Next APPG on ME meeting: Delay in production of the Minutes

Heather Walker, Communications Manager, Action for M.E. has advised me, this morning, that the minutes of the last meeting will be delayed.

Shortlink: http://wp.me/p5foE-2qt

Ms Walker writes @ 25 November

On behalf of the APPG on ME Secretariat, my apologies for the delay in the production of minutes of the last meeting.

We are still awaiting arrival of the verbatim transcript, kindly produced by a Hansard stenographer, on which the minutes are based.

As has been pointed out, the APPG has a policy that any comments on the APPG minutes and transcript be sent in to the APPG Secretariat one week before the meeting. The meeting scheduled for Wednesday the 2nd of December would therefore indicate a deadline for comments and amendments to be submitted by Wednesday the 25th of November

The delay means the usual procedure will have to be changed – what to will depend on when the transcript and minutes become available.

We will circulate them as soon as possible.

Meanwhile, the agenda for next week’s meeting is as follows:

1. Welcome by the Chairman
2. APPG Report on the Inquiry into NHS Services
3. Speaker: Mike O’Brien MP, Minister of State for Health Services
4. Minutes of the last meeting
5. Matters arising

- APPG legacy paper (in preparation for the General Election)

- New research: murine leukaemia virus-related virus (XMRV)

- Accessibility of venues for future meetings

6. Welfare update

- Employment and Support Allowance

- Welfare Reform Bill

7. Any other business

8. Date of next meeting

Heather Walker

Communications Manager
Action for M.E
Direct line: 0117 930 1323

Action for M.E. is the leading charity dedicated to improving the lives of people affected by M.E.
Action for M.E., Canningford House, 38 Victoria Street, Bristol BS1 6BY, 0117 927 9551
Registered charity number: 1036419. Registered in Scotland: SCO40452
www.afme.org.uk

The Role of Viruses in ME/CFS, XMRV and the MRC PACE Trial: Margaret Williams 21 November 2009

The Role of Viruses in ME/CFS, XMRV and the MRC PACE Trial – Margaret Williams – 21st November 2009

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Permission to Repost

Note:  This is a long and heavily formated document and I am posting only the introduction here:

The full document can be accessed here on MEActionUK website:

http://www.meactionuk.org.uk/The-role-of-viruses-in-ME.htm

http://tinyurl.com/ykjveep

http://www.meactionuk.org.uk/The-role-of-viruses-in-ME.pdf

http://tinyurl.com/y8m8s8h

The role of viruses in ME/CFS: what, if any, will be the effect of the discovery linking XMRV to ME/CFS on the MRC PACE Trial?

by Margaret Williams

21 November 2009

For decades it has been known and shown that viruses play a role in ME/CFS; some illustrations from the literature are provided below (all of which are relevant and significant).

In relation to “CFS”, the most-studied viruses have been the Epstein-Barr Virus (EBV) and the Human Herpes Virus-6 (HHV-6). In relation to “pure” ME, the most studied viruses (and for which there is extensive evidence) have been the enteroviruses, usually Coxsackie B (CBV). Some illustrations from the literature of the role that viruses play in ME/CFS are provided at the end of this paper; all are significant.

There is increasing awareness that the dysregulated immune system that is a hall-mark of ME/CFS allows multiple latent viruses and microbial agents to become reactivated (Co-Cure NOT:12th November 2009).

Moreover, recent research has shown that even viruses which were hitherto believed not to persist after an acute infectious episode are capable of long-term viral persistence.

Nora Chapman et al from the Enterovirus Research Laboratory, Department of Pathology and Microbiology, University of Nebraska Medical Centre, have shown that human enteroviruses Coxsackie B can naturally delete sequence from the 5’ end of the RNA genome and that this deletional mechanism results in long-term viral persistence, which has substantially altered the previously held view

(http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2440640/?tool=pubmed ). In a specially commissioned piece for the charity Invest in ME, the researchers say: “This previously unknown and unsuspected aspect of enterovirus replication provides an explanation for reports of enteroviral RNA detected in diseased tissue in the apparent absence of virus particles” (Journal of IiME 2009:3:1).

Dr John Chia, an infectious diseases specialist from Torrance, California, who specialises in ME/CFS, is on record: “I believe that the main reason (ME)CFS patients are symptomatic is due to continuing inflammatory response toward viruses living within the cells, enteroviruses in most of the cases I see. We have clearly documented certain enterovirus infections triggering autoimmune responses in some patients…Can you imagine how we would feel if there are viruses surviving in our muscles, brains, hearts and gastrointestinal tracts triggering ongoing immune responses?”  
(http://aboutmecfs.org/blog/?p=865 ).

The CFIDS Chronicle (Research Update, Summer 1993) explained viruses and retroviruses as follows:

“A virus is a microscopic organism that lives within the cells of another living organism. Viruses cause disease at the most basic level, by damaging the cells of living things. By themselves, viruses are lifeless particles incapable of reproduction, but once they enter the cell of another living thing they become active organisms that can multiply hundreds of times.

“Viruses are comprised of two parts – a core of either deoxyribonucleic acid (DNA) or ribonucleic acid (RNA) and a protective envelope of protein. RNA viruses are smaller than DNA viruses and sometimes contain a special enzyme called reverse transcriptase which allows them to convert RNA to DNA. These specialised viruses are known as retroviruses and have a unique ability to merge with the host’s own genetic material.

“Retroviruses have the unique ability to replicate themselves by (i) making a double-stranded DNA copy called a ‘pro-virus’ once they enter living cells. Pro-viruses integrate themselves into the human chromosome and become part of the host’s genetic code (ii) alter the host’s immune response by evading detection as a ‘hidden invader’ (iii) remain hidden and latent, spliced within the host’s DNA, for long periods of time. Retroviruses are known to be potent stimulators of cytokines”.

On 8th October 2009 the premier journal Science published a paper online showing a direct link between a retrovirus and ME/CFS (Detection of infectious retrovirus XMRV, in blood cells of patients with chronic fatigue syndrome. Lombardi VC, Ruscetti FW, Peterson DL, Silverman RH, Mikovits JA et al) which caused global reverberations.

However, this was not the first time that a retrovirus had been associated with ME/CFS.

In 1991, using polymerase chain reaction and in situ hybridisation, Dr Elaine De Freitas, a virologist at the Wistar Institute, Philadelphia (which is America’s oldest independent institution devoted to biological research) and Drs Daniel Peterson, Paul Cheney, David Bell et al found such an association (Retroviral sequences related to human T-lymphotropic virus type II in patients with chronic fatigue immune dysfunction syndrome. Proc Natl Acad Sci USA 1991:88:2922-2926). It is notable that co-author Hilary Koprowski is a distinguished virologist and Professor Laureate who was Director of the Wistar Institute from 1957-1991; he is a member of the US National Academy of Sciences and is Director of the Centre for Neurovirology at Thomas Jefferson University.

Before publication, the findings were presented on 4th September 1990 by Elaine De Freitas at the 11th International Congress of Neuropathology in Kyoto, Japan.

Ten days later, on 14th September 1990 Dr Peter White (as he then was) and other members of the Wessely School dismissed the findings: “in the vast majority of CFS cases there is a psychological component. About 75% of CFS sufferers are clinically depressed, according to Peter White, senior lecturer in the department of psychiatric medicine at St Bartholomew’s Hospital in London. White said he believes depression is often a cause, rather than a consequence, of CFS…Les Borysiewicz, a clinical virologist at Addenbrookes Hospital in Cambridge (now Chief Executive of the MRC, having succeeded Professor Colin Blakemore) (said) ‘Whatever causes CFS, it isn’t the virus itself’…Anthony Clare, psychiatrist and medical director of St Patrick’s Hospital in Dublin (now deceased), pointed out that…there have been many ‘fatigue’ diseases with shifting causes: ’Neurasthenia, food allergies, now viruses. Some people would always rather have a disease that might kill them than a syndrome they have to live with’ ” (Science 1990:249:4974:1240).

