THE CARER TIMES

THE FUTURE OF ME SERVICES

What people with ME need and have always wanted , is a biomedical service based upon clear , fundamental values that validate the physical disease and multisystem dysfunction. They have never wanted a therapy-led, psychosocial service.

Without the separation of Myalgic Encephalomyelitis , as defined by the Canadian Criteria and Chronic Fatigue, loosely defined within the Oxford Criteria, patients with ME and specifically the most severely affected, will continue to receive an inadequate or no service at all, while the people, easily treated by CBT and a therapy clinic will continue to dilute the reality of this serious disease .

The urgent biomedical need is for tests and new treatments to be developed and provided on the NHS.

What is going so wrong ?

The severely affected will continue to be neglected all the time that the emphasis is on management techniques. With severe multi system dysfunction , they need investigations, including PECT and SPECt scans, fat biopsies, blood tests etc and other specific ME tests that are not currently available on the NHS and new treatments that will attempt to alleviate the suffering and combat the disease process.

Where does the misunderstanding come from?

The terms Chronic Fatigue Syndrome (CFS) and Myalgic Encephalomyelitis (ME) cover a condition or a group of conditions which manifest in many different ways but have some common features. This is potentially seriously misleading : the desire to treat ME and CFS as one illness belongs to the Wessely School. Given the hostile political climate it must be explained that while just about all patients with M.E. will fit the definition for CFS, not all of those with CFS will fit the definition for M.E. As Dr Byron Hyde explains : Where the one essential characteristic of M.E. is acquired CNS[central nervous system] dysfunction, that of CFS is primarily chronic fatigue."

ME has been classified by the WHO as a neurological disorder since 1969 (currently in WHO ICD-10 at G93.3, with "post-viral fatigue syndrome" as a synonym). Since 1992 "Chronic Fatigue Syndrome" (CFS) has been indexed only to G93.3 as an alternative name for ME, hence the use of the term "ME/CFS" adopted by The International Association of ME/CFS (although many international research papers use the single term "CFS").

The international evidence-base is that ME/CFS is a serious, inflammatory multi-system disorder with well-documented abnormalities in the central nervous system, the autonomic nervous system, the cardiovascular, respiratory, neuroendocrine, immune and gastro-intestinal systems, with convincing evidence of muscle pathology, defects in gene expression, specific HLA antigen expression, and with irrefutable evidence of chronic inflammation.

Moreover, since 2008 the US Government (which co-funded the assay research with $1 million) has, after eight years, accepted a specific assay as a proven biomarker for all autoimmune diseases which, according to some researchers, means it has been proven that ME/CFS is an autoimmune disease

The greatest myth of them all

The prevailing orthodoxy , that research on ME is so incomplete that there is continuing uncertainty as to whether the term encompasses one condition or several and where, if anywhere, the divisions lie with other diagnoses such as Fibromyalgia or Post Viral Fatigue Syndrome, is incredibly misleading .

It must be stressed that despite the absence of a definitive test, ME/CFS is clinically recognisable. Professor Nancy Klimas has stated : "There are diagnostic criteria that enable clinicians to diagnose (ME)CFS in the primary care setting" (CDC Press Conference to launch the (ME)CFS Toolkit, November 2006) which enable all conscientious clinicians to feel confident in making the diagnosis."

Although there is as yet no definitive test, there are numerous accredited biomarkers of pathology in ME all of which lend support to the diagnosis.

As stated by Dr Suzanne Vernon , there are now over 5,000 worldwide peer-reviewed scientific papers (and numerous textbooks) showing that ME/CFS is a complex multi-system disorder involving demonstrable pathology not only of the central and autonomic nervous systems but also of the immune, cardiovascular and endocrine systems, and that on-going inflammation is a significant feature, with damage to skeletal and cardiac muscle as well as to other end organs including the pancreas and liver.

