THE NICEGUIDELINES BLOG

New Vaccine Tested Against Autoimmune Diseases

2012-01-26T08:22:00.000-08:00

BY NATASSIA GERRARD, NOCAMELS · JANUARY 24, 2012:Autoimmune diseases, such as Chrohn’s disease and Rheumatoid Arthritis, or even allergies, are one of the trickiest in the medical world because they occur when the immune system mistakenly attacks itself, causing damage to the entire body.

Israeli scientists from the Weizmann Institute of Science think they have made progress what could be significant progress in the treatment of autoimmune diseases by developing a vaccine.

Traditional treatment for patients with such diseases generally involves taking anti-inflammatory drugs along with immune suppressants. However, these drugs come with serious side effects, and can even increase the risk of patients developing an infection.

Tested on mice, the research team developed a new vaccine that tricks the immune systems into attacking one of the players in the autoimmune processes – an enzyme known as MMP9. When working properly, this enzyme plays an important role in mobilizing cells and healing wounds. However, when the MMP-9 dysfunctions it can “aid and abet” autoimmune diseases as well as cancer metastasis.

The vaccine developed by the researchers uses a smart synthetic molecule that artificially mimics the functional metal site at the heart of the MMP enzyme. This molecule, in turn, tricks the immune system into creating antibodies named “metallobodies” that block the enzyme at its active site.

Head of the research team at the Weizmann Institute of Science, Professor Irit Sagi, told NoCamels: “An antibody is a protein produced by the body’s immune system. Each antibody can bind to a specific antigen, or target; an interaction similar to a ‘lock and key’”. According to Sagi, “just as immunization with a killed virus induces the immune system to create antibodies that attack live viruses, an MMP immunization in theory could create antibodies that block the MMP-9 enzyme and help combat the disease.”

When mice during the research were treated with metallobodies, it significantly prevented various symptoms associated with autoimmune diseases, including diarrhea, weight loss and tissue destruction. According to Professor Sagi, “metallobidies treatment was effective in both preventative and therapeutic mode of application.”

Sagi believes that the effects of this vaccine can work better than current treatment methods. “Our antibodies will mimic the natural protective process in vivo,” she says. “In this respect, the new drug may be more efficient than other therapeutics such as steroids.”
At present, however, the researchers cannot predict which side effects can arise from using this vaccine on humans, so further research must be conducted.

“Yeda”, the technology transfer arm of the Weizmann Institute, has applied for a patent for the synthetic immunization molecules as well as the generated metallobodies. According to Sagi, this treatment will be available to the public in the next five to eight years, pending the next stage of drug development. She hopes that the future of this vaccine technology is to “target various metal dependent enzymes that play important roles in different diseases.”

See also: "Our thought is that in fact CFS is an autoimmune disease in most patients," says oncologist Olav Mella. Mella and his colleague, Oystein Fluge, MD, PhD, say they accidentally discovered that rituximab might help chronic fatigue syndrome

See also: Study demonstrates that 95% of ME/CFS Patients have Anticardiolipin Antibodies, suggesting that ME/CFS may be an autoimmune condition

Margaret Williams: The biopsychosocial model has no empirical foundation in relation to ME/CFS

2012-01-25T11:39:00.000-08:00

More concerns about the current UK Welfare Reform

Margaret Williams 22nd January 2012:

Attention is drawn to a letter recently sent to two high-profile members of The House of Lords by Douglas Fraser, a former professional violinist but now severely affected by ME/CFS (http://www.meactionuk.org.uk/FraserToTGTandMM.htm ).

In it, Fraser sets out his concerns about a paper circulated by Lord (David) Freud, Parliamentary Under Secretary of State (Minister for Welfare Reform) to certain members of the House of Lords (this being “Models of Sickness and Disability” by Waddell G and Aylward M, whose track record on the alleged deviance of sick people -- those with ME/CFS being specifically targeted -- is documented in “Magical Medicine: how to make a disease disappear” by Professor Malcolm Hooper available at www.meactionuk.org.uk/magical-medicine.htm ).

David Freud’s history is interesting: he previously worked as a journalist for the Financial Times and then joined a leading UK investment bank (UBS investment banking), where he was on record as saying to his deputy: “If the rest of the country knew what we were being paid, there would be tumbrels on the streets and heads carried round on pikes”. In his city career he frequently got things seriously wrong. As one reviewer of his book put it, Freud “will be remembered in the City as one of the key players in several of the most embarrassing and badly managed deals in investment banking”. His revenue forecasts were, in his own words: “completely potty”; according to the Daily Telegraph, his financial plans for Euro Disney “went so goofy they almost wrecked his career” and on the Channel Tunnel Rail Link he got his sums wrong by £1.2 billion and had to be bailed out by the Government (www.variant.org.uk/events/Doc7Poverty/BankerBankies.pdf ).

Nonetheless, as the “To Banker from Bankies” 2009 report (which was supported and funded by Oxfam) states, in 2007 Freud was appointed as the key Government advisor on welfare reform by Labour’s John Hutton, having been commissioned to produce a report “Reducing Dependency, Increasing Opportunity” on the “Welfare to Work” programme. This was despite the fact that, in his own words, Freud “didn’t know anything about welfare at all” (Daily Telegraph, 4th February 2008). Despite the great complexity of the welfare system, Freud researched and wrote his welfare “shake-up” plan in just three weeks. It recommended that the existing role of private firms (such as the French company Atos) in the Government’s “Welfare to Work” programme be dramatically increased; he acknowledged that there was no evidence to suggest that private contractors were any better than the Department for Work and Pensions, but he still concluded that it would be “economically rational” to pay them tens of thousands of pounds for every person they removed from benefits.

The Daily Telegraph subsequently reported that Freud himself had severed all ties with Labour Ministers and was joining the Conservatives’ Work and Pensions team “after being put forward for a peerage”.

In May 2010 the Coalition Prime Minister (David Cameron) appointed him to his current post as Minister for Welfare Reform.

On 17th January 2012 Hansard recorded that Lord Freud referred to the “Models of Sickness and Disability” document that he had handed round to some members of the House of Lords (http://www.publications.parliament.uk/pa/ld201212/ldhansrd/text/120117-0001.htm), this being the document which will apparently underpin the transition from Disabled Living Allowance (DLA) to the Personal Independence Payment (PIP) and from which document it is clear that the biopsychosocial construct now permeates medical assessments for state benefits (so it may come as no surprise that Professor Peter White is acknowledged as an advisor).

Lord Freud explained: “I am hopeful that PIP will do a better job than DLA….I shall now turn to the more technical aspects of this issue – that is, looking at what we are doing with the PIP and its assessment. Is it a medical assessment…? It absolutely is not.

“…Our approach is – and this is rather a mouthful – akin to the biopsychosocial model…

“I sent round a rather interesting piece of analysis to many noble Lords in the Committee, called Models of Sickness and Disability, which showed the differences between the models, explaining the medical model, the reaction of the social model against the pure medical model and the synthesis of the biopsychosocial model. The summary of the biopsychosocial model in the analysis is that: ‘Sickness and disability are best overcome by an appropriate combination of healthcare, rehabilitation, personal effort and social/work adjustments’. There is a coherent theory behind this assessment”.

There are about 170 references to “models” scattered throughout the 40 page document and Fraser points out that readers may get the impression when it comes to the “biopsychosocial model” that a rigorous and scientific approach has been taken, yet it may be argued that there is no coherent theory whatsoever behind that “model”.

Fraser draws attention to the authors’ footnotes, which are rife with selective referencing and contain misquotations from and misrepresentations of the (not easily available) cited source.

In one instance the authors seem to infer (from their cited source) that it has been shown to be perfectly legitimate to proceed directly from biopsychosocial theory (or the “conceptual model”) to biopsychosocial practice and policy, when the cited author in fact concluded that the biopsychosocial model is “hardly a theory” and “certainly not a model”.

The central arguments surrounding issues of bias and confounding in relation to the biopsychosocial model that are exposed within the cited source are not -- as they should have been -- made known by Waddell and Aylward.

Notably, the impression from the footnotes is that it was Professor Peter White who provided “classic” examples on “how the biopsychosocial model is not an aetiological model of disease, and (how) arguments about whether the cause of a particular disease is biological or psychosocial obscure the main issue”, when in reality it was George Davey-Smith, Professor of Clinical Epidemiology at the University of Bristol who urged caution and who carried the torch for intellectual integrity: it was he who showed that bias can generate spurious findings and that when interventional studies to examine the efficacy of a psychosocial approach have been used, the results have been disappointing, and he who pointed out that cholera was attributed to “moral” factors and that peptic ulcer was attributed to stress before the appliance of science (Proof Positive? Eileen Marshall & Margaret Williams, 30th August 2005 http://www.meactionuk.org.uk/PROOF_POSITIVE.htm ).

According to Waddell and Aylward (and White), both these examples are of “specific diseases of doubtful relevance to common health problems” and they are dismissed because they appear to threaten the biopsychosocial philosophy, which Waddell and Aylward claim applies to “any illness”.

However, when one examines Waddell and Aylward’s claim of supporting evidence for the biopsychosocial model in the management of low back pain (“extensive scientific evidence that the biopsychosocial model provides the best framework for the modern management of low back pain”), one finds from the latest Cochrane meta-analysis examining the results of behavioural interventions for low back pain that: “the risk of bias of the trials included in this review was generally high” and, in relation to the addition of behavioural therapy to in-patient rehabilitation over the longer term, that: “there was only low or very low quality evidence, which was based on the results of only two or three small trials” (Behavioural treatment for chronic low-back pain; 7 JUL 2010. The Cochrane Collaboration. http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD002014.pub3/full ).

Such seeming sleight of hand by Waddell and Aylward in seriously misleading a Government Minister and members of the House of Lords is to be deplored.

When it comes to ME/CFS, over 20 renowned international experts on ME/CFS have provided written statements of concern effectively stating that cognitive behavioural therapy and graded exercise therapy used to support the alleged existence of the “biopsychosocial model” do not work for people with ME/CFS (Magical Medicine pp 88-92).

Furthermore, numerous trials have shown that not only is the “biopsychosocial model” unsuccessful in the management of ME/CFS but that the model itself is not evidence-based and it may be actively harmful:

(i)              the evidence that behavioural modification techniques have no role in the management of ME/CFS is already significant and has been confirmed by a study in Spain, which found that in ME/CFS patients, the two interventions used to justify the biopsychosocial model (CBT and GET) did not improve HRQL (health-related quality of life) scores at 12 months post-intervention and in fact resulted in worse physical function and bodily pain scores in the intervention group (Nunez M et al; Health-related quality of life in patients with chronic fatigue syndrome: group cognitive behavioural therapy and graded exercise versus usual treatment. A randomised controlled trial with 1 year follow-up. Clin Rheumatol 2011, Jan 15: Epub ahead of print)

(ii)            “Notwithstanding the medical pathogenesis of ME/CFS, the (bio)psychosocial model is adopted by many governmental organizations and medical professionals to legitimize the combination of Cognitive Behavioral Therapy (CBT) and Graded Exercise Therapy (GET) for ME/CFS…. Justified by this model CBT and GET aim at eliminating presumed psychogenic and socially induced maintaining factors and reversing deconditioning, respectively. In this review we invalidate the (bio)psychosocial model for ME/CFS and demonstrate that the success claim for CBT/GET to treat ME/CFS is unjust. CBT/ GET is not only hardly more effective than non-interventions or standard medical care, but many patients report that the therapy had affected them adversely, the majority of them even reporting substantial deterioration…. We conclude that it is unethical to treat patients with ME/CFS with ineffective, non-evidence-based and potentially harmful ‘rehabilitation therapies’ such as CBT/GET” (A Review on Cognitive Behavioural Therapy (CBT) and Graded Exercise Therapy (GET) in Myalgic Encephalomyelitis (ME) / Chronic Fatigue Syndrome (CFS). Neuroendocrinol Lett 2009:30(3):284-299)

(iii)          The Wessely School’s much-vaunted FINE (Fatigue Intervention by Nurses Evaluation) Trial could not by any standards be judged to have been successful: the results showed that “pragmatic rehabilitation” (PR, based on CBT/GET) was minimally effective in reducing fatigue and improving sleep only whilst participants were engaged in the programme and that there was no statistically significant effect at follow-up. Furthermore, pragmatic rehabilitation had no statistically significant effect on physical functioning; equally, its effect on depression had diminished at follow-up. Moreover the other intervention being tested (“supportive listening” or SL) had no effect in reducing fatigue, improving physical functioning, sleep or depression (AJ Wearden et al; BMC Medicine 2006, 4:9 doi:10.1186/1741-7015-4-9

(iv)          Equally, the widely acclaimed but statistically unsustainable PACE Trial cannot be said to have been successful since, uniquely, ratings that would qualify a potential participant as sufficiently impaired to enter the trial were considered “within the normal range” when recorded on completion of the trial and no recovery statistics have been published by the Chief Principal Investigator, Professor Peter White (Comparison of adaptive pacing therapy, cognitive behaviour therapy, graded exercise therapy, and specialist medical care for chronic fatigue syndrome (PACE): a randomised trial. PD White et al. Lancet 2011 Mar 5;377(9768):823-36).

It has not been possible to determine Lord Freud’s awareness of the need to distinguish biomedical science from biopsychosocial ideology before he formulates Government policies that will have a profoundly detrimental impact on sick and frightened people whose means of survival is threatened if their state support is withdrawn.

The term “biopsychosocial model” is used almost exclusively by Wessely School psychiatrists to refer to disorders that they continue to regard as psychosomatic (especially ME/CFS) and it is not used by other disciplines. For example, cardiologists do not refer to patients as having a “biopsychosocial” disorder and oncologists do not refer to cancer as a “biopsychosocial” disorder, nor do they claim that their patients must be coerced back to work by the withdrawal of their state benefits because it is patients’ aberrant belief that they are physically sick which maintains their disease.