In their PNAS article that was published in April 1991, De Freitas et al noted that chronic fatigue immune dysfunction syndrome (CFIDS) “may be related or identical to myalgic encephalomyelitis” and examined adult and paediatric CFIDS patients for evidence of human retroviruses (HTLV types I and II). As the CFIDS Chronicle article noted, the Wistar team looked at the peripheral blood DNA to see if they could find messenger RNA (mRNA) encoding for a viral segment of the HTLV-II virus.

At that time, known human retroviruses were the human immunodeficiency viruses 1 and 2 (HIV-1 and HIV-2) which are known to cause AIDS, and human T-lymphotropic viruses HTLV-I which causes lymphoma and HTLV-II which causes leukaemia (Hunter-Hopkins ME-Letter, October 2009). The four segments of the HTLV-II virus are referred to as the env, gag, pol and tax.

After a two year study, De Freitas et al provided evidence for HTLV-II-like infection of blood cells from CFIDS patients (and also to a lesser extent from people closely associated with them). This evidence was further substantiated by patient reactivity to proteins with the molecular weights reported for HTLV-I and HTLV-II antigens.

In their article, De Freitas et al said: “The frequency of these antibodies in CFIDS patients compared with healthy non-contact controls suggests exposure / infection with an HTLV-like agent rare in healthy non-contact people”.

Following the Wistar findings, researchers at the US Centres for Disease Control (CDC) allegedly attempted to replicate De Freitas’ work but failed to do so; this was suggested to be because certain scientists appeared eager to discount any possibility of a retroviral association with CFIDS. De Freitas defended her work and insisted that the CDC investigators had modified her assays, with the result that her work could not be replicated by the CDC.

De Freitas was publicly discredited; her research funding was discontinued and her research abandoned; she was subjected to what appeared to be attempts to destroy her professional reputation. Commenting on the subsequent discovery of XMRV (see below), ME/CFS expert Dr Paul Cheney of The Cheney Clinic was unambiguous: “Her work was unfortunately assaulted by the CDC. Her proposal to fly to the CDC in Atlanta to physically run the assays side by side with the CDC scientists was dismissed by the CDC” (http://cheneyclinic.com/a-retrovirus-called-xmrv-is-linked-to-cfs/538  ).

Read full article here:

http://www.meactionuk.org.uk/The-role-of-viruses-in-ME.htm

http://tinyurl.com/ykjveep

http://www.meactionuk.org.uk/The-role-of-viruses-in-ME.pdf

http://tinyurl.com/y8m8s8h

APPG on ME: Agenda meeting 2 December 2009

APPG on ME: Agenda meeting 2 December 2009

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The APPG on ME maintains a website here: http://www.appgme.org.uk

Agenda APPG for ME 2 Dec 2009

APPG agenda 02/12/2009

19 December 2009

The next meeting of the All Party Parliamentary Group (APPG) on M.E. will be held 3.15-4.45pm, Wednesday 2 December 2009 in Committee Room 15, House of Commons.

1. Welcome by the Chairman

2. APPG Report on the Inquiry into NHS Services

3. Speaker: Mike O’Brien MP, Minister of State for Health Services

4. Minutes of the last meeting

5. Matters arising

- APPG legacy paper (in preparation for the General Election)

- New research: murine leukaemia virus-related virus (XMRV)

- Accessibility of venues for future meetings

6. Welfare update

- Employment and Support Allowance

- Welfare Reform Bill

7. Any other business

8. Date of next meeting

Prof Peter D White: Neurology and Psychiatry SpRs Teaching Weekend

Prof PD White: Neurology and Psychiatry SpRs Teaching Weekend

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14 November 2009

THE BRITISH NEUROPSYCHIATRY ASSOCIATION

http://www.bnpa.org.uk

http://bnpa.org.uk/doc/HANDBOOK.pdf

Neurology and Psychiatry SpRs Teaching Weekend

12 to 14 December 2008 St Anne’s College – Oxford

THE ESSENTIALS OF NEUROPSYCHIATRY

Presentations:

[...]

09:50 Chronic fatigue syndrome: neurological, psychological or both?

Peter White, Professor of Psychological Medicine, Barts and the London Medical School

The extract I am appending is a summary of Professor Peter Denton White’s presentation (Page 46 of PDF) in which he talks about the taxonomy of CFS “being a mess”.

During his Royal Society of Medicine “CFS” Conference presentation, in April 2008, White had said, ominously:

“…So ICD-10 is not helpful and I would not suggest, as clinicians, you use ICD-10 criteria. They really need sorting out; and they will be in due course, God willing.”

See unofficial transcript of part of White’s RSM presentation, here, in which he presents his thoughts on current ICD taxonomy:

Prof Peter White discouraging RSM Conference from using ICD-10: http://tinyurl.com/PDW-RSM-ICD-10

In an April 2009 paper, co-authored by White, the authors propose a change to current ICD-10 codings:

http://www.ncbi.nlm.nih.gov/pubmed/19366500

Psychological Medicine Preprint “Risk markers for both chronic fatigue and irritable bowel syndromes: a prospective case-control study of primary care”

In the section “Implications for Further Research” the authors state that because the paper finds that:

“These data also suggest that fatigue syndromes are heterogeneous (Vollmer-Conna et al. 2006), and that CFS/ME and PVFS should be considered as separate conditions, with CFS/ME having more in common with IBS than PVFS does (Aggarwal et al. 2006). This requires revision of the ICD-10 taxonomy, which classifies PVFS with ME (WHO, 1992)”

 Presentation given at Neurology and Psychiatry SpRs Teaching Weekend

http://bnpa.org.uk/doc/HANDBOOK.pdf

[Extract]

Presentation:

Chronic fatigue syndrome: neurological, psychological or both?

Peter White, Professor of Psychological Medicine, Barts and the London Medical School

Epidemiology of fatigue and CFS

Fatigue is a common symptom in both the community and primary care. When asked, between 10 and 20 per cent of people in the community will report feeling abnormally tired at any one time.

At the same time, fatigue is continuously distributed within the community, with no point of rarity.

Therefore any cut-off is arbitrary and the prevalence will vary by how the question is asked, the symptom volunteered, and its context. Between 1.5 % and 6.5 % of European patients will consult their general practitioner with a primary complaint of fatigue every year, the incidence varying by age and population. Fatigue is more commonly reported and presented to general practitioners by women and the middle-aged, and is most closely associated with mood disorders and reported stress. It does not seem to vary by ethnicity in the UK, but there is an intriguing paradox in that it is reported more commonly by those in high income countries, yet is presented to medical care more often in low income countries.

Prolonged or chronic fatigue is significantly less common than the symptom of fatigue and it is only in the last 10 years that consensus has emerged about the existence of a chronic fatigue syndrome (CFS), also called myalgic encephalomyelitis (ME). CFS is now accepted as a valid diagnosis by medical authorities in the UK, in the United States of America, as well as internationally. About one third of patients presenting to their doctor with six months of fatigue will meet criteria for a chronic fatigue syndrome. The other two thirds have fatigue secondary to another condition, most commonly mood and primary sleep disorders. Its primary symptom is fatigue, both physical and mental, which particularly follows exertion. Other symptoms agreed in consensual guidelines include poor concentration and memory, sleep disturbance, headache, sore throat, tender lymph glands, muscle and joint pain.

There are several criterion based definitions of CFS. These definitions were derived by consensus and have not been supported by empirical studies, and continue to be refined. Their utility stems from providing reliable criteria for research studies, rather than clinical use. The prevalence of CFS is between 2.5 % and 0.4 % depending on the definition used and whether comorbid mood disorders are excluded (that is mood disorders that are not thought to be the primary diagnoses). It is most common in women, the middle-aged, and ethnic minorities (unlike fatigue) – at least in English speaking countries.