Recent research proves that ME is a serious physical disease

Recent scientific research has revealed that there are known biomarkers for ME/CFS. From a comprehensive list of 30,000 peptides, 738 proteins were found only in (ME)CFS subjects' cerebrospinal fluid (ie. not in normal controls or other disorders), which the authors contend adds to the ever-increasing number of biomarkers for ME/CFS (Schutzer SE et al; PloS ONE 6(2): e17287. doi:10.1371.journal.pone.0017287).

Many other such biomarkers exist for the identification of ME/CFS.

For many years research has shown evidence of enterovirus (Coxsackie B) in the tissues of people with ME/CFS, which was roundly dismissed by Wessely School psychiatrists. More recent work of Douche-Aourik F et al (Journal of Medical Virology 2003:71:540-547) confirmed earlier work: " Enterovirus RNA has been found previously in specimens of muscle biopsy from patients with ME. These results suggest that skeletal muscle may host persistent enteroviral infection. The presence of viral RNA is in favour of a persistent infection involving defective viral replication ".

Research has continued to provide evidence of long-term enteroviral persistence in the face of the adaptive immune response: "This previously unknown and unsuspected aspect of enterovirus replication provides an explanation for previous reports of enteroviral RNA detected in diseased tissue in the apparent absence of infectious viral particles" (Human Enterovirus and Chronic Infectious Disease. Steven Tracy and Nora M Chapman. Journal of IiME 2009: 3:1).

A recent paper reported that biopsy of muscle fibres in ME/CFS showed that fibre-type proportion was "significantly altered in (ME)CFS samples" and concluded: "Taken together, these results support the view that muscle tissue is directly involved in the pathogenesis of (ME)CFS" (Int J Immunopathol Pharmacol 2009:22(2):427-436).

Another recent paper demonstrated that a large percentage (95%) of patients clinically diagnosed with (ME)CFS have elevated levels of the IgM isotope to CL (cardiolipin), suggesting that acute phase lipids may be part of disease pathogenesis in patients with (ME)CFS.

These lipids may be analogous to acute phase proteins triggered by cytokines involved in the inflammatory processes in the liver, such as C-reactive protein and serum amyloid A (which have been reported in ME/CFS and other diseases attributed to toxic chemicals). The authors note that a survey of the literature reports ACAs (anticardiolipin antibodies) as common serological markers in many diseases, including diseases resulting from viruses and chemical exposure, as well as autoimmune diseases such as multiple sclerosis and lupus erythematosus.

The authors conclude that (ME)CFS may be an autoimmune disease, and that classification of it as such may serve to increase the availability options for patients suffering from the disease. They confirm that experiments are under way to elucidate why ACAs are produced in (ME)CFS, and that these studies are investigating the effects of specific chemical agents on mitochondrial metabolic pathways that are indicative of blocked energy production as occurs in (ME)CFS (Yoshitsugi Hokama et al. J Clin Lab Anal 2009:23:210-212).

Yet more research has shown that (ME)CFS is an autoimmune disorder: Ortega-Hernandez et al looked at the influence of autoantibodies, polymorphisms in the serotonin pathway, and HLA Class II genes in relation to (ME)CFS, and tested autoantibodies to different components of the central nervous system. They conclude: "Our results reveal that in (ME)CFS, like other autoimmune diseases, different genetic features are related to age at onset and symptoms"(Ann N Y Acad Sci 2009:1173:589-599).

Blaney et al looked at a number of chronic and autoimmune conditions (including multiple sclerosis, lupus, fibromyalgia and (ME)CFS) and demonstrated the use of 1,25-D (1,25-dihydroxyvitamin D3) as a clinical marker in autoimmune conditions, with results that "showed a strong positive association between these autoimmune conditions and levels of 1,25- D greater than 110 pmol/L", noting that high levels of 1,25-D may result when dysregulation of the vitamin D receptor prevents it from expressing enzymes necessary to keep 1,25-D in a normal range (Ann N Y Acad Sci 2009: 1173:384-390).