The use of such a term can be seen as a linguistic misdirection by these psychiatrists, allowing them to conceal their belief that ME/CFS is not a physical disease but an aberrant state of mind maintained by psychological and behavioural factors (ie. the psychosocial components of “biopsychosocial”). The only “bio” in their “biopsychosocial model” is their reluctant concession that ME/CFS is sometimes preceded by a self-limiting viral infection (and, despite the overwhelming international evidence to the contrary, they insist it is maintained by psychosocial elements that do not result from any organic pathology).

As Fraser states: “As the tortured arguments continue, one suspects that the authors (Waddell and Aylward) are keenly trying to ensure something is kept out of public view….Had Lord Freud said ‘We have not gone for the medical model; we have gone for the psychosomatic model’, I do not think that members of the House would have been impressed for a moment”.

Informed readers of “Models of Sickness and Disability” might wonder why something that has been repeatedly shown not to be a successful model is being promoted by a UK Government.

As Fraser points out, an explanation may be found from a 2005 issue of “Decision Makers’ Exchange” (DME), the monthly newsletter for DLA and Attendance Allowance decision makers: “Confirmation that Medical Services (ie. the DWP) have adopted the Biopsychosocial Model for assessing not just claims based on incapacity for work but also DLA and AA came in the July edition of Decision Makers’ Exchange…An item explained that Medical Services have recently introduced a change in the way that they assess a customer’s disabilities and the effect it has on their lives. The Biopsychosocial Model aims to address how a person’s disability has an effect on that individual’s life”. The newsletter features an article by Mansel Aylward, former Chief Scientist at the DWP, entitled “Professor Aylward endorses the Biopsychosocial Model of Disability….Conditions for which there is limited or no recognised pathological basis, such as chronic fatigue, fibromyalgia…feature regularly in disability assessments for state benefits….The Biopsychosocial Model is the answer to the disability analyst’s plight”.

Fraser then quotes from an Atos Origin Medical Services meeting in 2004 which sets out just how the dogma that underpins the “biopsychosocial model” is being authoritatively promulgated, and he notes “the convenient fictions and lack of logic those responsible would…refuse to tolerate if applied to their own family and friends”.

The Atos Origin 2004 Conference report is explicit: “Psychosocial factors…are at least as important as physical factors in the onset and maintenance of these conditions. Patients can make a number of ‘secondary gains’ with these unexplained illnesses, such as…turning a socially unacceptable disability into a more acceptable ‘organic’ disability caused by injury or disease beyond their control. They can blame their failures on the illness; elicit care, sympathy and concern from family and friends; avoid work or even sex; and there are financial rewards associated with disability.

“…if a patient believes their illness was caused by a virus and there’s nothing they can do about it, their prognosis is not likely to be positive. But if the patient believes…that the symptoms won’t last long and they have control over them, then the prognosis will be better…. We need patients to understand their situation, so they are more likely to go back to work” (http://www.meactionuk.org.uk/AtosConference2004.pdf).

Fraser concludes in his letter: “Given the combined forces of what appears as an unseen (and) corporate-generated self-serving attitude (tacitly approved by “Models of Sickness and Disability” authors as perfectly moral) in the guise of the…psychosomatic model…promoting the prejudice of…pop-psychology directed at vulnerable and relatively powerless others…and a profit-driven foreign company…it is unsurprising that so many of the bad decisions they help facilitate are overturned on closer examination at costly appeals. It would of course, be much cheaper in the long run to adopt some of the higher standards of appeal tribunals in the first place”.

This non-evidence-based but pervasive biopsychosocial ideology is now being foisted on the unsuspecting people of Australia and New Zealand, because in May 2010 Aylward wrote a report for the Australasian Faculty of Occupational and Environmental Health (Realising the Health Benefits of Work: A Position Paper. Professor Sir Mansel Aylward CB; Director: Centre for Psychosocial Research and Disability Research, Cardiff University (the Centre being funded by the health insurance company UNUM Provident). In it, Aylward asserts:

“Fundamental Precepts:
Main determinants of health and illness depend more upon lifestyle, socio-cultural environment and psychological (personal) factors than they do on biological status and conventional healthcare
Work: most effective means to improve well-being of individuals, their families and their communities
Objective: rigorously tackling an individual’s obstacles to a life in work.

“Making the distinction: definitions and usage:
Disease: objective, medically diagnosed pathology
Illness: subjective feeling of being unwell
Sickness: social status accorded to the ill person by society

In that report Aylward claims that largely subjective complaints (such as ME/CFS) are often associated with psychosocial issues, not with pathology, and that “bio-psycho-social factors” may aggravate and perpetuate disability and that they may also act as obstacles to recovery and barriers to return to work. He refers to the UK Government’s “Pathways to Work” initiative, with its mandatory work-focused interviews for sick people and the use of CBT to change people’s alleged misperceptions about their health; his message is: “Barriers to recovery and return to (retention in) work are primarily personal, psychological and social rather than health-related ‘medical problems’ and that “Perceptions lie at the ‘heart’ of the problem”.

His report provides guidance on “ Engaging and Exploiting Stakeholders”, which he says must include
changing the beliefs and attitudes of politicians, civil servants, health professionals, employers etc and changing the present culture about health and well-being in order to deliver “visible hard outcomes”.

Even more disturbingly, Aylward’s report asserts that there must be new roles for health professionals, who must no longer permit their patients to believe that they are incapable of work if they have a disease but must instead propel them back into work even if they do have a legitimate medical disease. In the UK, there are recorded accounts of people with cancer being forced back to work and of a cancer sufferer dying whilst awaiting an appeal against a refusal of benefits by Atos.

Unsurprisingly, since he has invested so much into the promulgation of it, despite the accumulating evidence to the contrary, Aylward claims that the biopsychosocial principles of management are evidence-based, when the “biopsychosocial model” can be readily shown to have no empirical foundation, particularly in relation to ME/CFS.

It has nevertheless been used to justify beliefs and policies, for example, in his letter to the two members of the House of Lords, Douglas Fraser quotes the following:

"Benefits and Work has seen one recent medical report in which a DWP doctor explicitly stated that he had used the Biopsychosocial model. The claimant has Chronic Fatigue Syndrome and was seeking renewal of an award of the middle rate of the care component and the higher rate of the mobility component. His condition had deteriorated since his last award over two and a half years ago. The doctor who visited him recorded that: ‘There are few significant findings other than subjective tenderness and stiffness. But the customer is clearly living the life of a disabled person and I have applied the Biopsychosocial model’. The doctor then stated, without explaining how the conclusion had been reached, that the claimant’s condition was just 40% physical and ‘60% psychosocial’…. This allowed the decision maker to conclude that the claimant’s award of higher rate mobility was no longer appropriate as the primary reason for his virtual inability to walk was psychosocial rather than physical".

The specific numbers given (40/60 split) provided a superficial appearance of scientific objectivity to cover what was in fact no more than a highly-prejudiced guess, because such things cannot be measured or quantified, but they achieved the required outcome (which was to strip this person of his benefits and for which the company to which the DWP has delegated its medical assessments would receive a handsome financial reward).

It is, of course, imperative to seek out and remove from state benefits the cheats and idle lead-swingers, but it is even more imperative to take appropriate medical care of the sick, yet what underpins current Government welfare reform is the un-evidenced conviction that work is always good for people, no matter how ill they may be.

Commenting on a response to her article “Illness as Deviance, Work as Glittering Salvation and the ‘Psyching-up’ of the Medical Model: Strategies for Getting the Sick ‘Back to Work’ ” (http://www.democraticgreensocialist.org/wordpress/?page_id=1716), Gill Thorburn says: “I was appalled to discover what they have been doing to the ME community for so many years. Its nothing short of legitimised abuse. The one discouraging thing I’ve experienced in all my research so far has been discovering for how many years how much authentic evidence has been simply disregarded by those in power in favour of this spurious psychological approach. Some of the accounts on the net are simply heartbreaking, and it beggars belief that these people should have been allowed to continue with their ‘methods’ and ‘theories’. As someone pointed out recently, they ‘intervene’ in peoples’ lives with impunity, disregarding their negative effects, for which they are never held to account”.

A UK Government is democratically elected to look after the best interests of the nation and of its citizens, not to abuse and persecute the sick in favour of foreign corporate profits by imposing the “biopsychosocial model” that is promoted by UK psychiatrists who have vested financial interests in such a “model” because they work for the health insurance industry, whose profits benefit from its use.

See also: Another cracker from the CBT school of denial: “The bastards don’t want to get better”…

See also: Harvard Medical School: EEG spectral coherence data distinguish chronic fatigue syndrome patients from healthy controls and depressed patients

See also: The putative agent of ME/CFS can be transferred to monkeys
See also: Almost 5% of ME/CFS patients contracted ME/CFS from a blood transfusion

See also: Cerebrospinal fluid profiles can differentiate between Lyme disease, ME/CFS and healthy controls

See also: The main characteristic of ME is an abnormally delayed muscle recovery after doing trivial things, if you don't have that, you don't have ME
See also: GET (graded exercise therapy) is torture for ME patients and directly contravenes the do NO Harm principle of the GMC

See also: I never imagined my sister would die from ME

Douglas Fraser's letter to two high-profile members of The House of Lords

2012-01-25T11:26:00.000-08:00

Douglas Fraser, a former professional violinist but now severely affected by ME:

Dear Lady Grey-Thompson and Lady Mar,

Thank you for your hard work in the debate around the Personal Independence Payment and other matters.

I am writing because of my concerns over a paper that I believe was circulated on the 17th January 2012, and shall try to be brief.

Before illness struck I was a musician and have no scientific training, but sometimes I think I spot the odd misleading analogy or argument, although of course there are no guarantees, and I'm often more wrong than right, but I would like to respectfully beg your indulgence on this occasion.

There is much I find worrying in "Models of Sickness and Disability" ('MoSaD' hereafter) by Waddell G and Aylward M, referred to by Lord Freud as "a rather interesting piece of analysis", which will underpin the PIP assessment in the form of the so-called biopsychosocial assessment, behind which Lord Freud, mistakenly in my view, claimed "there is a coherent theory".

Among questionable claims and semantic acrobatics, especially in areas where the MoSaD authors appear to lack expertise, one finds examples of some rather disrespectful suggestion, seemingly being harnessed for effect, pointing away from scholarship and objectivity towards polemic, popular prejudice, and the troubling bias of the self-referential e.g. "These have been described as common health problems - Waddell & Burton 2004 .. similar in nature and sometimes even in degree to the bodily and mental symptoms experienced at times by most adults of working age". [6]

One example of the use of "suggestion" might be the following (I've removed the connecting camouflage with '...' ):

"Many incapacity benefit recipients are not completely incapacitated but still retain (some) capacity for (some) work, although this does not mean that they are all malingerers or scroungers ... malingering ... is extremely rare ... even if some degree of exaggeration may be much more common." [5]

Not a few of the MoSaD author claims appear to me to be closer to fiction than fact, for example, when they suggest that "schizophrenia and a subjective complaint of stress" are but "two ends" of a "spectrum". [8]

Although at root there are probably just clashing values, some claims appear to border on the nonsensical (perhaps with 'purpose'), for example: "The medical model is so implicit in modern medicine that it is often taken for granted". [8]

I am not sufficiently well to attempt a comprehensive overview and rebuttal, which would run to many pages, but I hope that someone may be able to deal with this thoroughly, before it is too late.

Instead, I will only focus on two details and their implications as I see them.

Interestingly, the article is peppered with the technical term 'model', at about 170 occurrences within the space of some 40 pages, excluding those at the top of each page (I am assuming I have the correct version of the article).

Some people may associate the term 'model' with science, or at least, some readers might tend to trust that a rigorous kind of approach has been taken, but I believe that would be mistaken in the main case being advanced by the authors of MoSaD, and Government.

There are two footnotes with (reluctant?) references to two articles (most people will not be able to access) which may help illuminate, and perhaps signal, the need for considerable caution.

I believe both of these articles are useful study before reading, or re-reading, and trying to decipher the "Models of Sickness and Disability" article, apparently so pertinent to PIP assessment.

The first can be found on page two of MoSaD:

"2. Scientific models are ‘simplified representations or descriptions of the structure of a complex system, which seek to explain phenomena based on theory and mechanisms, and are designed to facilitate testing and predictions’ (McLaren 1998, Llewellyn & Hogan 2000). Models provide a practical means of moving from theory to reality. The caveat is that models are not ‘real’ and should not be adopted uncritically: they are simply a tool that is useful only so long as it aids understanding, research and management".

One of the references concerns a paper: "McLaren N (1998) A critical review of the biopsychosocial model. Aust N Z J Psychiatry 32: 86–92" (I am unable to access the other).

It is interesting to note how the MoSaD authors shift the meaning intended by McLaren (when discussing Dennett) from: "A model is the practical means of matching a theory to reality" to: "a practical means of moving from theory to reality" (perhaps McLaren ought to know about this).

There is a considerable of difference between the two, the implications of which I hope will become apparent, but the paper would surely fail peer review at this early point.

The next sentence by McLaren (on Dennett) reads: "He emphasises that models must be distinguishable from the real things they model". Whereas the next sentence by the MoSaD authors reads: "The caveat is that models are not ‘real’.." (but aid in "understanding, research and management" - only when it suits one's own agenda, I presume) .

Meaning is again shifted, and likewise most readers would not be aware of the original context, McLarens intention, or the sleight of hand.

McLaren continues in his paper: "At this stage, the two meanings which attach to the noun 'model' are quite clear. A minority of authors use 'theory' and 'model' more or less interchangeably to represent an idea or notion. The majority, however, use the terms quite separately, reserving theory to nominate unembodied concepts or abstract notions, and model as the name for a class of real things, usually simplified diminutives of the unseen objects and processes outlined in the theories". [88]

Later on in this detailed analysis, McLaren states: "The common element in these accounts of models (physical, diagrammatic and mathematical), lies in their function: models model. What do they model? They model theories or theoretical constructs, meaning they embody, actualise or realise an idea, notion or concept". [88]

Before discussing the Biopsychosocial Model (BPS) in some detail, McLaren concludes: "Regardless of the validity of the theory, if the model is wrong, investigating it is non-science".