The diagnosis and classification of CFS

The clinical taxonomy for CFS is a mess. The ICD-10 classification defines CFS within both the neurology chapter and mental health chapters. Myalgic encephalomyelitis, the alternative name for CFS, is classified as a neurological disease (G93.3) (a.k.a. post-viral CFS), whereas neurasthenia (a.k.a. CFS not otherwise specified) is classified within mental health (F48).

[Ed: Note that White does not mention, here, that Chronic fatigue syndrome is listed in ICD-10: Volume 3, The Alphabetical Index* at G93.3, the same coding as for Benign myalgic encephalomyelitis, and for Postviral fatigue syndrome (ICD-10: Volume 1: The Tabular List).]

*ICD-10: Volume 3, The Alphabetical Index:
http://www.scribd.com/doc/7350978/ICD10-2006-Alphabetical-Index-Volume-3

[Back to PDW]

(Incidentally, this mess is not specific to CFS, since there are several conditions within the neurology chapter of ICD-10 that are also classified in the mental and behavioural disorders chapter. For instance, Alzheimer’s disease is classified within neurology, whereas dementia due to Alzheimer’s disease is classified under mental health. My personal view is that it is high time that all mental health disorders and neurological diseases affecting the brain were classified within the same chapter, simply called diseases/disorders of the brain and nervous system.)

[Ed: The WHO Department of Mental Health and Substance Abuse, which is overseeing the revision of Chapter V (Mental and Behavioural Disorders), is also managing the technical part of the revision of Chapter VI (Diseases of the Nervous System). According to Dr Geoffrey Reed, Senior Project Officer, WHO Department of Mental Health and Substance Abuse, Proposal forms for ICD Chapter V and Chapter VI are in preparation and expected to be released shortly.]

[Back to PDW]

There is also a current debate between “lumpers” and “splitters” about the nosology of “functional” somatic syndromes (symptom defined conditions), such as CFS, IBS and “fibromyalgia”. Some argue that the close associations between the syndromes (those with CFS are also more likely to have fibromyalgia and/or IBS) argues in favour of their being different manifestations of one over-arching functional somatic syndrome (the “lumpers”). Others argue that these syndromes are best understood by exploring their heterogeneity (the “splitters”). There is evidence to support both arguments, but two large and recent epidemiological studies suggest that chronic unexplained fatigue, for one, is both associated with and separate from other “functional” somatic syndromes. In particular, predisposing risk factors are shared whereas triggering factors are different.

CFS is not an easy diagnosis to make, since misdiagnosis is common in patients diagnosed as having CFS. A recent audit of my CFS clinic revealed that 4 out of 10 new patients (n = 250) assessed did not have CFS, and that was after a third of referrals had already been rejected as not being CFS.

The most common misdiagnoses were mood disorders, especially depressive disorders, and primary sleep disorders, particularly sleep apnoea. Other misdiagnoses included coeliac disease and autoimmune conditions. Alternative neurological diagnoses were made in 2%.

Aetiology and pathophysiology

The aetiology of CFS is unknown, but there is evidence that different risk markers are associated with predisposition, triggering, and maintenance of the illness. Predisposing risk markers include female sex, middle age, mood disorders (especially depressive disorders), other symptom defined syndromes, such as irritable bowel syndrome, and possibly either sedentary behaviour or excessive activity. As might be expected CFS patients are more likely to have attended their GP, than healthy matched controls, even up to 15 years before onset, but recent work shows that those with IBS (and no CFS) have the same tendency.

Triggering risk markers are less well established, but there is sufficient evidence to support certain infections as aetiological factors not only for fatigue but also CFS, with the best replicated evidence supporting a role for Epstein-Barr virus infection, which triggers CFS in 10% of those infected.

Maintaining or perpetuating risk markers are most important in determining treatment programmes, since reversing maintaining factors should lead to improvement. Reasonably well established factors include mood disorders, such as dysthymia, illness beliefs such as believing the whole condition is physical, pervasive inactivity, avoidant coping, membership of a patient support group, and being in receipt of or dispute about financial benefits.

Few pathophysiological findings in CFS have been replicated in independent studies. Those that have been include down-regulated hypothalamic pituitary-adrenal axis, physical deconditioning, and discrepant reports between perception of symptoms and disability and their objective tests.

The latter finding is now supported by functional brain scanning studies suggesting altered brain activity with specific tasks. The discrepancy between subjective states and objective tests has been found before in other symptom defined syndromes, such as “fibromyalgia”, and may be related to enhanced interoception (the perception of visceral phenomena), a concept first described by Charles Sherrington in 1904. One hypothesis currently being tested is that the common predisposition to “functional” somatic syndromes is caused by enhanced interoception.

Recent work suggests that these factors may be reversed by rehabilitation.

Prognosis

Without treatment the prognosis of CFS is poor with a systematic review of outcomes finding the median full recovery rate was 5 % (range 0-31%) and the median proportion of patients who improved of 39.5% (range 8-63%). Being younger, having less fatigue baseline, a sense of control over symptoms and not attributing illness to a physical cause were all associated with a better outcome. The prognosis is considerably better after treatment.

Treatment

The NICE guidelines, published in 2007, were based on an updated systematic review. The essence of specialist care is rehabilitation, provided on an individual basis with an appropriately qualified and trained therapist. The two approaches with the greatest evidence of efficacy are cognitive behaviour therapy (CBT) and graded exercise therapy (GET). Approximately 60% of patients report significant improvement with these approaches and about 25%report full recovery, which lasts. No pharmacological treatments are recommended (antidepressants are ineffective), but symptomatic pharmacotherapy for specific symptoms (such as pain) or comorbid conditions such as depressive illness) can be helpful complementary treatments.

These rehabilitation approaches have not received universal approval from patient charities, with concerns that patients may be harmed by exercise therapies or that CBT implying that the condition is psychological.

Is CFS neurological or psychological?

This is a nonsensical question when one considers the neuroscience of consciousness and recent advances in functional brain physiology. The philosopher, John Searle, stated the answer to this Cartesian dualism that still bedevils western medicine. “Conscious states are caused by neurophysiological mechanisms, and are realised in neurophysiological systems.” Therefore it is not possible to have a psychological process or event without a neurological mediating process. It is neither of the mind or body; it is both.

Fatigue secondary to neurological diseases

Fatigue is commonly associated with chronic medical disorders, but it should be differentiated from fatiguability. Fatiguability is the onset of a physical sensation of fatigue and weakness after exertion and is commonly reported with neurological diseases such as multiple sclerosis and myopathies.

Apart from measures of disease activity, other associations of secondary fatigue in general that have been repeatedly found include sleep disturbance, mood disorders, inactivity and physical deconditioning. Studies of fatigue associated with multiple sclerosis are instructive and exemplary. As in all studies of secondary fatigue, measures of the severity or pathophysiology of the disease itself are associated with fatigue. Some cytokines are associated, but others are not.

Associations vary depending on the fatigue measure, confirming the multidimensional nature of fatigue, but all measures are associated with depression. Objectively confirmed sleep disturbance is also associated with fatigue. Fatigue associated with MS therefore requires biopsychosocial management.

There have been a number of studies of various treatments aimed at reversing the associations of secondary fatigue in general, in the hope they would help fatigue directly, with variable results. As with CFS, the most consistent evidence of efficacy has been with graded exercise programmes and CBT.

Attarian HP, Brown KM, Duntley SP, et al. The relationship of sleep disturbances and fatigue in multiple sclerosis. Arch. Neurol. 61 (2004), 525-8.