It has long been known that the resting energy expenditure (REE) in ME/CFS patients is abnormally high (see, for example: J Neurol Sci 1997:150:S225; JCFS 1998:4:4:3-14; Medical Hypotheses 2000:54: (1):59-63). When individual resting energy expenditure (REE) was predicted on the basis of total body potassium values, 45.5% of the (ME)CFS patients tested had resting energy expenditure above the upper limit of normal, suggesting that there is upregulation of the sodium-potassium pump in (ME)CFS. There was no evidence that the results were due to lack of activity (which would have affected total body water estimates). Given that the energy expended at rest by the ME/CFS patient is significantly elevated when compared with controls, it is not difficult to understand what may be the result when the ME/CFS patient is subjected to even minimal exercise.

Confirmation that the UK Government recognises that ME is a real physical disease

ME was recognised as a specific disease entity by The Royal Society of Medicine in 1978 and was recognised as an organic disease by the Department of Health in November 1987. On the 25th November 2008, the Northern Ireland Minister for Health, Social Services and Public Safety, admitted that ME is "a very real and debilitating neurological condition". On 23rd February 2010, in an Adjournment debate on ME, Gillian Merron, Minister of State (Public Health), Department of Health, stated:"I want first to put on the record that we accept the World Health Organisation's classification of ME as a neurological condition of unknown cause.". On 28th May 2010, Kay Ellis confirmed on behalf of the UK Chief Medical Officer: " The Department's view is that it is important to recognise that CFS/ME is a genuine and disabling neurological illness and health professionals must recognise it as such".

On 11th October 2010, in a debate on ME in the House of Lords, the Countess of Mar asked the noble Earl , the Parliamentary Under Secretary of State for Health, (Earl Howe) whether the coalition accepts that CFS/ME is a neurological condition and he replied that the " Government accepts that it is a neurological condition". On 19th June 2008, Stephen Atkinson on behalf of the Department of Health confirmed:"I would like to assure you that the Department recognises CFS/ME as a neurological disease"". On Feb 2nd 2011 Paul Burstow, Minister of State, Department of Health, in response to Ian Swales MP, confirmed that there is :"strong international consensus that CFS/ME is a chronic and disabling neurological illness. I want to stress that it is a neurological illness; it is not a mental health problem " .

The severity of ME has been compared to : to late stage AIDS , chronic obstructive lung disease and end stage renal failure .

ME has been documented in the medical literature from 1934. The Wallis description of ME (not Chronic Fatigue Syndrome, known as CFS) was in 1957. Sir Donald Acheson's (a former UK Chief Medical Officer) major review of ME was in 1959. In 1962, the distinguished neurologist Lord Brain included it in the standard textbook of neurology.

ME has been formally classified by the World Health Organisation as a neurological disorder in the International Classification of Diseases (ICD) since 1969 (ICD-8: Vol I: code 323, page 158; Vol II (Code Index) page 173). On 7th April 1978 the Royal Society of Medicine held a symposium on ME at which ME was accepted as a distinct entity. The symposium proceedings were published in The Postgraduate Medical Journal in November that same year. The Ramsay case description was published in 1981. Since 1989, the Medical Information Service of the British Library has produced quarterly updates on the disorder: these updates (known as CATS, or Current Awareness Topics) compile published international research and clinical evidence about the condition and contain abstracts of published articles.

The Centres for Disease Control (the US federal agency charged with the containment of diseases and known internationally as the CDC) designates it for funding status as "A serious legitimate diagnosis CDC PRIORITY 1 disease of public health importance".

The large and significant published international evidence-base that ME/CFS is a legitimate medical disorder with numerous reproducible biomarkers of organic pathologyhas been consistently buried in the UK by "Wessely School" psychiatrists (so named after its leading activist Professor Simon Wessely) who have vested interests in promulgating their own hypothesis that ME is nothing but an "aberrant illness belief" that is best managed by compulsory "behavioural rehabilitation" regimes.

According to the CDC, as many as 900,000 Americans have (ME)CFS.(To put this in a UK perspective: 130 cases per 100,000 equates to 78,000 people out of the UK population of 60 million and 2,600 cases per 100,000 equates to 1,560,000 out of the UK population of 60 million; by comparison, 83,000 people out of the UK population of 60 million suffer from multiple sclerosis, which is 139 cases per 100,000).