Following a lengthy dissection of the flawed thinking behind the BPS model and illegitimate attempts to borrow from systems theory, McLaren remarks: "[But] of the model itself, there is nothing to be seen. Engel simply demonstrated a need for a particular approach, talked about it for a while then announced that he had found it. He had not. All he offered was an emotive case for more humanity and less technology in medicine, little more than a heartfelt plea based in a particular ontological stance. It was hardly a theory, and it was certainly not a model". [89]

He elaborates how: "Engel did not define his biopsychosocial model; instead, he hoped its definition would emerge ostensively, through a description of how it might function, with the emphasis on 'might'. His model can therefore never reach scientific status: a description of what something does can never be an explanation of why or how it does it". [90]

After detailed and logical consideration, the situation becomes clear: "In practice, if we want to know whether Engel's biopsychosocial model is truly a model, or just a case of wishful thinking, then a simple test will decide the issue. Try making, say, a prediction about a man's psychological state from his biological data, or vice versa. Or perhaps try to predict wholly from sociological data which girls will develop post-partum mental disorders as young women or psychoses in old age. Since nothing like this can be done, Engel's 'model' is not a model in any interesting sense of the term". [91]

However, in spite of their knowledge of the paper by McLaren, it is not clear that the MoSaD authors have understood the serious issues facing them (although much of what they write appears to me to ignore the challenges of scientific responsibility coming from McLaren - who's published article the authors presumably could not easily avoid).

In MoSaD the authors write:

"The biopsychosocial model recognizes that biological, psychological and social factors, and the interactions between them, can influence the course and outcome of any illness. Human beings are biopsychosocial – an integrated whole of body and mind in a social being – so a comprehensive model of human illness must be biopsychosocial ... The term ‘biopsychosocial’ is a catchy shorthand that expresses the key features of the model. The disadvantage is that it is ‘professional’, technical and clumsy, but no one has yet produced a simple yet adequate alternative". [22]

Perhaps it should simply read: "We believe that we know what modulates the effects of an illness".

On this point it is rather remarkable that the MoSaD authors can only recommend developing "messages" to change outcomes. [28]

However when one is confronted with the novelty that : "human beings are biopsychosocial ... so a comprehensive model human illness must be biopsychosocial" (humans beings are bipedal ... so a comprehensive model of human illness must be bipedal), it would be wise to be on the alert for any non-scientific, as it were, agenda. [22]

There is of course an abundance of experimental research (some of it contradictory, some with uncertain practical application) showing both predictable and unpredictable effects on organisms from poverty, isolation, social hierarchies etc., which for their proper amelioration perhaps only the bravery of a radical overhaul of a currently unfair and hypocritical capitalist system would be required. However, that might be antithetical to the dogma of MoSaD, which I view more as part of the problem than part of any of realistic solution.

As the tortured arguments continue, one suspects that the authors are keenly trying to ensure something is kept out of public view, and I believe that it may simply be the term "psychosomatic" (linked to 'hysteria'), which is made very conspicuous by it's virtual absence (it reluctantly appears once, somewhat disingenuously in my estimation).

In the same way the authors invoke Hippocrates as some justification for allegedly treating 'the whole' person' without mentioning his dismal failure to spot the important difference between causes and mere associations, the authors unaccountably fail to mention why "Engel introduced the term biopsychosocial" (to replace psychosomatic), and perhaps the authors should be called on this. [23]

Had Lord Freud said: "We have not gone for the medical model; we have gone for the psychosomatic model", I do not think Members of the House would have been impressed for a moment, given its misogynist overtones and tragic history as a means to deny women medical treatment, among other things.

The second footnote and reference that I found of interest is on page 26 of MoSaD, and concerns a chapter-length article by George Davey-Smith, a Professor of Clinical Epidemiology, entitled "The biopsychosocial approach: a note of caution" (in White P (2005) Biopsychosocial Medicine: An Integrated Approach to Understanding Illness. Oxford: Oxford University Press). Very few people will have access to this article.

Interestingly, without mentioning Davey-Smith by name, the footnote reads: "26. White (2005) gives the classic examples of this debate: in previous times, cholera was attributed to ‘moral’ factors and more recently peptic ulcer was attributed to psychosocial stress (before the discovery of the bacterium Helicobacter pylori). Both examples are of specific diseases and of doubtful relevance to common health problems".

A previous footnote, to "Proponents of the medical model argue that its achievements justify expectations that all illness will eventually succumb to biomedical advances,9 ..", simply states: "9 Historical examples of cholera or peptic ulcer, originally attributed to various psychosocial ‘causes’ and subsequently shown to be physical pathologies, are not relevant to the present discussion. These were always objective diseases, even if the aetiology was unknown". [11]

And later, following the section on "The biopsychosocial model applied to common health problems", at footnote 39 "Thanks are due to Bob Grove and Peter White for suggestions on this section". [37]

The summary of the chapter by Davey-Smith begins:

"This chapter will provide a cautionary critique of whether the biopsychosocial (BPS) model is useful in understanding aetiological factors in chronic diseases. I will illustrate the arguments by referring to studies of peptic ulcer and ischaemic heart disease. I will show that bias and confounding can generate spurious findings and associations, especially in observational studies. When interventional studies have been used to examine the efficacy of a psychosocial approach the results have been disappointing".

Davey-Smith points to various historical precedents that eventually undermined popular assumptions underpinning the BPS model including:

"Over the past 50 years many psychosocial factors have been proposed and accepted as important aetiological agents for particular diseases and then they have quietly been dropped from consideration and discussion. If this meeting had been held 15 years ago we would have discussed type A behaviour at great length. Type A behaviour will hardly be mentioned at this meeting, because it no longer appears to be an important cause of coronary heart disease. People versed in the history of epidemiology will know that conditions such as cholera, pellagra, ben ben, asthma, Down’s syndrome, scurvy, yellow fever, typhoid, and peptic ulcer were all at one time seen as diseases that were importantly influenced by stress or (in earlier times) ‘moral’ factors. In 1832 William Beaumont, for example, considered that such factors underlaid ‘the greater proportional number of deaths in the cholera epidemics'. He would doubtless have considered the BPS model an ideal way of conceptualizing the causes of cholera, while pouring scorn over those studying the geographical distribution of cases and relating this to water supply." [3]

Before discussing the well known & misleading stress theories of peptic ulceration, where it was claimed in 1948 that a "better appreciation of the natural history of the disease has directed the treatment away from the ulcer towards the individual as a whole" [4], Davey-Smith introduces Sontag.

"An important critic of the BPS model—although she never explicitly talks about it— is Susan Sontag. She published a remarkable book, Illness as Metaphor, a year after Engel's 1977 article appeared.

Sontag wrote about how in plague-ridden England in the late sixteenth and seventeenth centuries, it was believed that a happy man would not get the plague. She stated that,

'The fantasy that a happy state of mind would fend off disease flourished for all infectious diseases before the nature of infection was understood. Theories that diseases are caused by mental state and can be cured by willpower are always an index of how much is not understood about the physical basis of the disease. The notion that a disease can be explained only by a variety of causes is precisely the characteristic of thinking about diseases where causation is not understood'

Diseases that are thought to be multi-determined have the widest scope for becoming metaphors for what is felt to be socially or morally wrong.

Sontag was writing at least partially in response to her own diagnosis with cancer. Her reason for being sceptical of the BPS model was that she saw it as a way of putting blame for disease on the people with disease. This metaphorical treatment of disease can lead to internalized blame and guilt. Sontag therefore wanted to strip these metaphors away and see disease principally as a biological, not psychological, phenomenon". [3]

I found his rich tour of confounding and bias incisive and disturbing, given the current uncritical climate. As with the McLaren paper, it seems odd that the MoSaD authors fail to acknowledge the meat of the argument, which concerns bias and confounding, while dismissing the paper on seemingly spurious grounds, without mentioning the authors name.

He concluded [GeorgeDaveySmith_White_BPS.doc]:

"In this presentation I have suggested that the epidemiological evidence supporting important contributions of psychosocial factors as direct causes of disease is limited. However, it might be suggested that despite this, a doctor who is influenced by the BPS is the sort of doctor one would like to consult when sick. I am not so certain about this. When writing about a myocardial infarction patient whom he had seen, Engel stated, `In the end, whether the patient lives or dies, the biopsychosocial model further provides the physician with the conceptual tools to clearly think and plan the implications of the cardiac arrest.' If I have a heart attack, I want to be treated by a doctor who cares about whether the patient lives or dies. I'm not really concerned about whether the doctor has the above-mentioned conceptual tools, I would rather have a doctor who keeps up to date with the best evidence on somatic treatments and gives me morphine, a thrombolytic, and aspirin, then puts me on appropriate long-term treatments". [12]

The MoSaD authors claim both, that the reasonable position of Davey-Smith is of "doubtful relevance to common health problems" (without credibly establishing how that might be possible), apparently dismissing inconvenient truths, and, that their BPS model "recognizes that biological, psychological and social factors, and the interactions between them, influence the course and outcome of any illness". [26 & 22]

However, as McLaren has pointed out: " ... it might be argued that an approach which considers biological, psychological and social factors necessarily amounts to a biopsychosocial model but, for several reasons, this is not the case. To begin with, we must clearly distinguish theories with real predictive value (i.e. they can predict something we didn't know or which was counter-intuitive) from those which can only 'explain' or rationalise what we already know. The former are science, but the latter are just self-reinforcing prejudice.

Only highly improbable predictions can test a theory's basic assumptions. Furthermore, researchers who gather data from a variety of theoretically unrelated fields will not be able to test the basic assumptions which led them to collect just those data and not others. They may be able to detect associations but, critically, not errors in their own basic assumptions. Only a model with true predictive value can do that, and then not always.

Unless there is an integrating theory already in place, gathering biological, psychological and sociological data about people will only yield scattered lumps of information which don’t relate to each other in any coherent sense. Without an over-arching theory to integrate the fields from which the data derive, associations between differing classes of information are meaningless". [90]

Some readers of "Models of Sickness and Disability" might wonder why something, that is "hardly a theory" and "certainly not a model" that produces "self-reinforcing prejudice", that "can lead to internalized blame and guilt" and can be used "as a way of putting blame for disease on the people with disease", according to McLaren, Davey-Smith and Sontag respectively, is being promoted by a UK Government.

Providing some possible insight into this, one organisation had already reported as far back as 2005 that:

"Confirmation that Medical Services have adopted the Biopsychosocial Model for assessing not just claims based on incapacity for work but also DLA and AA came in the July edition of Decision Maker’s Exchange (DME), the monthly newsletter for DLA and AA decision makers ... An item in DME explained that:

“Medical services have recently introduced a change in the way that they assess a customer's disabilities and the effect it has on their lives. The Biopsychosocial Model aims to address how a persons disability has an effect on that individuals life”.

The newsletter features an article by Mansel Aylward, former Chief Scientist at the DWP, self-effacingly entitled “Professor Aylward endorses the Biopsychosocial Model of Disability”. In it, the Professor asks, but doesn’t actually answer in any tangible way, the questions:

"Why is it that in disability assessment medicine we see two individuals, of the same age and with the same illness or pathological condition, but with very different resulting levels of disability? How, as medical disability analysts, do we assess the level of disability in people with conditions whose effects are predominantly or wholly subjective? People with "medically unexplained symptoms" - conditions for which there is limited or no recognised pathological basis, such as chronic fatigue, fibromyalgia, chronic low back pain - feature regularly in disability assessments for state benefits. How do we evaluate and reasonably validate the functional limitations that affect people with such conditions?"

Whilst not giving any clear explanation of how it is to be applied, the Professor does explain that the Biopsychosocial Model is the answer to the disability analyst’s plight".

"Genuinely disabled

Whatever the philosophy behind the model, Medical Services doctors are now being taught that the most important test to be applied to DLA and AA claimants is whether they are “genuinely living the life of a disabled person”.

Doctors are being taught to look for evidence of:

“Consistency of disability within a typical day” – for example, someone with chronic fatigue might be expected to have a disturbed sleep pattern, often needing to sleep during the day.

“History involving chronic pain management” – this might be referral to a pain clinic, cognitive behavioural therapy, appropriate medication, physiotherapy or alternative therapies such as acupuncture.

“Home adaptations and adaptations to daily living” – this might include things such as the regular and consistent use of raised chairs, walking aids, a commode and a downstairs room for sleeping in.

“Appropriate intervention from a carer” – this might be assistance with things such washing and bathing, dressing, etc.

It’s nearly all in your mind

In theory, such an assessment which would require a more detailed and holistic assessment by doctors.

In practice, it seems likely to be used to dismiss a large part of a claimant’s needs as not physical but “psychosocial”.

"Benefits and Work has seen one recent medical report in which a DWP doctor explicitly stated that he had used the Biopsychosocial model. The claimant has Chronic Fatigue Syndrome and was seeking renewal of an award of the middle rate of the care component and the higher rate of the mobility component. His condition had deteriorated since his last award over two and a half years ago. The doctor who visited him recorded that:

“There are few significant findings other than subjective tenderness and stiffness. But the customer is clearly living the life of a disabled person and I have applied the Biopsychosocial model.”

The doctor then stated, without explaining how the conclusion had been reached, that the claimant’s condition was just 40% physical and “60% psychosocial: dependence on family members, depression and pain”. This allowed the decision maker to conclude that the claimant’s award of higher rate mobility was no longer appropriate as the primary reason for his virtual inability to walk was psychosocial rather than physical". [New genuinely disabled test to cut DLA & AA awards.pdf - http://www.benefitsandwork.co.uk/news/news-archive/186-new-genuinely-disabled-test-to-cut-dla-a-aa-awards ]

In a 2005 Newsletter (containing the same material as the Decision Maker’s Exchange above) from UnumProvident Centre for Psychosocial and Disability Research, where Professor Aylward was "Sponsored by UnumProvident", Dr Peter Dewis of UnumProvident stated: "I think it is true to say that without the academic debate stimulated by the Unit, we would not have developed our thinking on the bio-psychosocial model of illness in the way we have.