Baker R, Shaw EJ. Diagnosis and management of chronic fatigue syndrome or myalgic encephalomyelitis (or encephalopathy): summary of NICE guidance. BMJ 2007 doi: 10.1136/bmj.39302.509005. AE

Chambers D, Bagnall A-M, Hempel S, Forbes C. Interventions for the treatment, management and rehabilitation of patients with chronic fatigue syndrome/myalgic encephalomyelitis: an updated systematic review. J R Soc Med 2006;99:506-20.

Cleare AJ. The neuroendocrinology of chronic fatigue syndrome. Endocr. Rev. 24 (2003), 236-52.

Flachenecker P, Bihler I, Weber F, et al., Cytokine mRNA expression in patients with multiple sclerosis and fatigue. Mult. Scler. 10 (2004), 165-9.

Fulcher KY, White PD. Strength and physiological response to exercise in patients with the chronic fatigue syndrome. J. Neurol. Neurosurg. Psychiatry 69 (2000), 302-7.

Joyce J, Hotopf M, Wessely S. The prognosis of chronic fatigue and chronic fatigue syndrome: a systematic review. Q. J. Med. 90 (1997), 223-33.

Kroencke DC, Lynch SG, Denney DR. Fatigue in multiple sclerosis: relationship to depression, disability, and disease pattern. Mult. Scler. 6 (2000), 131-6.

Lyall M, Peakman M, Wessely S. A systematic review and critical evaluation of the immunology of chronic fatigue syndrome. J. Psychosom. Res. 55 2003), 79-90.

National Institute for Health and Clinical Excellence. Clinical guideline CG53. Chronic fatigue syndrome/myalgic encephalomyelitis (or encephalopathy): diagnosis and management. London, NICE, 2007. http://guidance.nice.org.uk/CG53.

Reeves WC et al. Identification of ambiguities in the 1994 chronic fatigue syndrome research case definition and recommendations for resolution.BMC Health Serv Res 3 (2003), 25.

Romani A, Bergamaschi R, Candeloro E, et al., Fatigue inmultiple sclerosis: multidimensional assessment and response to symptomatic treatment. Mult. Scler. 10 (2004), 462-8.

M. C. Tartaglia, S. Narayanan, S. J. Francis, et al., The relationship between diffuse axonal damage and fatigue in multiple sclerosis. Arch. Neurol. 61 (2004), 201-7.

Wessely SC, Hotopf M, Sharpe M. Chronic Fatigue and its Syndromes (Oxford: Oxford University Press, 1998).

Wessely S, Nimnuan C, Sharpe M. Functional somatic syndromes: one or many? Lancet 354 (1999), 936-9.

Wessely S, White PD. In debate: there is only one functional somatic syndrome. Br. J. Psychiatry 185 (2004), 95-6.

White PD, Thomas JM, Kangro HO, et al., Predictions and associations of fatigue syndromes and mood disorders that occur after infectious mononucleosis. Lancet 358 (2001), 1946-54.

White PD, Sharpe MC, Chalder T, DeCesare JC, Walwyn R; on behalf of the PACE trial group. Protocol for the PACE trial: a randomised controlled trial of adaptive pacing, cognitive behaviour therapy, and graded exercise, as supplements to standardised specialist medical care versus standardised specialist medical care alone for patients with the chronic fatigue syndrome/myalgic encephalomyelitis or encephalopathy. BMC Neurol 2007;7:6.

[ Extract ends, doc: http://bnpa.org.uk/doc/HANDBOOK.pdf ]

For detailed information on the proposed structure of ICD-11, the Content Model and operation of iCAT, the collaborative authoring platform through which the WHO will be revising ICD-10, please scrutinise key documents on the ICD-11 Revision Google site:
https://sites.google.com/site/icd11revision/
https://sites.google.com/site/icd11revision/home/documents

For information around the DSM and ICD revision processes see DSM-V and ICD-11 Directory page: http://meagenda.wordpress.com/dsm-v-directory/

Suzy Chapman
http://meagenda.wordpress.com
http://twitter.com/MEagenda

More evidence of inflammation in (ME)CFS: M Williams 14 November 2009

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Update: I am advised that the PDF referenced in the text of Ms Williams’ article, below, is no longer available at the URL given. A cached html version of the document has been archived here:

http://www.meactionuk.org.uk/Infectious-mononucleosis-as-a-model-for-chronic-fatigue-syndromes.htm

Permission to Repost

http://www.meactionuk.org.uk/More-evidence-of-inflammation-in-(ME)CFS.htm

http://www.meactionuk.org.uk/More-evidence-of-inflammation-in-(ME)CFS.pdf

More evidence of inflammation in (ME)CFS

Margaret Williams

14 November 2009

In his presentation in Bergen on 20th November 2009, Professor Peter White’s power point slides state about (ME)CFS that maintaining factors include illness beliefs, the search for legitimacy, being on benefits, and the diagnostic label, and that immune or viral measures are NOT involved in the maintenance of the disorder

( http://www.unifobhelse.no/upload/Bergen%20What%20is%20CFS%202009.pdf )

White’s assertion that immune or viral measures are not involved in the maintenance of the disorder would seem to be a direct denial of the evidence of two of the world’s leading immunologists who specialise in ME/CFS, Professors Mary Ann Fletcher and Nancy Klimas, who recently published yet more confirmatory evidence of immune dysfunction in the maintenance of the disorder (Journal of Translational Medicine 2009:7:96: doi:10.1186/1479-5876-7-96). Their peer reviewed article was published immediately upon acceptance.

Fletcher and Klimas et al are clear that cytokine abnormalities are common in (ME)CFS and that the cytokine changes observed are more likely to be indicative of immune activation and inflammation, rather than specific for (ME)CFS, as people with fibromyalgia, Gulf War Illness, rheumatological disorders and multiple sclerosis may also have similar cytokine patterns.

The authors do, however, demonstrate that several of the abnormal cytokines show promise as potential biomarkers for (ME)CFS.

As Fletcher and Klimas et al point out:

“CFS studies from our laboratory and others have described cytokine abnormalities. Other studies reported no difference between (ME)CFS and controls. However, methodologies varied widely and few studies measured more than 4 or 5 cytokines. Multiplex technology permits the determination of cytokines for a large panel of cytokines simultaneously with high sensitivity.

“In this study, 10 of 16 cytokines examined showed good to fair promise as biomarkers. However, the cytokine changes observed are likely to be more indicative of immune activation and inflammation…Many of the symptoms are inflammatory in nature.

“There is a considerable literature describing immune dysfunction in (ME)CFS.

“The goal of this study was to determine if, using new technology, plasma cytokines had sufficient sensitivity and specificity to distinguish (ME)CFS cases from age-matched healthy controls….Amounts of cytokines in plasma or serum are often below the level of detection in traditional ELISA assays.

“The availability of sensitive multiplex technology permitted the determination of 16 cytokines simultaneously…In the (ME)CFS cases, we found an unusual pattern of the cytokines that define the CD4 T cell.

“Pro-inflammatory cytokines: A significant elevation in the relative amounts of 4 of 5 pro-inflammatory cytokines in peripheral blood plasma of patients with (ME)CFS was found when compared with the controls. In cases, lymphotoxin (LT)a was elevated by 257% and IL-6 by 100% over the controls.

“TH2 cytokines: Both interleukin (IL)-4 and IL-5 were elevated in (ME)CFS, with the median of IL-4 (being) 240% and of IL-5 (being) 95% higher in cases than controls.

“Anti-inflammatory cytokines: IL-3 was significantly lower in (ME)CFS patients.

“TH1 cytokines: IL-12 was significantly elevated (120%) and IL-15 decreased (15%) in cases compared to controls.

“IL-8 (CXCL8): this chemokine was 42% lower in the (ME)CFS patients.

