome. Naschitz JE, Rozenbaum M, Rosner I, Sabo E, Priselac RM, Shaviv N, Ahdoot A, Ahdoot M, Gaitini L, Eldar S, Yeshurun D. Departments of Internal Medicine A, Rheumatology, Anesthesiology, and Surgery, Bnai Zion Medical Center and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.

OBJECTIVE: To compare the cardiovascular response during postural challenge of patients with fibromyalgia (FM) to those with chronic fatigue syndrome (CFS). METHODS: Age and sex matched patients were studied, 38 with FM, 30 with CFS, and 37 healthy subjects. Blood pressure (BP) and heart rate (HR) were recorded during 10 min of recumbence and 30 min of head-up tilt. Differences between successive BP values and the last recumbent BP, their average, and standard deviation (SD) were calculated. Time curves of BP differences were analyzed by computer and their outline ratios (OR) and fractal dimensions (FD) were measured. HR differences were determined similarly. Based on the latter measurements, each subject's discriminant score (DS) was computed. RESULTS: For patients and controls average DS values were: FM: -3.68 (SD 2.7), CFS: 3.72 (SD 5.02), and healthy controls: -4.62 (SD 2.24). DS values differed significantly between FM and CFS (p < 0.0001). Subgroups of FM patients with and without fatigue had comparable DS values. CONCLUSION: The DS confers numerical expression to the cardiovascular response during postural challenge. DS values in FM were significantly different from DS in CFS, suggesting that homeostatic responses in FM and CFS are dissimilar. This observation challenges the hypothesis that FM and CFS share a common derangement of the stress-response system.


 
Somatomedin C (insulin-like growth factor I) levels in patients with chronic fatigue syndrome. Bennett AL, Mayes DM, Fagioli LR, Guerriero R, Komaroff AL. Journal of Psychiatric Research 1997; 31(1): 91-96.

Abstract: Chronic fatigue syndrome is a disorder clinically quite similar to fibromyalgia syndrome, and it is of interest to examine if these two syndromes have pathogenetic as well as clinical features in common. Somatomedin C levels have been found to be lower in patients with fibromyalgia syndrome than in healthy controls. An attractive hypothesis relating sleep disturbance, altered somatotropic neuroendocrine function and fibromyalgia symptoms has been put forward as a plausible pathogenic mechanism for fibromyalgia syndrome. We therefore sought to investigate the level of somatomedin C in patients with chronic fatigue syndrome. Somatomedin C levels were determined by radioimmunoassay in frozen serum specimens from 49 patients with CFS and 30 healthy blood donor control subjects of similar age and gender. Somatomedin C levels were higher in patients with CFS than in healthy control subjects (255.3 ± 68.5 vs 211.9 ± 76.2, P = 0.01). There was no effect of gender, use of nonsteroidal anti-inflammatory drugs or tricyclic drugs on levels of somatomedin C. There was a tendency for somatomedin C levels to fall with age. In contrast to patients with fibromyalgia, in whom levels of somatomedin C have been found to be reduced, levels in patients with CFS were found to be elevated. Thus, despite the clinical similarities between these two conditions, they may be associated with different abnormalities of sleep and/or of the somatotropic neuroendocrine axis.

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The book 'Caring For The M.E. Patient' by Jodi Bassett includes a Foreword by international M.E. expert Dr Byron Hyde.

He writes:

"There is so much false information that is picked up and disseminated it is near impossible to hold one’s head above the water and sift through this morass of misinformation. Any attempt to seek the truth is always a major difficulty. Somehow, Jodi Bassett and Hummingbird have managed to plow through this field of weeds."

"This is a book that deserves being read, not only by patients and physicians with an interest in M.E. but the bureaucrats in the USA Centers for Disease Control who have done so much damage to the understanding of M.E. I recommend her book to all and wish it every best success."

Paperback $18.95
Hardcover $22.95