Without this developing understanding, we would not have been in a position to make the changes we did to our claims team structure in November". [Issue 1.pdf]

And at an Atos Origin Medical Services meeting in 2004, the manner in which BPS dogma were being authoritatively promulgated, the convenient fictions and lack of logic those responsible would no doubt refuse to tolerate if applied to their own family and friends, was reported thus:

“Psychosocial factors – such as personality, life events and psychiatric disorders – are at least as important as physical factors in the onset and maintenance of these conditions. Patients can make a number of ‘secondary gains’ with these unexplained illnesses, such as: work absence as a reward for years of struggle; turning a socially unacceptable disability in to a more acceptable ‘organic’ disability caused by injury or disease beyond their control. They can blame their failures on the illness; elicit care, sympathy and concern from family and friends; avoid work or even sex; and there are financial rewards associated with disability.”

" ... if a patient believes their illness was caused by a virus and there’s nothing they can do about it, their prognosis is not likely to be positive. But if the patient believes stress may have contributed towards their symptoms, that the symptoms won’t last long and they have control over them, then the prognosis will be better.”

“What people believe influences how they react and what they do about it. The mind and the body interact and we need to understand how this works. We need patients to understand their situation, so they are more likely to go back to work.” [AtosConference2004.pdf]

The MoSaD authors express their questionable beliefs about all of their fellow humans, apparently without exception, and their own values: "Human beings are driven by both self-interest and altruism, but self-interest is generally dominant. There is nothing morally wrong with self-interest, and it should not be misinterpreted as selfishness or greed". [21]

Being a foreign company, Atos, like UnumProvident, would probably then (and perhaps conveniently for those promoting Government short-term-ism) have no natural interest or concern in the well-being of British citizens, and probably even less for the real long term economy of this country.

Given the combined forces of what appears as an unseen mainly corporate-generated self-serving attitude (tacitly approved by MoSaD authors as perfectly moral) in the guise of the BPS psychosomatic model, possibly applied to the disadvantage of others, its systematic corporate inculcation promoting the prejudice of a weak pop-psychology directed at vulnerable and relatively powerless others, masquerading as benign science while probably routinely overriding serious factual matters of other individuals health, and a profit-driven foreign company (who may not hesitate to sack their British employees first, should their profits fall), it is unsurprising that so many of the bad decisions they help facilitate are overturned on closer examination at costly appeals.

It would be of course be much cheaper in the long run to adopt some of the higher standards of appeal tribunals in the first place.

On the BBCs "This Week" programme of the 19th of January, after raising awareness of the steep rise in UK disability hate crime, the comedienne and writer Francesca Martinez summed up the situation succinctly: "...this financial crisis we're in was caused by a very elite few at the top and once again the vulnerable in society are being made to pay for the greed of those at the top so really I think the government is morally disabled".

However, apart from wider such implications, I am hoping that someone, or some individuals have identified just how disingenuous and misleading the alleged biopsychosocial model could be in all its slippery expediency, and the serious threat to the health of others it may well represent, possibly now with a vengeance.

Although it is probably not the case, if anything in my email (and files) may be of interest or of use to anyone, please feel free to forward it.

I shall place relevant documents on-line via 'mediafire' for download, with a text-file index.

Thank you for taking the time and trouble to read this.

Yours sincerely,
Douglas T Fraser

I never imagined my sister would die from ME

2012-01-24T03:52:00.000-08:00

The Irish Times - Tuesday, January 24, 2012:MY HEALTH EXPERIENCE: RÓISÍN WILSON Sophia’s nervous system had been ravaged by ME

BEFORE MY sister Sophia got Myalgic Encephalomyelitis (ME), I had subconsciously developed a disparaging view of the disease. The little I knew about ME at the turn of the century was from how it had been portrayed in the tabloid press.

ME had been painted as some kind of luxury illness, labelled “yuppie flu”. It seemed a very boring disease and I can’t say I had any interest in it.

I had got the impression ME was kind of a sabbatical illness, an excuse for a few weeks off work to recharge the batteries. So when my mum told me Sophia had ME, I wasn’t that worried.

Sophia, two years my junior, had had meningitis before and malaria twice. What was ME compared to those bad boys? My feisty sister could easily whip this lily-livered ME.

I was living in New York at the time and on transatlantic phone calls with our Irish mum, she would tell me how my sister had had to leave her London life because she was too ill to look after herself. She told me Sophia was getting worse and that nearly everything hurt my sister.

I thought my mum was exaggerating; how can everything hurt Sophia?

Light hurt my sister, noise, smells, vibrations, the list went on. My then 26-year-old sister had almost zero energy and had to lie in a blackened room day and night, wearing a blindfold and earplugs, in constant pain.

If that wasn’t bad enough, the doctors treating her said this disease was a mere “wrong belief”, despite doing no physical tests on their patient. And just for good measure they called my mum an enabler, for believing her youngest child was genuinely ill and threatened to remove her as Sophia’s carer.

I listened to what my mum told me, but I couldn’t really take it in. How could Sophia be so desperately ill for months on end? The ME my mum described was like nothing I had read about on the net. ME is often referred to as Chronic Fatigue Syndrome (CFS) and the information my Google searches revealed at the time did not correspond with what my mum was describing about Sophia. I believed my mum, but I could not grasp just how ill my sister was.

By the time I came back to Britain, I was still none the wiser, but I was more clued up about telling people about my sister’s disease, or rather not telling people about it.

Upon hearing of my sibling’s ME, people’s reactions ranged from “Is that all? I thought you were going to say something serious from your tone of voice”, to polite “humour-her” nodding and baffled, sympathetic faces, and then the slam dunk of some responses.

“Maybe your sister has got issues with your mum/dad/whoever,” or words to that effect. “Issues!” I snapped at the last person who suggested that, “Issues! If you got ME from having f***ing issues, then the whole b*****d country would be down with it!”

Not long after I returned to Britain, 9/11 happened. My then husband was in the Twin Towers that day, and with hindsight, I can see I over-reacted to 9/11, because it was on the strength of that, that I decided to become a nurse.

Throughout my three years of nurse training, I didn’t tell a soul about Sophia and the ME. I don’t think I even mentioned I had a sister. I saw how ME was viewed from the other side of the fence and it wasn’t good or accurate. One day during my second year of training, I was on my cardiac placement and telephoned my mum on my break.

She was distraught, because at that very time I was calling her, the police were breaking down the door so Sophia could be sectioned into a mental hospital.

I didn’t know what to do, so I called my brother Shane, who went straight down to help mum and Sophia. I then went back to the ward and couldn’t say anything to anyone.

And it was around that time I nearly cracked. I very nearly told my personal tutor about my fears and concerns for my sister. I was about to blurt it out once when my tutor mentioned that our confidentiality could be broken if somebody was at risk or over something illegal.

Confiding about Sophia could have me seen as an enabler, it could have jeopardised Sophia even more; I couldn’t risk it. I stayed schtum and blamed my tears on PMT and the stress of course work.

Visits to Sophia were rare and precious, they had to be in the dark with only a smidgen of light. Her body may have been torturing her, but Sophia’s mind was still all there. Those 13 days in the mental hospital had done irreparable damage to my sister, though, she went downhill from there.

I never imagined Sophia would die from ME, I thought she would outlive the lot of us, by years. But my sister became the first person in England to officially die from ME, a dubious honour indeed.

Sophia was 32 and had been bedridden for the last six years of her life. I was in shock and grief-stricken for months after her death, but in among all the pain, there was a tiny part of me that felt lighter; that tiny light was one of relief, relief my sister was not suffering so unbearably anymore.

The post-mortem revealed the physical evidence of Sophia’s ravaged nervous system, proof at last her disease was of physical origin. Sophia’s death from ME made news around the world, but it hasn’t changed how people with ME get treated in Britain – well not yet it hasn’t.

When Sophia got sectioned, the event was tape-recorded. This profoundly moving audio is included in the award-winning documentary Voices from the Shadows , a film made out of sheer desperation by the family of a girl who suffers with severe ME.

This documentary includes the stories of other ME sufferers and carers, as well as expert medical opinion and facts. This film needs to be shown to as wide an audience as possible.

Voices from the Shadows will literally save lives and spare much unnecessary suffering and bring much-needed understanding about the reality of ME. This documentary urgently needs a way to be seen by the masses. Please go to Voicesfromtheshadowsfilm.co.ukfor more information.

Sophia suffered and died from ME, but nobody else should have to.

Cardiac autonomic impairment and chronotropic incompetence in fibromyalgia

2012-01-20T04:51:00.000-08:00

Roberta P da Cunha Ribeiro1, Hamilton Roschel1,2, Guilherme G Artioli1,2, Thalita Dassouki1, Luiz A Perandini1, Ana L Calich1, Ana L de Sá Pinto1, Fernanda R Lima1, Eloísa Bonfá1 and Bruno Gualano1,2*:

Corresponding author: Bruno Gualano gualano@usp.brAuthor Affiliations1 Division of Rheumatology, School of Medicine, University of Sao Paulo, Brazil. Av. Dr. Arnaldo, 455, Cerqueira César, Brazil2 School of Physical Education and Sport, University of Sao Paulo, Brazil. Av. Prof. Mello Moraes, 65, Butantã, BrazilFor all author emails, please log on.Arthritis Research & Therapy 2011, 13:R190 doi:10.1186/ar3519

The electronic version of this article is the complete one and can be found online at: http://arthritis-research.com/content/13/6/R190Received: 19 May 2011Revisions received: 25 August 2011Accepted: 18 November 2011Published: 18 November 2011© 2011 da Cunha Ribeiro et al.; licensee BioMed Central Ltd.

This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited

Abstract

Introduction
We aimed to gather knowledge on the cardiac autonomic modulation in patients with fibromyalgia (FM) in response to exercise and to investigate whether this population suffers from chronotropic incompetence (CI).

Methods
Fourteen women with FM (age: 46 ± 3 years; body mass index (BMI): 26.6 ± 1.4 kg/m2) and 14 gender-, BMI- (25.4 ± 1.3 kg/m2), and age-matched (age: 41 ± 4 years) healthy individuals (CTRL) took part in this cross-sectional study. A treadmill cardiorespiratory test was performed and heart-rate (HR) response during exercise was evaluated by the chronotropic reserve. HR recovery (deltaHRR) was defined as the difference between HR at peak exercise and at both first (deltaHRR1) and second (deltaHRR2) minutes after the exercise test.

Results

FM patients presented lower maximal oxygen consumption (VO2 max) when compared with healthy subjects (22 ± 1 versus CTRL: 32 ± 2 mL/kg/minute, respectively; P < 0.001). Additionally, FM patients presented lower chronotropic reserve (72.5 ± 5 versus CTRL: 106.1 ± 6, P < 0.001), deltaHRR1 (24.5 ± 3 versus CTRL: 32.6 ± 2, P = 0.059) and deltaHRR2 (34.3 ± 4 versus CTRL: 50.8 ± 3, P = 0.002) than their healthy peers. The prevalence of CI was 57.1% among patients with FM.

Conclusions
Patients with FM who undertook a graded exercise test may present CI and delayed HR recovery, both being indicative of cardiac autonomic impairment and higher risk of cardiovascular events and mortality.

David Tuller: It’s not rocket science to figure out that The PACE study included people who are depressed and don’t have CFS

2012-01-18T11:10:00.000-08:00

Posted by Julie Rehmeyer on January 18th, 2012:

When I wrote that first story about the PACE study, I’d been focusing primarily on XMRV, not CFS more generally. I didn’t understand the problem with case definitions [a set of criteria for what symptoms should be required for a person to be diagnosed with CFS], and there was a context of controversy that wasn’t part of my awareness at the time. I wrote that story in a couple hours on deadline. It wasn’t until afterward that I realized that this wasn’t the piece I would have written had I known more about it.

I will say, though, that my story was better than most of the others on it, which for the most part didn’t have any caveats.

What dissatisfied you about the story?

I was driving home when it appeared, and by the time I got home I had half a dozen emails about the piece. I realized that I hadn’t focused on the issue of the case definition. I’ve been a public health student and I teach reporting about public health [at the University of California-Berkeley Graduate School of Journalism and School of Public Health’s new concurrent Master of Public Health/Master of Journalism program]. In the first semester, all public health students have to take epidemiology, and one of the things they learn is that if you’re doing research, you have to have a good case definition so that you know which patients have the illness and which don’t. The PACE study’s definition of CFS is six months of unexplained fatigue — period. It’s not rocket science to figure out that that’s likely to include people who are depressed and don’t have CFS. Fatigue is a common symptom of depression, but people with CFS have some symptoms that are not typical of depression.

It was really because of that that I ended up writing a second story, a month or so later, about case definition in CFS. I tried to put it in a larger context — that this issue had been fought over for years, and the PACE trial was the latest variation on it.

What made you want to write an even more in-depth piece, explaining the history of CFS research and relating that to the recent XMRV mess?

Writing the case definition story led me to start looking into the Centers for Disease Control’s role in defining the disease. I found that in 2005, the CDC created a new way of defining the illness. Using that framework, the agency calculated that the prevalence of CFS was four times what everyone else thought it was, and ten times their own previous estimate. But if four to ten times as many people now have it, obviously something is really wrong with your case definition, before or after. William Reeves was head of the CDC’s research program for CFS for two decades, and two years ago, they moved Reeves aside. They never publicly said why, as far as I could tell. Furthermore, in the 1990s, the CDC spent funds allocated for CFS research on other projects, then lied to Congress about it.

I think all of this is really important for understanding why patients can be so suspicious and paranoid. In most of the coverage, the XMRV situation was decontextualized from the experience of patients and history of the illness, although Amy Dockser Marcus did some terrific reporting in the Wall Street Journal about the back story. But no one had really focused in depth on the case definition problem and the CDC’s role in perpetuating that problem.

I didn’t want to write a rant. I wanted to write, “This is what happened with the epidemiology, and this is why the situation is so screwed up.” I wanted something that patients felt represented some of the frustration they’d experienced in the past 20 years.