“Along with the TH1 abnormalities, we found up-regulation of TH2 associated cytokines, IL-4 and IL-5, in the (ME)CFS subjects. Allergy is common in (ME)CFS cases. Years ago, Straus et al reported >50% atopy in 24 CFS patients.

“The probability of chronic inflammation in (ME)CFS patients is supported by the elevation of four members of the pro-inflammatory cytokine cascade , LTa, IL-1a, IL-1b and IL-6, in the (ME)CFS samples compared to controls.

“Interleukin-13, associated with inhibitory effects on inflammatory cytokine production, was lower in cases compared to controls.

“The inflammatory mediator IL-8 (a chemokine known as CXCL8) known to be responsible for migration and activation of neutrophils and NK cells was decreased in plasma of (ME)CFS patients.

“The observations of abnormal cytokine patterns in (ME)CFS patients support the reports of retrovirus infections.

“Recently, DNA from a human gammaretrovirus, xenotropic murine leukaemia virus-related virus (XMRV) was found in the PBMC of 68 of 101 patients compared to 8 of 218 healthy controls. Patient–derived, activated PBMC produced infectious XMRV in vitro. Both cell associated and cell-free transmission of the virus to uninfected primary lymphocytes and indicator cell lines was possible.

“The decreased natural killer (NK) cell cytotoxic and lymphoproliferative activities and increased allergic and autoimmune manifestations in (ME)CFS would be compatible with the hypothesis that the immune system of affected individuals is biased towards a T-helper (TH) 2 type, or humoral immunity-orientated cytokine pattern.

“The elevations in LTa, IL-1a, IL1b and IL-6 indicate inflammation, likely to be accompanied by autoantibody production, inappropriate fatigue, myalgia and arthralgia, as well as changes in mood and sleep patterns.

“This study is among the first in the (ME)CFS literature to report the plasma profiles of a reasonably large panel of cytokines assessed simultaneously by multiplex technique.

“Cytokine abnormalities appear to be common in (ME)CFS. The changes from the normal position indicate immune activation and inflammation.

“The results imply a disorganised regulatory pattern of TH1 function, critical to antiviral defence.

“The results from this study support a TH2 shift, pro-inflammatory cytokine up-regulation and down-regulation of important mediators of cytotoxic cell function”.

Since it is now unequivocal that people with (ME)CFS show markers of inflammation, what will be the impact on the Wessely School’s MRC PACE Trial that is predicated on the assumptions of deconditioning, on the “perception” of effort and on aberrant illness beliefs and whose participants are instructed about “sleep hygiene”?

Correspondence between Stephen Ralph and Dr Charles Shepherd

Correspondence between Stephen Ralph and Dr Charles Shepherd

WordPress Shortlink: http://wp.me/p5foE-2jm

The opinion piece below, which includes extracts from recent correspondence with Dr Charles Shepherd is authored and published by Stephen Ralph; the views and opinions expressed are the views and opinions of Mr Ralph and any comments or queries resulting out of this opinion piece should be addressed to Mr Ralph and not to ME agenda.

Stephen Ralph maintains a website at  www.meactionuk.org.uk 

Dr Charles Shepherd is an Honorary Medical Advisor and a Trustee/Director of the ME Association http://www.meassociation.org.uk/

A copy of the statement which Stephen Ralph quotes from is here:

 XMRV and ME/CFS: WHAT DO WE KNOW SO FAR? AND WHAT DON’T WE KNOW? (VERSION 3) (04.11.09)  http://wp.me/p5foE-2kq

—————–

By Stephen Ralph  ME Action UK

Permission to Repost

06 November 2009

Like many of you, I was alarmed when I read the recent MEA XMRV Statement No.3 particularly because of one telling sentence.

I decided to ask Dr Shepherd a series of questions and although I had several answers, I had no answer at all to one important question that I asked several times.

I asked Dr Shepherd about this statement.

“Demonstrating a link between a retrovirus and ME/CFS does not, by itself, resolve the physical vs psychological debate.

Research studies have demonstrated links between retroviruses and diseases as diverse as autoimmune disorders (which could be relevant to ME/CFS), immunodeficiency diseases, multiple sclerosis, tumours, anaemias and even schizophrenia.”

In reply I got the following from Dr Shepherd.

“I don’t think this comment will have any effect whatsoever on psychiatry.

Psychiatrists already know that viruses and psychiatric illness can sometimes be linked.

I put this info into version 3 because some people are wrongly assuming that having a viral link in an illness means that it must be physical rather than psychological. And that the physical vs psychological battle in ME/CFS is now almost over. I only wish…..

Retroviruses may be involved in schizophrenia and it is being said the up to 40% of people with autism have XMRV.”

I then asked Dr Shepherd what he would do if he found he was XMRV negative and how this might impact on his judgment.

In reply I had the following from Dr Shepherd…

“I don’t know my XMRV status. I obviously could have access to XMRV testing facilities. But as knowing my XMRV result isn’t going to affect either my diagnosis of ME or the management of my illness at this stage I don’t see any point in being tested.”

Lastly, I asked Dr Shepherd if he did or did not support the views of Professors Simon Wessely, Michael Sharpe and Peter White.

I asked this question twice for the sake of clarification.

Dr Shepherd has decided not to answer that question.

I asked the question because on numerous occasions the MEA have released hedge betting, sitting-on-the-fence statements or cheek turning Statements that effectively support the agenda of Somatoform Psychiatry or completely ignore the agenda of Somatoform Psychiatry.

The statement regarding XMRV not ending the debate on mental v physical is for my eyes indicating that yet again the MEA and Dr Shepherd are entertaining the possibility that Wessely White and Sharpe are right.

Dr Shepherd – you should be actively ending the involvement of Professors Wessely, White and Sharpe and you should be representing the total “State of Science” from across the Atlantic as is the case with the ESME – see their website for example…

http://esme-eu.com/news/category7.html

…instead of selectively picking what you want to feed your members and back peddling on the profound implications of XMRV and what was said at the CFSAC last week.

As we all know, the liaison faction of psychiatry firmly and militantly assert that CFS is a functional psychosomatic syndrome and that ME does not exist at all.

We know that the likes of Wessely, White and Sharpe are trying to get CFS into the next edition of the DSM – DSM-V and reclassified in ICD-11.

Both Action for ME and the ME Association are doing nothing to stop this agenda.

I asked Dr Shepherd some time ago if he or the MEA were going to do anything about the CSSID DSM-V ICD-11 agenda and Dr Shepherd said he was too busy and it wasn’t on his list of things to do.

In my view, the ME Association is not a lot more than the Public Relations arm of Action for ME.

Yes they seem approachable and yes they seem to press all the buttons that please some of their members.

But as soon as you ask anything considered “controversial” or important – then Dr Shepherd and/or the MEA goes silent and refuses to answer the question as is the case by default with Action for ME.

It seems to me that here in the UK and for many years, the ME population are being held hostage by the mental health movement who seem to have castrated both Action for ME and the ME Association who between them dominate the arena yet lay silent and do nothing to counter the mental health agenda…

So it seems to me that neither charity actually give a damn about the concerns of the ME community unless those views accord with their agenda that they will not discuss when challenged in ANY detail.

They say the devil is in the detail but we do not know what the detail is because when we ask we get nothing back.

Under these circumstances we need those over in the USA and those in the UK with Independence of mind and purposes such as ME Research UK, the 25% ME Group and Invest in ME – to come to the rescue of the UK ME patient population.

If people are not happy with this e-mail I have written and you think I am being unfair then you should ask Dr Shepherd and the MEA yourselves and get the answers he would not give to me or the many others who have asked similar questions over the years that never get answered.

Why does the MEA turn the other cheek and choose not to robustly challenge the views of Professor Wessely and his colleagues and instead state that “they already know” so that these individuals are therefore beyond challenging…

How exactly does liaison psychiatry “already know” that retro-viruses cause mental illness and does the MEA believe that XMRV potentially causes functional mental illness in people with ME? If not then why stay silent – creating a space for the opposition to occupy.

Why does the MEA put out neutered statements that reflect the views of liaison psychiatry instead of using all the evidence available to robustly and technically challenge those views?

Why is the ME Association calling for the use of the CDC Fukuda Criteria in UK XMRV research when the Fukuda criteria has been and is still being exploited by Wessely et al due to its well known ability to produce a heterogeneous patient group and therefore research results that are by default inconclusive and “mixed” and challengeable by those with a mental health agenda?

Why does the ME Association not firmly call for the use the Canadian criteria or use both Fukuda and the Canadian criteria in parallel research to make the research outcomes more meaningful and less open to exploitative deconstruction when the ME Association at one time adopted the Canadian Criteria by a democratic vote and then quietly swept that democratic vote under their carpet?

This is all about accountability. We should be given full answers to all of the above questions.

What is wrong in asking?  Why does that make us bad?

Yours sincerely,

Stephen Ralph

www.meactionuk.org.uk

RiME: Newsletter No. 11

Paul Davis of RiME has recently issued a Newsletter.

WordPress Shortlink: http://wp.me/p5foE-2iE

RiME Newsletter No. 11

Permission to Repost

Campaigning for Research into ME (RiME)  www.rime.me.uk

RiME Newsletter No. 11 is now available. Items include:

ME: Activism + Organisation: The Need for Change

MPs Referendum on ME Research

NHS Services Inquiry: RiME Bank of Evidence

ME Association – Running with Hare and Hounds?

What does Lady Mar stand for? Forward-ME Condemned

MRC – Freedom of Information

Lightning Process

Conservatives + Lib Dems – latest.

If you want a copy posted to you, please send SAE plus 4 unused postage stamps (the few who have sent contributions over last year will get it anyway).

In order to survive, RiME depends on contributions from its supporters. We welcome unused postage stamps.

Paul Davis

10 Carters Hill Close, Mottingham, London, SE9 4RS   rimexx@tiscali.co.uk  

www.rime.me.uk

MEA summary of meeting of APPG on ME (21 October 2009) and APPG Legacy paper

http://www.meassociation.org.uk/content/view/1053/161/

1] MEA summary of meeting of APPG on ME (21 October 2009)

(Note this is a brief personal summary published by Dr Charles Shepherd on behalf of the ME Association and not the official meeting Minutes.  The Minutes and possibly a verbatim transcript will be issued at a later date by the  secretariat on behalf of Dr Des Turner, Chair, APPG on ME.)

2] APPG on ME launches legacy paper consultation

WordPress Shortlink: http://wp.me/p5foE-2cK

MEA summary of meeting of APPG on ME (21 October 2009)

This is a very brief summary of key points from the APPG meeting held on Wednesday 21 October in Committee Room 21 at the House of Commons.

The meeting was Chaired by Dr Des Turner MP.

Among parliamentarians present were the Countess of Mar, Russell Brown MP, Andrew Stunell MP, Bill Wiggin MP, and Tony Wright MP..

Representatives from charities and other organisations included those from AfME, BRAME, Kent and Sussex Alternative Group for ME, The MEA, reMember, RiME, Sussex and Kent ME Society, WMMEG and the 25% Group. There were also several members of public present.

A more detailed account of the meeting will appear in the Minutes, which will be posted on the APPG website when they have been through the drafting process and agreed.

PRESENTATION FROM THE RT HON YVETTE COOPER MP, SECRETARY OF STATE FOR WORK AND PENSIONS (DWP)

The main item was a presentation from the Rt Hon Yvette Cooper MP, Secretary of State for Work and Pensions, on benefit issues. Yvette was accompanied by Dr James Bolton, Deputy Chief Medical Adviser at the DWP.

Yvette explained that she had a strong personal interest in ME having suffered from it for a period starting in 1993 before entering parliament. During this time she was very ill for a period of roughly two years and completely off work for a year. This was followed by a period of recovery with more variable health over another two years. She has now made a full recovery and manages to combine being an MP, Minister and bringing up three children! During her early days in parliament she was actively involved with the APPG when it was chaired by Tony Wright MP. However, she did not feel it was appropriate to make general assumptions about ME/CFS based on her own experience.

Yvette briefly outlined the aims behind changes to the care, welfare and benefit systems that are now taking place –in particular the introduction of Employment and Support Allowance (ESA) to replace Incapacity Benefit and the role of the Work Capability Assessment (WCA) in deciding eligibility for ESA. Following on from her personal experience with ME she fully understood the concerns being expressed about assessing the fluctuating nature of ME/CFS and the need for a flexible approach regarding any possible return to work. She believed that the new WCA for ESA claimants took these problems into account. However, she was very willing to look at the problems that were raised during the meeting.

Yvette answered a series of questions from the Chair, who also read out written questions that had been submitted in advance of the meeting, along with questions from those attending the meeting. Yvette had only intended to be there for around 20 minutes but managed to stay for about an hour.

Questions relating to all the common and very familiar problems facing people with ME/CFS were discussed. In particular:

• The role of the new Work Capability Assessment for ESA claimants – especially in relation to people being unable to sustain physical/mental activity and the post-exertional symptomatology experienced by people with ME/CFS. In response, Yvette pointed out that this assessment should not depend on a precise diagnosis but on what a claimant could and could not do from the point of view of physical and mental function.

• The type of information and training on ME/CFS that is given to DWP decision makers and examining doctors. In response, Yvette maintained that adequate training in relation to specific illnesses such as ME/CFS was part of the DWP programme.

• Difficulties in accessing assessment centres. In response, she noted these concerns, agreed that the centres must be accessible to people with disabilities, and said she is very keen to hear of specific examples.

• The way in which a patient’s own GPs and specialist were progressively being removed from the opinion gathering process and replaced by doctors who knew nothing about the patient’s social and medical background. In response she noted these concerns but did not indicate that there would be any shift in the DWP position.

• Providing real help for people who can and want to return to work on a flexible and/or part time basis. In response, she agreed that this was vital – citing her own experience of a gradual and flexible return to work after having quite severe ME.

• Reviewing the permitted work rules – which can be very unhelpful in the case of ME/CFS. These concerns were sympathetically noted.

• Des Turner raised the specific issue of problems with tribunals and the knowledge about ME/CFS of those who sat on the panels making these decisions. Examples of very unsatisfactory procedures at tribunals were mentioned by several of those present. In response, Yvette managed to somewhat duck the issue by explaining that the tribunals are classed as being ‘independent’ and their administration comes under the Ministry of Justice. This is clearly going to remain an important issue on the parliamentary agenda.

• Tony Wright MP made the point that something was clearly wrong with the benefit assessment system when so many people with ME/CFS were failing on their first application but then being successful on appeal.

• Charles Shepherd questioned the DWP auditing and monitoring of the success/failure rate of applications for ESA from people with specific illnesses, including ME/CFS. In response, Dr Bolton explained that no figures are available.

• With regard to DLA and the government Green Paper, Yvette was asked about the mixed messages coming from ministers on the future of DLA. In reply, she acknowledged the concerns being expressed and made it clear that DLA for people of working age was not under review. She stated that a government statement on DLA would be made on Wednesday 22 October by the Rt Hon Andy Burnham.

At the end of this presentation. Charles Shepherd asked Dr James Bolton if he would be willing to meet with ME/CFS charity representatives to discuss these concerns in more detail and he agreed to do so. This meeting is now being followed up through the Forward ME group.