Did you think of the story as an advocacy piece?

No. I’m not a patient. I didn’t want to write it as an advocate for people with CFS. I wrote it because there was an undertold story. I understood that it was something that would likely be useful to the patient community; to the extent that that’s the case, that’s great. My goal is to tell a story that’s interesting, and one that I think is important. Obviously I do think that the CDC has not done what people expected it to do in this case. I think of writing this piece as being a proper watchdog of a government agency in an area that hasn’t gotten much attention.

Read more>>

See also: World exclusive: Prof Wessely admits in the BMJ that there were no ME/CFS patients in the ME/CFS PACE trial
See also: PACE trial results are out: ME is caused by an oncogenic virus
See also: Cerebrospinal fluid profiles can differentiate between Lyme disease, ME/CFS and healthy controls
See also: The main characteristic of ME is an abnormally delayed muscle recovery after doing trivial things, if you don't have that, you don't have ME
See also: Operation Mincemeat aka the PACE trial, a thrilling true story of deceit and survival

Oh Lord, Please Don’t Let Me Be Misunderstood

2012-01-18T10:54:00.000-08:00

Oh Lord, Please Don’t Let Me Be Misunderstood

by Margaret Williams 16th January 20121

Professor Simon Wessely has recently published his own account of his involvement since the late 1980s with what he refers to as Chronic Fatigue Syndrome but does not clarify that he and his colleagues regard CFS as synonymous with ME and that they regard – and treat—it as a behavioural disorder (“CFS Personal Story”: simonwessely.com/faq.html).

His story as published on his new website makes a smooth and impressive read, at least for the uninitiated, as it refers to numerous biomedical studies with which Wessely says he was involved during his “CFS” career.

What he fails to make clear is the number of those biomedical studies that had negative findings, or that he uses the Oxford case definition that specifically excludes those with a neurological disorder such as ME, so he may be studying only those with unexplained “fatigue”.

Equally, he claims “considerable success” with cognitive behavioural therapy but again he does not explain the cardinal importance of case definition.

Wessely states that he is “proud” of having contributed to neuroendocrine studies and seems to be claiming the honour for having discovered HPA axis dysfunction in “CFS”, whereas this was first demonstrated by Mark Demitrack in the US (Journal of Clinical Endocrinology and Metabolism 1991:73:6:1224-1234; Biol Psychiatry 1992:32:1065-1077).

Wessely specifically mentions Professor Tony Cleare (a member of Wessely’s group) and his work on neuroendocrine aspects of CFS, but does not explain that Cleare regards the disorder as being “most likely of biopsychosocial origin”, concluding that there is “no evidence for a specific or uniform dysfunction of the HPA axis” and that confounding factors such as inactivity and psychiatric comorbidity may influence the observed endocrine changes (Endocrine Reviews 2003:24:236-252). Cleare is also on record as stating that “HPA axis changes can be reversed by modifying behavioural features of the illness, such as inactivity (and) deconditioning” and that “current evidence suggests that neuroendocrine changes are not a central core of the condition, but occur…at least partly as a response to certain features of the illness such as …physical deconditioning” (TRENDS in Endocrinology and Metabolism 2004:15:2).

Notably, Wessely fails to report his own view on the cortisol abnormality: -

“I will argue that this line here represents not the line between low and high cortisol responses…but the line between real and unreal illness” - Simon Wessely - Microbes, Mental illness, the Media and ME: The Construction of Disease; 9th Eliot Slater lecture given at The Institute of Psychiatry, 12th May 1994
Wessely mentions the immunological studies with which he has been involved, but again he does not explain that his group failed to find the immunological abnormalities documented by experts such as Professor Nancy Klimas, nor that he argues against immunological testing, for example:

“Though disordered immunity and persisting viral infection have recently attracted attention, it is important that immunologists do not deflect attention away from the wider (ie. psychiatric) aspects of the chronic fatigue/postviral syndrome” (Anthony David, Simon Wessely, Anthony Pelosi. Lancet 1988: July 9th: 100-101).
Notably, in his “CFS Personal Story” Wessely says:

“We showed that immune dysfunction didn’t relate to clinical outcomes” but experts have found the exact opposite, for example: “We demonstrated changes in different immunological parameters, each of which correlated with particular aspects of disease symptomatology” (Hassan I, Weir WRC et al. Clin Immunol & Immunopathol 1998:87:1:60-67); “The findings suggest that the degree of cellular immune activation is associated with severity of physical symptoms” (Immunological Status Correlates with Severity of Physical Symptoms in Chronic Fatigue Syndrome Patients. S Wagner, N Klimas et al; Fourth International AACFS Research & Clinical Conference 1998; abstract page 28) and “Among (ME)CFS subjects, those who had been sick longer had higher rates of autoantibodies” (S Vernon et al. Journal of Autoimmune Diseases 2005: May 25th: 2:5).

Wessely mentions his work looking at HLA phenotypes but does not reveal that his team found no association with any specific phenotype, whereas others have shown direct linkage:

“A significant association between CFIDS and the presence of HLA-DQ3 was noted” (RH Keller, N Klimas et al. Clin Inf Dis 1994:18: (Suppl 1): S154-S156) and “The frequency of the HLA-DQ1 antigen was increased in patients compared to controls. This association between (ME)CFS and the HLA-DQ1 antigen translates into a relative risk of 3.2” (RS Schacterle, Anthony L Komaroff et al. JCFS 2004:11(4):33-42).

Wessely also fails to mention that in the 1996 Joint Royal Colleges’ Report on CFS his advice to Government bodies was that the reported biomedical abnormalities “should not deflect the clinician away from the biopsychosocial approach and should not focus attention towards a search for an ‘organic’ cause”, or his recommendation that no advanced tests should be carried out on these patients when it is those very tests that reveal the organic nature of the disorder (Joint Royal Colleges’ Report 1996: CR54).

He refers to his work on vitamin levels without mentioning his disparaging dismissal of vitamin supplementation or his unsupported conclusion that “many” people with “CFS” are taking vitamin B supplementation with no evidence of benefit (JRSM 1999:92:183-185).

Wessely concedes that he has changed his “writing style” but does not appear to comprehend the extent to which his earlier published views are perceived almost universally as being denigratory and sometimes mocking (as is to be found, for example, in the audiotape and his own notes for his 1994 Eliot Slater lecture), nor does he mention the harm in the form of medical rejection and dismissal, as well as the financial hardship, that have resulted from the widespread adoption of his views by the medical fraternity, government departments and private health insurers.

Indeed, he entirely fails to mention his published views, for example:

“neurasthenia would readily suffice for ME”; “It seems that ME sufferers prefer to feel that they have a ‘real’ disease – it is better for their self-esteem”; “many patients become…over-sensitised to physical sensations”; “Blaming symptoms on a viral infection conveys certain advantages, irrespective of its validity…It is also beneficial to self-esteem by protecting the individual from guilt and blame”; that patients obtain “secondary gain” by “adopting the sick role”; that “fear of illness is an important part of (the disorder)”; that patients are not suffering from any organic disorder because he believes their symptoms have no anatomical or physiological basis; that “The term ME may mislead patients into believing they have a serious and specific pathological process” and that “Several studies (often Wessely’s own) suggest that poor outcome is associated with social, psychological and cultural factors”.

Wessely says in his account of his involvement with “CFS”:

“I remain proud of the work myself and colleagues did in the early days of CFS…But there has been a downside”, and here he appears to seek sympathy from his readers by referring to alleged threats made to him by “activists”.

He continues:

“Right from the start, myself and all my colleagues had from the start (sic) been targeted by a small group of activists who (sic) mission was, and still is, to impede our work in as much as they are able. Thankfully… they haven’t succeeded and won’t”.

He goes on to say:

"I do not blame those who repeat some of the things they have read about me.. I feel however differently towards those who originally extracted or altered the quotes, and persist in doing so over the years despite knowing that these are wrong”.
No, Professor Wessely: responsible people who quote your published or recorded spoken words can readily demonstrate that these are not wrong.

He continues:

“So next time you come across something that purports to be an unfavourable or unflattering quote from myself or one of my colleagues, make sure you check it out first with the actual article”.

For those who wish to “check it out first with the actual article” and to verify for themselves the quotations from his own work to which attention needs to be repeatedly drawn but which Wessely now plays down, the full references can be accessed in “Quotable Quotes Updated” (can be ordered from Invest in ME - click here) and in “Magical Medicine: how to make a disease disappear” (http://www.investinme.org/Documents/Library/magical-medicine.pdf ).

Readers of Professor Wessely’s website may not recognise his version of medical history but they may recognise a recurring theme, which is his apparent lack of self awareness.

He presents himself in a heroic role as a patient advocate determined to dispel unhelpful stereotypes whilst, many would argue, he is in fact the source of those stereotypes.

He seems unable to grasp why those suffering from a disease he regards as “somatisation par excellence”, whose symptoms he describes as being “perpetuated predominantly by dysfunctional illness beliefs and coping behaviours” and whose “[negative automatic thoughts] are explained as distortions of reality” (Manual of cognitive-behavioural treatment for CFS, Chalder T, Deale A, Sharpe M, Wessely S. 19/6/2002) should fail to be grateful for his interventions.

The essence of his apologia may perhaps amount to no more than two lines from a Nina Simone song:

“But I'm just a soul whose intentions are good;

Oh Lord, please don't let me be misunderstood”.

Lyme Disease as a Cause of Supraspinatus tendinitis

2012-01-18T08:47:00.000-08:00

Lyme Disease as an Underlying Cause of Supraspinatus Tendinopathy in an Overhead Athlete.

Coulon CL, Landin D., Phys Ther. 2012 Jan 12. [Epub ahead of print]:

SourceC.L. Coulon, PT, Peak Performance Physical Therapy, 11320 Industriplex Blvd, Baton Rouge, LA 70809 (USA).

Abstract

BACKGROUND AND PURPOSE:/b>Supraspinatus tendinopathy is a common cause of shoulder pain seen in overhead athletes, but to our knowledge no published cases present Lyme disease as the underlying cause of tendinopathy. Lyme disease is diagnosed primarily by clinical signs and symptoms and then supported by laboratory tests including western blot and enzyme-linked immunosorbant assay (ELISA). This case demonstrates the importance of a physical therapist's input and clinical role in reaching the correct diagnosis in an athlete with Lyme disease, who presented with a diagnosis of rotator cuff impingement and tendinitis.

CASE DESCRIPTION:/b>A 34-year-old male tennis player presented to physical therapy with right shoulder impingement and tendinitis diagnosed by an orthopedic surgeon. He was unable to participate in sporting activities due to impairments in strength and pain. Initial examination revealed distal supraspinatus impingement and tendinopathy.

OUTCOMES:/b>The patient was not progressing with commonly accepted interventions and began to have "arthritis-like" shoulder pain in the uninvolved left shoulder. Suspicious of an underlying condition, the physical therapist informed the physician of the patient's updated status and referred to the physician to discuss the current symptoms in therapy. After testing, the patient was diagnosed with chronic Lyme disease and underwent antibiotic therapy.

DISCUSSION:/b>Many active patients spend time in the outdoors increasing their risk of exposure to a vector for Borrelia burgdorferi. Physical therapists spend a larger portion of time with patients than other health care professionals, and due to this extended contact and musculoskeletal knowledge are able to recognize atypical musculoskeletal disorders or musculoskeletal manifestations of unusual pathologies including Lyme disease.

PMID: 22247404 [PubMed - as supplied by publisher]

For years medics were baffled by her catalogue of problems

2012-01-17T12:03:00.000-08:00

By SADIE WHITELOCKSLast updated at 6:27 PM on 17th January 2012:

A mother-of-three plagued by illness has told how her problems have been linked to an insect bite suffered 20 years ago.

Adelle Huckins, 31, has been blighted by a range of medical conditions including migraines, severe fatigue, sickness, hearing difficulties and a drooping left eye.

But it was only last year that she was able to understand the route of her failing health when medics diagnosed her with Lyme Disease, a bacterial infection carried by ticks.

She suddenly remembered a school trip to Germany in 1991 when she was 11-years-old, during which she was bitten on the leg by a tick.

Despite the bite causing a rash she thought nothing of it, but now she believes it is responsible for years of poor health, which have made her feel like she has the body of 'a 90-year-old'.

Mrs Huckins, of New Marske, Cleveland said: 'I was never the same after coming home from that trip. I couldn’t get better afterwards but they couldn’t find what was wrong with me.

For years medics were baffled by her catalogue of illnesses but it was only when she chanced upon Lyme Disease on the internet last year that she realised it could hold the key to her health problems.

A basic NHS test came back negative, so Mrs Huckins turned to the Nuffield Hospital in Newcastle upon Tyne where results, sent off to a U.S. specialist, proved positive.
Read more>>

Differences in metabolite-detecting, adrenergic, and immune gene expression after moderate exercise in patients with chronic fatigue syndrome, patients with multiple sclerosis, and healthy controls

2012-01-16T09:07:00.000-08:00

Psychosom Med. 2012 Jan;74(1):46-54. Epub 2011 Dec 30.

White AT, Light AR, Hughen RW, Vanhaitsma TA, Light KC.:Department of Anesthesiology, University of Utah, 30 N 1900 E, Room 3C444, Salt Lake City, UT 84132-2501. Kathleen.c.light@hsc.utah.edu.