OTHER MATTERS

APPG INQUIRY INTO NHS SERVICES IN ENGLAND Des Turner explained that the report was now being written with the intention of having it ready for presentation to the APPG at the next meeting in early December. A Minister from the Department of Health will be invited to attend this meeting to respond to the report.

APPG LEGACY PAPER Des Turner explained that the APPG would have to be reformed after the general election – which will have to take place before June 2010. And with him standing down as an MP we would need to find a new Chair in 2010. To coincide with the winding up of the APPG, a Legacy Paper is being prepared which outlines the key areas of work and actions that have been taken by the APPG during the current parliament, as well as future actions. The APPG is keen to receive input on this from people with ME/CFS and a copy of the current draft will be posted on the APPG website. Comments on this draft must be received by the Secretariat by 19 November – so that further discussion on a further draft can take place at the December meeting.

STATEMENT BY WMMEG (West Midlands ME Groups Consortium): Jill Cooper read out a further statement relating to issues about patient representation, transparency and the suitability of the education and training programme provided by the ME/CFS Clinical and Research Network and Collaborative (CCRNC) This was followed by a very lively discussion on the current state of NHS services for people with ME/CFS.

XMRV: A rather informal discussion on various aspects of the new viral research findings took place.

Date of next meeting: Provisionally fixed for Wednesday 2 December

APPG website: www.appgme.org.uk

——————

http://www.meassociation.org.uk/content/view/1052/161/

APPG on ME launches legacy paper consultation

A consultation on the Legacy Paper for the All Party Parliamentary Group (APPG) on M.E. was launched yesterday (October 22).

The current Chair of the APPG, Dr Des Turner, intends to stand down at the next General Election, due sometime before 3 June 2010.

Comments on the draft APPG legacy paper should be sent to the Secretariat tristana.rodriguez@afme.org.uk  

This email address is being protected from spam bots, you need Javascript enabled to view it no later than 19 November 2009.

The Countess of Mar, who is Secretary of the Group, thanked people with M.E. and Action for M.E. for the work done so far in producing the draft.

The main speaker at the meeting was the Rt Hon Yvette Cooper MP, Secretary of State for Work and Pensions, who described her own personal experience of M.E. and answered a number of questions. In particular, she reassured people with M.E. that it was not the Government’s intention to change working-age Disability Living Allowance under current care reform proposals.

Other topics on the agenda included an update on the APPG Inquiry into NHS services, which is expected to produce a report before the next meeting of the APPG, which will take place on Wednesday 2 December 2009. A Minister from the Department of Health would be invited to attend.

In addition to the Chair, Dr Turner and the Secretary, the Countess of Mar, the meeting was attended by Vice Chairs Andrew Stunell MP and Tony Wright MP (Vice Chairs), plus Bill Wiggin MP and Russell Brown MP.

Minutes and a transcript of the meeting will be produced in due course.

Download Draft Legacy Paper in PDF

Professor Peter D White document to CNCCs re XMRV and CFS

Professor Peter D White document to CNCCs re XMRV and CFS

22 October 2009

A copy of the document below was passed anonymously to ME agenda, yesterday, together with evidence that it originates from Professor Peter White (Barts and The London NHS Trust).

It is being circulated by Professor White to the Clinical Network Co-ordinating Centres (CNCCs).

Professor White is also a co-PI (Principal Investigator) of the MRC funded PACE Trials.

Caveat: Amongst other issues, there have been expressions of concern over Professor Lloyd’s use of the term “‘endogenous retroviruses’ (ERVs)” in his original commentary, a term reproduced in the document being circulated by Professor Peter White to CNCCs.

Note: The original commentary by Professor Andrew Lloyd is published here

http://www.me-cfs.org.au/node/448  on the website of The ME/CFS Society of NSW Inc.

————————–

Document Properties:

MS Word Document file name: xenotropic murine leukemia virus-related virus XMRV and CFS.doc

Document Created: 15 October 2009

Document Title: Dear ME/CFS Society,

Author: Andrew LLoyd

Company: Barts and The London NHS Trust

————————–

Document text:

Dear colleagues,

In light of the recent publication in Science regarding a new retrovirus discovered in patients with CFS and the attendant widespread publicity, the following is a scientific appraisal of this publication and the evidence so far. It has been adapted almost in full with permission from an article by Professor Andrew Lloyd, Director, Centre for Infection and Inflammation Research, University of New South Wales.

The first comment is that the findings are potentially important to our understanding of the illness. The paper describes the detection of genetic material of a virus known as xenotropic murine leukemia virus-related virus (XMRV) in 68 of 101 (67%) patients in the US, described as having illness “fulfilling the 1994 CDC Fukuda Criteria for Chronic Fatigue Syndrome and the 2003 Canadian Consensus Criteria for Chronic Fatigue Syndrome/myalgic encephalomyelitis (CFS/ME) and presenting with severe disability”, compared to 8 of 218 (3.7%) healthy individuals. The significance of this finding was further supported by detection of XMRV proteins in the blood of 19 0f 30 patients, but none of 5 healthy subjects. Antibodies against XMRV were found in the blood of 9 of 18 patients and none of 9 healthy individuals. The XMRV was shown to grow in cell culture in the laboratory. As the retrovirus family also includes HIV, on face value this finding raises the suggestion that CFS may be caused in some cases by infection with XMRV which may affect both the immune system and the brain.

However, several strong notes of caution need to be applied:

1) Research into CFS has been plagued over several decades by studies using sophisticated molecular laboratory techniques to examine poorly characterised subjects and samples. In the recent study, the 101 patients are reported to have met diagnostic criteria for CFS, but perplexingly no details of their age, gender, or illness characteristics were provided – except the indication that the illness in these patients was causing “severe disability”. This information is critical to allow the reader to understand how comparable the patients in the study were to ‘typical’ patients with CFS in the USA and worldwide. Disconcertingly, one of the authors of the study, Judy Mikovits has suggested during interviews with the Amy Dockser Marcus in the Wall Street Journal, that “20 patients of the 101 in the study have lymphoma” – if this statement is accurate the reliability of the designation of the 101 patients must be cast into serious doubt (as diagnosis of lymphoma precludes a diagnosis of CFS). Perplexingly, the paper also does not describe how the healthy control subjects were selected – for instance if the controls were family members of the cases, or individuals working in the laboratory where the studies were performed this would be inappropriate as they may have altered rates of contact with the XMRV.

2) the finding of a retrovirus in the blood would seem to be highly significant, however so called ‘endogenous retroviruses’ (ERVs) are actually found commonly in humans and generally cause no ill effects. These retroviruses are derived from ancient viral infections of germ cells in humans, mammals and other vertebrates; and so are passed on through generations and now remain in the genome. Some research suggests that human ERVs may cause certain  autoimmune diseases and cancers. XMRV has previously been associated with prostate cancer. Accordingly, the finding of XMRV in the recent study raises the possibility that infection with this virus may cause CFS in some patients – alternatively it may become active as a result of CFS – or it may have no role whatsoever in the illness (i.e it may be an epiphenomenon).

3) those of us who have been undertaking research into CFS for a long period will remember the remarkably comparable “discovery” of a retrovirus in patients with CFS made by Elaine Defreitas which was published in the similarly prestigious journal, Proceedings of the National Academy of Sciences in 1991. In brief, the initial report was of a retrovirus with both genetic material and viral proteins, as well as antibodies against the virus, identified in a significant proportion of patients and not in healthy individuals. A series of subsequent studies failed to confirm the findings – or find evidence for any known retroviral infection. This outcome is an important reminder that biomedical research is highly complex process and often uses new technologies to make discoveries – some are confirmed and found to have lasting significance – many are not. This process is a necessary element in the pathway to improved understanding of disease.

There can be no doubt that CFS is one of the most challenging on the list of unsolved medical conditions, hence the last two decades have witnessed many such ‘discoveries’ – time will tell whether this one stands the key test of independent replication, which is verification of the same finding in other laboratories and using other patient samples. A number of research groups will be undertaking this task over the next several months – until these results are in – there is no likelihood of a meaningful “diagnostic test”. If the findings were confirmed the likelihood of an effective treatment would be several years away at the earliest.

[Ends]

APPG on ME: Minutes and Transcript for 8 July 2009 meeting

All Party Parliamentary Group on ME meeting 8 July 2009

The last meeting of the APPG on ME took place on 8 July 2009.  The Minutes are published below, in both PDF format and as text.  The transcript of the entire meeting is posted in PDF format only.

Minutes APPG on ME 8 July 09

Transcript APPG on ME 8 July 09

 

Text of Minutes:

All Party Parliamentary Group on M.E.

Chair: Des Turner MP
Vice-Chairs: Andrew Stunell MP
Tony Wright MP
Secretary: Countess of Mar
Treasurer: David Amess MP

 

Minutes of the meeting of the All Party Parliamentary Group on M.E.
held at 1.30-3pm, Wednesday 8 July 2009
Committee Room 13, House of Commons

 

Present:

Parliamentarians
Dr Des Turner MP
Andrew Stunell MP
Countess of Mar
Peter Luff MP
Edward Davey MP

Secretariat
Sir Peter Spencer (Action for ME)
Heather Walker (Action for ME)
Kimberley Hogarth (Action for ME)
Charles Shepherd (MEA)

Organisations and individuals
Paul Davis (RiME)
Jane Colby (Tymes Trust)
Christine Harrison (BRAME)
Doris Jones (25% Group)
Joy Birdsey (K&SAME)
Jill Cooper (Warwickshire Network for ME)
Bill Kent (reMEmber)
Janice Kent (reMEmber)
Augustine Ryan
Michelle Goldberg

Apologies:

1. Welcome

The Chairman welcomed those present and apologised to those who may have been inconvenienced by a change of room. Two further apologies were made: that unfortunately there would be no speaker today, and that the chair would have to leave the meeting at 2 p.m. but that the Countess of Mar had kindly agreed to complete the meeting.

2. Annual General Meeting

Current officers were re-elected with the exception of Dr Ian Gibson, who had resigned as an MP. The Countess of Mar was elected to replace him. The elected Officers for 2009-2010 are therefore:

Chair: Dr Des Turner MP
Vice-Chairs: Andrew Stunell and Anthony Wright
Treasurer: David Amess
Secretary: Countess of Mar

The Chair pointed out that he is not standing at the next general election, so a new Chair will have to be found at that point.

3. Minutes of the last meeting

The Chair reminded the Group that the minutes are not intended as a verbatim record; they are business minutes. However he accepted that Paul Davis had said at the last meeting: “There is a road map that goes back to the CMO report, York review 1, and a certain school of psychiatry.” The reference to the CMO report had been omitted from page six of the transcript.

4. Matters arising

Jane Colby asked that it be noted that the BBC Politics Show, filmed in part during the last meeting, was transmitted in ME awareness week, and that everybody was very grateful to the APPG for allowing it to happen.

5. APPG Inquiry into NHS Services

The Chair reported that evidence sessions were due to start at 2pm the next day in Committee Room 19. The first session would hear from patients and patient organisations. He hoped that the next week’s session would include a Minister, the Chief Medical Officer and service providers. Many patients had submitted evidence. Questionnaires had been sent to all Primary Care Trusts. The aim was to produce a report which would act as a campaigning tool to improve services for people with ME.

During the discussion which followed, Dr Turner had to leave and the Countess of Mar took the chair. Some concerns were raised eg. that:

i. Existing services were not focused on neurological ME and over-emphasised the psychosocial model
ii. Some people would not respond to the survey for that reason
iii. Some panel members had made favourable comments about existing services in the past
iv. Evidence sessions clashed with key local meetings elsewhere, affecting attendance
v. People submitting evidence had not received confirmation of receipt due to the inquiry’s lack of administrative support
vi. Publicity for the inquiry had been limited and would not reach the majority who were not in touch with certain charities, support groups or services
vii. Some patients do not collate evidence
viii. How issues not covered by surveys, such as the replacement of consultants by new services in some areas, could be addressed.

Some issues could be raised via questions through the panel eg. support for severe cases.

It was noted that the decision had been taken by parliamentarians at the last meeting, to drive forward the inquiry quickly, because of the imminence of a general election.

The hope was for a report by the inquiry which would have sufficient credibility, evidence and parliamentary authority for consideration by the Health Select Committee.

6. Statement from WMMEG (West Midlands ME Groups) Consortium on ME/CFS – Education and Training in the NHS

i. Heather Walker apologised formally for tabling the wrong statement on their behalf at the last meeting.
ii. Jill Cooper asked that sufficient time to be allocated to discuss the key issues of appropriate NHS training at a future APPG meeting.
iii. Sir Peter Spencer responded to the WMMEG statement saying that he did not believe that NHS staff were being ‘trained’ to treat this illness as a psychological illness and that Action for M.E.’s involvement in the last NHS collaborative conference had resulted in delegates hearing Professor Stephen Holgate emphasise the importance of getting new research talent into the field, plus discussion on the need for properly derived patient reported outcome measures.
iv. Noting to the statement’s reference to Pathways to Work, the Countess of Mar reported that the Welfare Reform Bill was going through the House of Lords. She had been fighting hard to have ME and other fluctuating conditions recognised in their own right by the Grand Committee and not “lumped in” with mental illness.

The meeting acknowledged its appreciation of all the work that the Countess had done.

7. Future Work of the APPG

Ideas included:

i. Inviting Baroness Young, Care Quality Commission, to address the Group
ii. Maintaining focus on the DWP and Welfare to Work
iii. Follow-up on the presentation made by Jane Colby and Mary-Jane Willows about child protection problems, by asking the Inspector of Social Services to come to the APPG to listen to parents, consider how social services might be alerted to the possibility of M.E. in children and examine how parents could be informed of their rights eg. though a simple leaflet signposting information and organisations that could help them.

8. All Party Parliamentary Group Legacy Paper

As a General Election was due and the Chair had noted his intention to stand down, it was suggested that it might be useful to draw up a short summary of the APPG’s recent activities, outstanding concerns and objectives for consideration by the new Chair and any other new officials.

People with M.E. could be invited to put forward three or four bullet point suggestions for the key issues and objectives and to submit them to Heather Walker, Action for ME and Charles Shepherd. On behalf of the Secretariat, Action for M.E. would produce a draft consensus document from the results.

Action: Heather Walker to supply a copy of the Legacy Paper produced by the Cross Party Group on ME in the Scottish Parliament before their last General Election.

Click for Legacy Paper

9. Website

A website had been set up for the APPG at www.appgme.org.uk. Although the impetus for the site had come from the inquiry, the site would continue after the inquiry and would be the central focal point of information about meetings and activity.

10. Any Other Business

Michelle Goldberg raised the case of Kay Gilderdale 54 and the assisted suicide of her daughter, Lynn, after 17 years of M.E.

Michelle described the lack of support she herself had faced and highlighted problems experienced by another woman proven innocent after receiving an ASBO.

Christine Harrison reported on her campaign about pets in holiday accommodation. Currently, customers with allergies can not be guaranteed a holiday property in which a registered guide and/or support dog has not stayed. The Countess of Mar had kindly taken this up in the House of Lords, asking for a new clause to be added to the Disability Discrimination Act to say that people who rent out holiday accommodation are permitted/allowed to have a policy of no pets and no smoking to allow them to offer accommodation to guests who may have health conditions  and/or allergies that might be exacerbated by the presence of pets and smoke.

11. Date of Next Meeting

The chair advised the group that the next meeting would be in the Autumn