Abstract
Objective Chronic fatigue syndrome (CFS) and multiple sclerosis (MS) are characterized by debilitating fatigue, yet evaluation of this symptom is subjective. We examined metabolite-detecting, adrenergic, and immune gene expression (messenger ribonucleic acid [mRNA]) in patients with CFS (n = 22) versus patients with MS (n = 20) versus healthy controls (n = 23) and determined their relationship to fatigue and pain before and after exercise. Methods Blood samples and fatigue and pain ratings were obtained at baseline and 0.5, 8, 24, and 48 hours after sustained moderate exercise. Leukocyte mRNA of four metabolite-detecting receptors (acid-sensing ion channel 3, purinergic type 2X4 and 2X5 receptors, and transient receptor potential vanilloid type 1) and four adrenergic (α-2a, β-1, and β-2 receptors and catechol-O-methyltransferase) and five immune markers (CD14, toll-like receptor 4 [TLR4], interleukin [IL] 6, IL-10, and lymphotoxin α) was examined using quantitative polymerase chain reaction. Results Patients with CFS had greater postexercise increases in fatigue and pain (10-29 points above baseline, p < .001) and greater mRNA increases in purinergic type 2X4 receptor, transient receptor potential vanilloid type 1, CD14, and all adrenergic receptors than controls (mean ± standard error = 1.3 ± 0.14- to 3.4 ± 0.90-fold increase above baseline, p = .04-.005). Patients with CFS with comorbid fibromyalgia (n = 18) also showed greater increases in acid-sensing ion channel 3 and purinergic type 2X5 receptors (p < .05). Patients with MS had greater postexercise increases than controls in β-1 and β-2 adrenergic receptor expressions (1.4 ± 0.27- and 1.3 ± 0.06-fold increases, respectively, p = .02 and p < .001) and greater decreases in TLR4 (p = .02). In MS, IL-10 and TLR4 decreases correlated with higher fatigue scores.

Conclusions
Postexercise mRNA increases in metabolite-detecting receptors were unique to patients with CFS, whereas both patients with MS and patients with CFS showed abnormal increases in adrenergic receptors. Among patients with MS, greater fatigue was correlated with blunted immune marker expression.

PMID: 22210239 [PubMed - in process] PMCID: PMC3256093 [Available on 2013/1/1]

Persistence of Borrelia burgdorferi in Rhesus Macaques following Antibiotic Treatment of Disseminated Infection

2012-01-14T08:05:00.000-08:00

Monica E. Embers1*, Stephen W. Barthold4, Juan T. Borda2, Lisa Bowers1, Lara Doyle3, Emir Hodzic4, Mary B. Jacobs1, Nicole R. Hasenkampf1, Dale S. Martin1, Sukanya Narasimhan5, Kathrine M. Phillippi-Falkenstein3, Jeanette E. Purcell3¤, Marion S. Ratterree3, Mario T. Philipp1*

1 Divisions of Bacteriology & Parasitology, Tulane National Primate Research Center, Tulane University Health Sciences Center, Covington, Louisiana, United States of America, 2 Comparative Pathology, Tulane National Primate Research Center, Tulane University Health Sciences Center, Covington, Louisiana, United States of America, 3 Veterinary Medicine, Tulane National Primate Research Center, Tulane University Health Sciences Center, Covington, Louisiana, United States of America, 4 Center for Comparative Medicine, Schools of Medicine and Veterinary Medicine, University of California Davis, Davis, California, United States of America, 5 Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, United States of America

Abstract Top

The persistence of symptoms in Lyme disease patients following antibiotic therapy, and their causes, continue to be a matter of intense controversy. The studies presented here explore antibiotic efficacy using nonhuman primates. Rhesus macaques were infected with B. burgdorferiand a portion received aggressive antibiotic therapy 4–6 months later. Multiple methods were utilized for detection of residual organisms, including the feeding of lab-reared ticks on monkeys (xenodiagnosis), culture, immunofluorescence and PCR. Antibody responses to the B. burgdorferi-specific C6 diagnostic peptide were measured longitudinally and declined in all treated animals. B. burgdorferi antigen, DNA and RNA were detected in the tissues of treated animals. Finally, small numbers of intact spirochetes were recovered by xenodiagnosis from treated monkeys. These results demonstrate that B. burgdorferi can withstand antibiotic treatment, administered post-dissemination, in a primate host. Though B. burgdorferi is not known to possess resistance mechanisms and is susceptible to the standard antibiotics (doxycycline, ceftriaxone) in vitro, it appears to become tolerant post-dissemination in the primate host. This finding raises important questions about the pathogenicity of antibiotic-tolerant persisters and whether or not they can contribute to symptoms post-treatment.

Citation: Embers ME, Barthold SW, Borda JT, Bowers L, Doyle L, et al. (2012) Persistence of Borrelia burgdorferi in Rhesus Macaques following Antibiotic Treatment of Disseminated Infection. PLoS ONE 7(1): e29914. doi:10.1371/journal.pone.0029914

Editor: Jean Louis Herrmann, Hopital Raymond Poincare - Universite Versailles St. Quentin, France

Received: July 22, 2011; Accepted: December 6, 2011; Published: January 11, 2012

Copyright: © 2012 Embers et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: This work was supported by NIAID grant R01-AI042352 (MTP), R01-AI26815 (SWB and EH), a TNPRC Pilot Study Grant (MEE), and NCRR grant RR00164. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

* E-mail: members@tulane.edu (MEE); Philipp@tulane.edu (MTP)

¤ Current address: Biologic Resources Laboratory, University of Illinois, Chicago, Illinois, United States of America

New study indicates that Gulf War Syndrome may be an autoimmune syndrome induced by adjuvant (ASIA)

2012-01-13T07:49:00.000-08:00

Israeli E:

Lupus. 2012;21(2):190-4.

Gulf War Syndrome as a part of the autoimmune (autoinflammatory) syndrome induced by adjuvant (ASIA).

Israeli E:.

Source

The Zabludowicz Center for Autoimmune Diseases, Tel-Hashomer, Israel.

Abstract

Gulf War syndrome (GWS) is a multi-symptom condition comprising a variety of signs and symptoms described in the literature, which not been fully resolved. The various symptoms of the condition include muscle fatigue and tiredness, malaise, myalgia, impaired cognition, ataxia, diarrhoea, bladder dysfunction, sweating disturbances, headaches, fever, arthralgia, skin rashes, and gastrointestinal and sleep disturbances. In addition, excessive chemical sensitivity and odour intolerance is reported. The aetiology of the condition is unclear, but many reviews and epidemiological analyses suggest association with pyridostigmine bromide (PB), certain vaccination regimes, a variety of possible chemical exposures, including smoke from oil-well fires or depleted uranium from shells, as well as physical and psychological stress. Recently, Shoenfeld et al. suggested that four conditions - siliconosis, macrophagic myofaciitis (MMF), GWS and post-vaccination phenomena - that share clinical and pathogenic resemblances, may be incorporated into common syndrome called 'Autoimmune (Autoinflammatory) Syndrome induced by Adjuvants' (ASIA). Symptoms and signs of the four conditions described by Shoenfeld et al. show that at least eight out of ten main symptoms are in correlation in all four conditions. Namely, myalgia, arthralgias, chronic fatigue, neurological cognitive impairment, gastrointestinal symptoms, respiratory symptoms, skin manifestations and appearance of autoantibodies. Regardless of the aetiology of GWS, be it exposure to environmental factors or chemical drugs, vaccinations or the adjuvants in them, GWS fits well with the definition of ASIA and is included as part of 'Shoenfeld's syndrome'.

PMID:: 22235052; [PubMed - in process]

Prof Racaniello: the CDC has stumbled when tackling CFS, dismissing evidence that CFS is an organic disease, diverting funds designated for CFS to other programs

2012-01-12T08:57:00.000-08:00

January 12th, 2012, by Vincent Racaniello, discovermagazine.com:

Vincent Racaniello is Higgins Professor of Microbiology & Immunology at Columbia University, where he oversees research on viruses that cause common colds and poliomyelitis. He teaches virology to graduate, medical, dental, and nursing students, and writes about viruses atvirology.ws.

The detection of a new virus called XMRV in the blood of patients with chronic fatigue syndrome(CFS) in 2009 raised hope that a long-sought cause of the disease, whose central characteristic is extreme tiredness that lasts for at least six months, had been finally found. But that hypothesis hasdramatically fallen apart in recent months. Its public demise brings to mind an instance when a virus *was* successfully determined to be behind a mysterious scourge: the case of HIV and AIDS. How are these two diseases different—how was it that stringent lab tests and epidemiology ruled one of these viruses out, and one of them in?

The first inklings of the disease now called AIDS surfaced in Los Angeles in the summer of 1981. The5 June 1981 issue of Morbidity and Mortality Weekly Report described 5 homosexual men withPneumocystis carinii pneumonia (abbreviated PCP), normally only observed in individuals with weakened immune systems. The article suggested the possibility of an immune dysfunction related to exposure to something that would make individuals vulnerable to opportunistic infections. Soon clusters of PCP and Kaposi’s sarcoma, a rare skin cancer, were observed in gay men in other urban centers. The Centers for Disease Control and Prevention established a simple case definition—Kaposi’s sarcoma or opportunistic infections—and began scouring hospital records. Over time this definition was modified, but its early use identified an ongoing epidemic, and identified groups at risk for the disease as men who have sex with men and injection drug users.

The next year the new disease was called AIDS, and soon the U.S. Public Health Service recommended that members of risk groups not donate blood or plasma. Soon came reports that the disease could be acquired by newborn babies from their mothers, and also by heterosexual contact. By the fall there were nearly 700 people who had been diagnosed with AIDS in the U.S., of whom almost 300 had died. The CDC and World Health Organization worked together to publish global data on the disease, and issue recommendations to prevent its spread.

During the early years, the epidemiology of AIDS suggested an infectious cause, and in 1983, just two years after the disease was identified, a novel retrovirus was isolated from a patient at risk for AIDS. A year later a commercial blood test was developed, which allowed comprehensive studies to be done that showed clearly that the virus, later named human immunodeficiency virus type I (HIV-1), was the cause of AIDS. This conclusion was strengthened by the transmission of AIDS to hospital workers when they inoculated themselves with HIV-containing blood by accidental needle sticks.

HIV (green) budding from an infected cell.

By 1987 the first anti-HIV drug, azidothymidine or AZT, was licensed for the treatment of AIDS. Today over 20 anti-HIV drugs have been approved. When given in combinations of three, the emergence of drug-resistant viral variants is minimized, transforming AIDS from a death sentence to a life-long chronic disease.

The story of CFS, generally defined as persistent fatigue of six months or greater not relieved by rest and accompanied by other specific symptoms, is markedly different. This syndrome was first reported in Los Angeles as well, but in 1934. There were subsequent sporadic outbreaks, some of which were reviewed by DA Henderson in 1959, who noted that females were more frequently affected, and suggested that a virus might be involved. In the 1980s Daniel Peterson identified antibodies against Epstein-Barr virus (EBV) in the blood of a group of CFS patients in Incline Village, Nevada. The CDC entered the investigation but was unable to confirm that antibodies to the virus were consistently present in patient blood. A subsequent case-control study failed to identify EBV as the causative agent of the disease, which was subsequently named chronic fatigue syndrome.

The search for that agent of CFS has continued to be fruitless. In addition to EBV, a host of other viruses have been found in CFS patients, including enteroviruses, measles virus, herpesviruses, and human T-lymphotropic virus type II. However, none have been consistently detected in CFS patients and therefore are not considered to cause the disease.

The possibility of a viral cause of CFS re-emerged in 2009 with the detection of a retrovirus called XMRV in the blood of a substantial fraction of CFS patients. A second laboratory subsequently identified sequences related to murine leukemia viruses, also retroviruses, in the blood of CFS patients. However, many other laboratories were unable to replicate these findings, and both papers have been retracted.

Why do the stories of AIDS and CFS have such different outcomes? One reason is that it has been difficult to reach a consensus on a clinical definition of CFS. At the onset the case definition of AIDS was simple—“Kaposi’s sarcoma or opportunistic infections”—which made it possible to rapidly and accurately identify new cases, especially among different research groups around the country. This led to the establishment of risk factors, and the epidemiological data obtained from this work made it highly likely that an infectious agent was involved, spurring the search for the causative pathogen. The case definition for CFS has undergone a number of revisions over the years. When different research groups use different definitions of the disease, it becomes difficult to compare findings. Most importantly, there is no indicator or diagnostic test that can be used to identify CFS, and since diagnosing CFS is a long and difficult process, cohorts established by different investigators vary, leading to different findings, confusion, and contention. In contrast, AIDS was readily identifiable and easily diagnosed once a blood test for HIV was developed.

Another problem is that in contrast to their excellent work on AIDS, the CDC has stumbled when tackling CFS. The CDC has dismissed evidence that CFS is an organic disease, and spent funds on investigating psychiatric and trauma-related causes, rather than infectious origins. The agency also diverted funds designated for CFS to other programs. These and other missteps alienated the CFS patient community—the opposite of what the agency accomplished with the AIDS community.

In part due to the standardized case definition of AIDS, identification of a candidate virus was relatively rapid. Determining its role in the disease was facilitated by the development of a blood test, which could be used to prove that HIV-1 caused AIDS. The relationship between HIV and AIDS was further confirmed by the development of antiviral drugs that inhibited viral replication and helped alleviate the symptoms of the disease.

Why have investigators failed to identify a virus behind CFS? (It is not due to the lack of appropriate technology; this has improved substantially since the 1980s with the development of polymerase chain reaction and rapid DNA sequencing.) One explanation for this dilemma is that an infectious agent does not cause CFS. However, there is plausible evidence for an infectious etiology, including observations that the disease is known to occur in outbreaks. Furthermore, in many cases the onset of symptoms appears to begin with a flu-like illness. Additionally, CFS is a heterogeneous disease, and may be caused by several different agents or a combination of viruses and non-infectious conditions. Another possibility is that an infection initiates an immune response that spirals out of control, leading to CFS symptoms. This scenario implies that at least some CFS patients have underlying deficits in immune regulation. If that’s true, it will be very difficult to identify the virus involved because it will likely have been eliminated from patients’ systems by the time CFS symptoms become apparent.

In retrospect, it is clear that the properties of AIDS made it an easy disease to understand. While the path to understanding CFS has been clouded by non-scientific issues, in the end the main reason why we do not understand this disease is because it is extraordinarily complex. But that never stopped a good scientist.

B-Cell Discovery Suggests Why Women Suffer More Autoimmune Disease

2012-01-12T04:51:00.000-08:00

ScienceDaily: — Researchers at National Jewish Health have discovered a type of cell that may contribute to autoimmune disease. The findings also suggest why diseases such as lupus, multiple sclerosis and rheumatoid arthritis strike women more frequently than men.

The cells, a subset of immune-system B cells, make autoantibodies, which bind to and attack the body's own tissue. The researchers report in the August 4, 2011, issue of the journal Blood, that they found higher levels of these cells in elderly female mice, young and old mice prone to autoimmune disease, and humans with autoimmune diseases. National Jewish Health has applied for a patent for a method to treat autoimmune disease by depleting these cells.

"We believe these cells could be useful in the diagnosis and treatment of autoimmune diseases, and may help us understand general mechanisms underlying autoimmunity," said senior author Philippa Marrack, PhD, Professor of Immunology at National Jewish Health and an investigator of the Howard Hughes Medical Institute.

Autoimmune diseases occur when the immune system begins attacking its own tissues rather than external pathogens. Several autoimmune diseases, including lupus, rheumatoid arthritis and multiple sclerosis, afflict women anywhere from two to 10 times as often as they do males. Although sex hormones are known to play a role in autoimmune disease, other factors are involved in these gender differences.

The research team came across the new cells when they were examining differential expression of X-chromosome genes in healthy male and female mice. They discovered a previously undescribed type of B cell, which expressed the cell-surface protein CD11c. The protein is an integrin, which helps cells attach to other cells or to an extracellular matrix. The researchers are not certain what role integrin might play in autoimmunity or if it is merely a marker for another mediator of autoimmunity.

These cells increase as healthy female mice age, but remain at constant low levels in healthy male mice. As a result, the researchers named the cells Age-associated B Cells or ABCs. The researchers also found higher levels of ABCs in young and old mice that are prone to autoimmune disease. They could detect the elevated ABC levels before any disease developed and even before autoantibodies appeared, suggesting a role for these cells in early detection of disease.

The researchers also found an almost identical type of cell in the blood of many human autoimmune patients. In women with rheumatoid arthritis the presence of these cells increased with age.
ABCs in mice produce antibodies against chromatin, the combination of proteins and DNA that make up chromosomes in the cell nucleus. When they depleted the ABCs in mice, autoantibody levels fell, suggesting a potential treatment for autoimmune diseases. National Jewish Health has applied for a patent on the method of depleting the cells to treat autoimmune disease.

The researchers also found that activation of these cells requires stimulation of TLR7, a cell-surface receptor involved in innate immune responses. The gene for TLR7 is located on the X chromosome. Women have two X chromosomes, men an X and a Y chromosome. Normally one copy of the X chromosome in women is silenced so that it does not produce excess protein. But the silencing is not always complete, and women commonly express elevated levels of some X-chromosome genes.

"Not only do these cells appear more frequently in females, their activation depends on a gene of which women have two copies and men only one," said Anatoly V. Rubtsov, PhD, first author and postdoctoral fellow at National Jewish Health. "This could help us understand why women suffer many autoimmune diseases more often than men."

100 year old prostitute still going strong

2012-01-11T11:33:00.000-08:00

By Tessie Theuma – Happy fluffy story correspondent

Sitting on her plastic-covered scarlet arm-chair in the boudoir of her Gzira home, one would be forgiven for thinking Doris Borg is just a regular sweet old granny. But while she is indeed sweet as kannoli, she also has a more illicit side: she is Malta’s oldest working prostitute.

The silver-haired “anzjana tat-triq“, as she calls herself, celebrated her birthday on January 2, surrounded by prominent politicians, businessmen, lawyers and members of the clergy, all of whom were in costume to protect their identities. “I so enjoyed lapping up their warm greetings,” she beams.

Doris says she has been in the world’s oldest profession ever since she can remember. She comes from a long line of ladies of the night. “My mother was a prostitute, and her mother before her. Her mother was a cloistered nun so I’m not sure what happened there. There hasn’t been a proper male member of the family for generations.”

During her long life, the centenarian has lived through her fair share of momentous events. She has particularly fond memories of World War II. “All those marines,” she says wistfully. “Some historians say the invasion of Sicily might not have succeeded had the entire British 51st infantry division not spent a morale-boosting night with me before they shipped out.”

How has she managed to live for so long? “Well I’m lucky enough to do what I love, even though I don’t love who I do most of the time. I’ve never had a break, except for my hip of course.

“Also, a Ghanaian former witchdoctor once told me his seed had life-giving properties. It appears to have worked.”

Doris admits that due to her advanced age, the market she caters for is somewhat niche. “For men who are almost into necrophilia but not quite” say her ads on Maltapark. “Oh yes, I’m very web savvy,” she says. “One of my last clients, bless him, was a shy computer programmer, and he set up a Facebook page for me, which really helps to set up appointments since I can only cover about 30 metres of pavement in a day nowadays, and that’s with my Zimmer frame.

She says advanced age has several advantages. “Losing all my teeth has been a Godsend, I can tell you. And if someone has a foot fetish, but also likes breasts, in my case they’re in the same general area.”

Being more than a century old certainly hasn’t diminished her creativity either. “I can do more things with a tire-swing and a rolling pin than you could ever possibly imagine.”

What does she think of her younger counterparts? “Bah, in my day we used to learn everything on the job, if you’ll pardon the pun. Hookers today don’t know they’re born, with their MCAST courses and ETC training schemes.”

Despite the fact that her more glamourous days are arguably behind her, Doris has no intentions of retiring any time soon. “No matter how old I get I won’t stop bending over backwards to make sure my clients are satisfied.”

We're all desperate for welfare reform, Mr. Cameron, but hiding the truth is not the way to achieve it

2012-01-10T10:58:00.000-08:00

By SONIA POULTONLast updated at 3:03 PM on 10th January 2012:

I BELIEVE that there comes a point in the life of any Prime Minister when the electorate is entitled to ask - and loudly - does this person actually know what they are doing?

So it is that I have just posed this question of our current PM and the answer to come back has greatly alarmed me.

David Cameron is lost in his role as PM. That much is apparent. Like a toddler at big school he has no true understanding of the issues before him and blunders in apparently unaware of danger or the need to tread carefully.

I can only conclude that being out of his depth is the problem because I can't, for the life of me, fathom some of his policies. They make no sense to me on any level, human or otherwise.

His current big idea - the Welfare Reform Bill - may yet prove to be his Margaret Thatcher - Milk Snatcher moment. The point when people will look back and shudder at the sheer callousness of it.

My problem is that I was hoping for too much from him when it comes to the sensitivity and understanding of the UK's disabled community.

Foolishly I believed that he, of all prime ministers, would be acutely aware and therefore appropriately empathetic of the difficulties that disability bring to the day to day existence of people.

Who can forget the national sorrow and compassion we all felt for him, regardless of our political persuasion - when he and his wife, Samantha, experienced the loss of their disabled son, Ivan?

Given David Cameron's painful, yet remarkable, insight into disability - and the wide and diverse range of needs that disabled people have - there was a general feeling that this would be a PM who would enable our country's disabled population to lead as full and secure a life as possible.

And this would occur without feeling humiliated to ask for assistance because, after all, the care of it's vulnerable should be a priority for any decent society.

So it is that I am barely shocked, but no less disappointed, to discover that when it comes to Welfare Reform - and disabled people in particular - David Cameron has been less than straightforward.

I refer to the Coallition's plans for Disability Living Allowance (DLA) and the proposed - and vast £9.2bn in cuts to services and benefits.

A great deal of opposition has been registered to these cuts but the chances are you won't have heard about them seeing as the Government has worked incredibly hard to keep it quiet.

Well, its an unpopular proposal for starters - and they've already had their fair share of those in less than two years in the job - so they can ill-afford any more initiatives that appear to have been conceived during a midnight feast on a dorm in Eton.

Do I need to recall the recent idea of having a taskforce show up on the doorstep of trauanting children/drug addicts of a morning and marching them off to their destination? Course not. We all remember that and some of us are still laughing.

But now they are more mean-spirited than ever - proving that when it comes to politics, David Cameron's Conservatives retain their place as 'the nasty party'.

Let me clue you up. For those of us fortunate enough not to need Disability Living Allowance, we would have remained in sweet ignorance about the untenable pressure and stress that is currently being applied to some of the most inordinately vulnerable members of society: our disabled.

That was until the Spartacus report published this week which blows the lid off the Government's plans and makes abundantly clear the true level of opposition to the intended reforms - and this includes the extent to which the Government misled MPs and Peers over the hostility to disability benefit reform.

Oh me, oh my. Surely Dave and his boys wouldn't only give us the information that they would want us to know about, would they? Apparently so.

Despite conducting a public consultation, the Department for Work and Pensions - whose arm DLA falls under - have chosen to blanket ignore the opinions of their respondents.

The unexpurgated version of the consultation goes something like this:

98 per cent of respondents objected to the qualifying period for benefits being raised from three months to six months. 99 per cent also objected to DLA no longer being used as a qualification for other benefits. And just to seal off the 90 percent-ers, 92 per cent of people opposed removing the lowest rate of support for disabled people.

In real terms what we are talking about here is less money in the disabled benefit pot and to the tune of billions. Yet despite the opposition to these intended cuts - and even Mayor of London Boris Johnson opposing the proposals so worried was he about how this would impact the disabled citizens of our capital city - no one knew about this.

It was kept away from public dissection and would've remained so had it not been for researchers using the Freedom of Information Act to obtain more than 500 responses to the consultation that were submitted by disabled people’s organisations, disability charities and other groups.

That was when the true scale of the deception became clear. And the alarm to these proposals - backed up by their iffy statistics - can be heard from Scunthorpe to Southend as thousands of disabled people come to terms with the fact that if the Welfare Reform Bill goes through then there is a very real chance that DLA will be abolished completely and replaced with a benefit that looks suspiciously like the Employment and Support Allowance (ESA) and utilises a number of flawed tests to ascertain eligibility.

The upshot is that 3.2 million people will be transferred to a system that will include yet more assessments and a cutting of existing claims by 20 per cent.

Even more savage are those disability cuts that will result in as much as 50 per cent of weekly benefit deducted. When you are receiving little more than seventy pound, as it is, then reducing the income by half is a frightening and shocking amount. People are already dying through lack of food and heat and it will surely only increase. Remind me. We are living in a privileged country in 2011, yes?

This Coalition love to talk about our 'shameless' generation but we are led by a shameless government. One that runs regular 'Sweetheart Deals' with multi-nationals and allow them to get away without paying billions - yes, that's right billions - of pounds in taxes and yet turn on the very people we need to protect.

My screen saver, taken from a popular poster, reads: 'Put politicians on minimum wage - and watch how fast things change.' I believe there is a great deal of truth in that.

Our MP's are entirely out of touch because they are not living hand to mouth like too many of us.

There's an absolute feeling now - and I certainly have it - that our politicians are nothing but self-serving egomaniacs. Across all parties there are reprehensible examples of people behaving in manners unbefitting of elected members of parliament.

Like their fatcat mates in The City - who they protected again last week when David Cameron vetoed a financial transaction tax for business - this Coalition is symbolic of the 'me, first' era.

Interestingly, four days after they voted to keep their city friends in the luxury to which they are accustomed, the House of Lords also voted to reduce top-up payments for disabled children.

Translated that means they will reduce some disabled benefits to less than $30 per week. Roughly the amount, no doubt, that David Cameron spends on toothpicks for a weekend party for his Chipping Norton set of elite friends.

The thing about disability or illness is they are not always visible. My fifty-something brother had a kidney transplant and has had a casebook of illnesses ever since - ranging from cancer to diabetes and depression - and yet, on a good day, he can walk for 10 or 15 minutes at a time with me. Admittedly, it's not very far but he can physically move.

Anyone seeing him may deduce that he is one of those fabled characters 'the benefit scrounger' but the reality couldn't be further from the truth. He requires literally hundreds of tablets each week, and daily injections, to keep him alive.

Like so many others now in receipt of disability benefits, my brother worked for decades, paid into the system and then found himself on the receiving end of detestable and diabolical behaviour when it comes to getting some support back.

He endured a year of utter misery at the hands of the Department for Work and Pensions who shuffled his claim back and forth and treated him with indifference on the one hand and belligerence on the other .

At one stage I worried for his mental health so severe was his depression when his DLA application was rejected, subject to several - and costly - appeals and then finally re-instated.

Disabled or sick people have more than enough to cope with without having to put out the begging bowl to be helped when they are entitled to be and should not be treated as a leper when they need it.

Regardless of whether this Coalition is determined to take us to hell in a handbasket we should really ask if we want to be represented in such a callous and coldhearted manner. And then when we've decided - we should make that clear by standing up and being counted.

That's not a country that represents me or, indeed, any of the decent and fair-minded people of my acquaintance. We want to know that should the worst happen and people need help and support that it is available for them without making them despair or feel humiliated.

To reprise a slogan, Mr. Cameron, one that was dreamt up when your predecessor, Tony Blair, was conducting his own dodgy dossier so that he, too, could push for action that few others agreed with - when it comes to your proposed welfare cuts, the ones you seek to change but by giving us only half the story in which to make up our minds, I say this: not in my name.

Whistleblower Scientist Dr. Lewis Accuses British Medical Journal of Institutional Research Misconduct

2012-01-09T11:28:00.000-08:00

Posted by Age of Autism at January 09, 2012:Actions of BMJ Editor and Reporter “More Tabloid News than Science” According to Dr. David Lewis, and “a Genuine Threat to Public Health”

WASHINGTON, D.C., Jan. 9, 2012 (SEND2PRESS NEWSWIRE) -- Dr. David Lewis, internationally known whistleblower and respected expert on institutional fraud, released a report today calling for a formal investigation into the practices of the British Medical Journal (BMJ), and specifically into the actions of its editor, Dr. Fiona Godlee, and Brian Deer, a reporter she hired to write a series of articles which appeared in the journal beginning on January 4, 2011.

The BMJ articles accuse Dr. Andrew Wakefield of committing scientific fraud in a 1998 Lancet publication he co-authored that brought global attention to a link many parents and physicians suspect may exist between autism and children who are genetically predisposed to adverse reactions from the Measles/Mumps/Rubella (MMR) vaccine.

The BMJ, Deer, and Godlee alleged that Wakefield fabricated a diagnosis of colitis in most of the 12 children described in The Lancet article — calling Wakefield’s work an "elaborate fraud" intended to create an "MMR scare" — so Wakefield could profit from a patent related to his research.

“Documents recovered from Dr. Wakefield's files during my investigation at the National Whistleblowers Center (NWC) - www.researchmisconduct.org - reveal that a pathologist associated with the study, Dr. Andrew Anthony, interpreted a number of the children's biopsies as evidence of colitis,” explained Dr. Lewis. “Altogether, the evidence contained in Wakefield's files suggested to me that the BMJ's fraud theory was more tabloid news than science.”

According to documents Lewis filed with Sir John Tooke, Vice-Provost for Health at the University College London (UCL) where The Lancet study was done, BMJ Editor Godlee responded to the Lewis revelations by “cherry-picking the evidence and coming up with a grand conspiracy theory involving ‘institutional research misconduct’. Alleged fraudsters now include University College London (UCL) administrators, the Royal Free Hospital, and all 13 co-authors of the Lancet study.”

UCL President Malcolm Grant notified Lewis that, because his charges were “so serious,” he urged Dr. Lewis to inform Dr. Godlee and Deer “at the earliest opportunity.”

Lewis also reports that Godlee has previously acknowledged the BMJ Group receives funding from the two manufacturers of the MMR vaccine, Merck and GlaxoSmithKline, and has testified in a Parliamentary inquiry that peer-reviewed medical journals are “the marketing arm of the pharmaceutical industry.” Lewis added: “Apparently scientists who question certain government policies and industry practices can be destroyed for a price. If so, this kind of tabloid science poses a genuine threat to public health.”

On January 3, 2012, Dr. Wakefield filed suit against the BMJ and Brian Deer ( http://www.courthousenews.com/2012/01/04/BritMedJ.pdf ). Last September, Columbia University published a major study supporting the link Dr. Wakefield established between autism and enterocolitis ( http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3174969/ ).

Lewis Investigation Available Online:

Dr. Lewis’ detailed investigation of the BMJ series in question can be downloaded here.pdf

----------------------------------------------------

Marketing drugs with tabloid science

Commentary
Editors at the British Medical Journal (BMJ) and Brian Deer, a freelance reporter
with no formal training in science or medicine, alleged that Andrew Wakefield
fabricated the diagnosis of colitis in a 1998 Lancet study involving 12 children with
autistic spectrum disorder (ASD). In the study, some parents and physicians linked
MMR vaccine to the children's gastrointestinal problems and rapid regression into
autism. In 2010, Deer alleged in the BMJ that Wakefield alone made up the diagnosis
by misinterpreting grading sheets from pathologists A.P. Dhillon and A. Anthony, who
reviewed the children's colonic biopsy samples.

In the article, Deer wrote that, according to specialists, grading sheets "don’t
generate clinical diagnoses such as colitis." Grading sheets I recovered from
Wakefield's files, however, show that Anthony wrote "colitis" in marginal notes on a
number of his grading sheets. And, Dhillon included boxes to check for various
diagnoses, such as Crohn's disease and "UC" for ulcerative colitis. Consistent with the
Lancet article, both pathologists found that only one child showed no evidence of
inflammation.

Last September, BMJ's chief editor, Fiona Godlee, rejected a commentary I wrote
about Wakefield's documents. In its place, she invited me to submit a Rapid Response,
which I did. But, instead of admitting she had falsely accused Wakefield of making up
the diagnosis of colitis, she and Deer simply cherry-picked the evidence to come up
with a new theory involving "institutional research misconduct." The alleged fraudsters
now include University College London (UCL) administrators, the Royal Free
Hospital, and all 13 authors of the Lancet study.

Their objective, according to an editorial and feature article Godlee and Deer
published with my Rapid Response, was to create the MMR scare so that UCL could
sell its own safer measles vaccine, diagnostic kits and "autism products." In her
editorial, Godlee acknowledged "the BMJ Group receives funding from the two
manufacturers of MMR vaccine, Merck and GSK."

To support their new fraud theory, Godlee rewrote my Rapid Response, removing
any evidence that undermined their allegations against Wakefield and others. Then, to
prevent me from publishing this evidence on my NWC website, Deer filed a flurry of
false allegations of ethical misconduct against me with the NWC. Godlee ignored my
protests over Deer's behavior; and some of his false and misleading characterizations of
my professional credentials and current work appeared in her editorial and Deer's
feature article

When testifying before Parliament in 2011, Godlee agreed that peer-reviewed
journals have become "the marketing arm of the pharmaceutical industry." Therefore, it
shouldn't surprise anyone if her fraud allegations turn out to be nothing more than a
scheme to protect the BMJ's financial interests in companies marketing the MMR
vaccine. What's frightening is that it requires one of Great Britain's leading medical
journals to utterly destroy the reputation of one of the world's most prestigious
academic institutions.

Dr. Lewis’ detailed investigation of the BMJ series in question can be downloaded here.pdf

Dr. Lewis's direct contact information:
(706) 296 3675LewisDaveL@aol.com .

ME/CFS: Into 2012 without Cure or Care

2012-01-09T08:05:00.000-08:00

By Llewellyn King, JANUARY 2, 2012:

It's an indecent disease, shrouded in mystery, endless in suffering, in stigma and in despair. It's a life sentence and many of those who are afflicted take their own lives, according to patient advocates.

Witness this e-mail I received from a woman on New Year’s Eve: “Today, December 31, is my birthday. I will not get to eat out, have a party tonight. ... I am not sure I can hang on another year, when every day is so hard to get through. Just a few weeks ago, a doctor laughed at me and said there was no such thing as [my disease], and my husband just sat there, not once backing me. That was more hurt than I can carry for another year. I pray every night, 'Now I lay me down to sleep and please, Lord, take me before I wake.' ”

This scourge, this foul and stealthy confiscation of life, is so little understood that there's even confusion about its name.

In the United States, the disease is known as Chronic Fatigue Syndrome (CFS): a bland and trivializing nom de plume bestowed on the disease by the Centers for Disease Control in Atlanta. Elsewhere in the world, it's known as myalgic encephalomyelitis (ME). American patients tend to use both names and the acronym ME/CFS.

I've been writing about ME/CFS for three years. But in more than 50 years of journalism, I've never had so much reader response. So many cries from the heart. So much gratitude for doing so little.

The disease is socially ecumenical and afflicts an estimated 1 million people in the United States and 17 million worldwide. I hear from a great cross section of the ME/CFS community who have access to a computer and are well enough to use it.

There are many sufferers who aren't well enough to e-mail; they're severely debilitated and bedridden for months and years.

Deborah Waroff, a colleague of mine from the 1970s, who's been sick for more than two decades, describes a period of total disability she suffered in 2003 and 2004, when she lay on her apartment couch too sick even to watch television, as “lying in your own coffin.”

There is no known route to infection, no diagnoses and no cure. Research has been scattered and funded grudgingly at such low levels that Dr. Fred Volinsky of Boston has calculated annual federal funding for ME/CFS at only $1.25 per patient compared to $400 for multiple sclerosis.

Last year was especially sad because many patients and some researchers had pinned their hopes on a retrovirus called XMRV. Most of the work on this line was done at the Whittemore Peterson Institute in Reno, Nev., a private research facility founded by the Whittemore family. It now appears that promising conclusions were the result of laboratory contamination, and a paper in Science magazine had to be withdrawn. Worse, there's an ugly dispute between the institute and its former chief research scientist Judy Mikovits. Because there's low-level contagion in families and cluster outbreaks of ME/CFS, the idea that there's a virus at work can't be discredited entirely.

There are parallels as well as dissimilarities to the early days of the AIDS. For AIDS, the stigma was sexual; for ME/CFS, the stigma is sloth.

As doctors have no diagnostic procedure for ME/CFS, they dismiss it as imaginary, psychosomatic or sloth. Families believe the disease is sloth: Sons have written to me because their fathers disowned them, believing that they are just layabouts.

Some sufferers are homeless, according to Dr. Leonard Jason of DePaul University, abandoned to life on the streets. He tells of one unfortunate living in a car.

Hospital emergency rooms have no tools, no knowledge. In the frenzy of the just-in-time nature of emergency room medicine, there's no care there for ME/CFS victims. There's precious little in the way of charity funding or home visits, unless the patient has family support they are on their own, alone.

A cure this year is unlikely, but better understanding can start today. Now.

Wanted: A high-energy, high-profile celebrity to do for ME/CFS what Elizabeth Taylor did for AIDS, what Jerry Lewis did for muscular dystrophy, and what Michael J. Fox is doing for Parkinson’s: raising concern, raising money and banishing stigma. Fox has raised $264 million for Parkinson’s. By contrast, the Chronic Fatigue Immune Deficiency Syndrome Association targeted raising just $2 million for research last year.

Maybe in 2012 the voiceless victims of ME/CFS will be heard, even faintly.

BMJ Editorial - Missing clinical trial data

2012-01-09T07:47:00.000-08:00

BMJ Editorial - Missing clinical trial data

http://www.bmj.com/content/344/bmj.d8158

BMJ2012;344doi: 10.1136/bmj.d8158(Published 3 January 2012)
Cite this as:BMJ2012;344:d8158

1.Richard Lehman, senior research fellow1,
2.Elizabeth Loder, clinical epidemiology editor2
Author Affiliations
1.eloder@bmj.com

A threat to the integrity of evidence based medicine

Clinical medicine involves making decisions under uncertainty. Clinical research aims to reduce this uncertainty, usually by performing experiments on groups of people who consent to run the risks of such trials in the belief that the resulting knowledge will benefit others. Most clinicians assume that the complex regulatory systems that govern human research ensure that this knowledge is relevant, reliable, and properly disseminated. It generally comes as a shock to clinicians, and certainly to the public, to learn that this is far from the case.

The linked cluster of papers on unpublished evidence should reinforce this sense of shock. These articles confirm the fact that a large proportion of evidence from human trials is unreported, and much of what is reported is done so inadequately. We are not dealing here with trial design, hidden bias, or problems of data analysis—we are talking simply about the absence of the data. And this is no academic matter, because missing data about harm in trials can harm patients, and incomplete data about benefit can lead to futile costs to health systems. Moreover,
researchers or others who deliberately conceal trial results have breached their ethical duty to trial participants.

The linked articles look closely at the extent, causes, and consequences of unpublished evidence from clinical trials. Hart and colleagues incorporated unpublished evidence into existing meta-analyses of nine drugs approved by the US Food and Drug Administration in 2001 and 2002.1 These reanalyses produced identical estimates of drug efficacy in just three of 41 cases (7%); in the remaining cases, estimates of drug efficacy were evenly split between more (19/41) and less (19/41). It is sometimes assumed that incorporation of missing data will reduce estimates of drug benefits, but this study shows that “publication bias” can cut both ways. Each increment of data can change the overall picture, but in most cases with no certainty that the picture is complete.

A fundamental step towards tackling this problem was taken in 2005, when, as Chan describes in the Research Methods and Reporting section, prior registration of all trials became a condition for later publication.2 Chan details the ways in which authors of systematic reviews can search for unpublished evidence, and he strikes an optimistic note when he states that “Key stakeholders—including medical journal editors, legislators, and funding agencies—provide enforcement mechanisms that have greatly improved adherence to registration practices.”

However, two studies we publish give little cause for optimism that this adherence extends to timely sharing of trial results. A survey of publicly funded research in the United States between 2005 and 2008 by Ross and colleagues shows that registration is not followed by reporting of summary results within 30 months of completion in more than half of trials.3 Even at three years, one third remain unpublished. The US Food and Drug Administration Amendments Act of 2007 made publication of a results summary on ClinicalTrials.gov within 12 months mandatory for all eligible trials in the US “initiated or ongoing as of September 2007”—Prayle and colleagues examine the extent to which this has happened.4 The tally stands at 22%. When the word “mandatory” turns out to mandate so little, the need for stronger mechanisms of enforcement becomes very clear.

Most clinical interventions in current use, however, are based on trials carried out before the era of mandatory registration, and here the task of data retrieval by systematic reviewers and national advisory bodies becomes impossible. Wieseler and colleagues show that the different documents available to researchers and regulators—internally produced study reports, study findings published in peer reviewed journals, and results posted in results registries—supplement each other, but that reporting quality is highest in study reports. However, the effort required to find and collate these sources can be prodigious and seldom guarantees completeness.5 In their just published Cochrane review update on antiviral treatments for influenza, Jefferson and colleagues describe a painstaking search for information from undisclosed trials stretching over several years.6

There is an “Alice in Wonderland” feel to these investigators’ efforts—acting on the public’s behalf, searching over hill and dale and among the paperwork of regulatory bodies and drug companies to put together pieces of data that should have been freely available in the first place. Even when data on individual participants are made available, they only form part of the jigsaw, and Ahmed and colleagues describe the problems of fitting in such data when the whole picture is not known.7

Finally, to find the randomised clinical trials that have been published in the medical literature, nearly every student, clinician, or researcher turns first to Medline among the biomedical databases. But Wieland and colleagues find that many reports of randomised controlled trials entered into Medline between 2006 and 2011 have not been indexed as such; thus, simply entering the search term “randomised controlled trial” into this database will miss many of these trials, despite the best efforts of the Cochrane Collaboration and the US National Library of Medicine.8

What is clear from the linked studies is that past failures to ensure proper regulation and registration of clinical trials, and a current culture of haphazard publication and incomplete data disclosure, make the proper analysis of the harms and benefits of common interventions almost impossible for systematic reviewers. Our patients will have to live with the consequences of these failures for many years to come. Retrospective disclosure of full individual participant data would be an important first step towards better understanding of the benefits and harms of many kinds of treatment. A model for this is provided by Medtronic’s recent agreement to release full individual participant data relating to its controversial bone product—recombinant human bone morphogenetic protein-2—to independent analysis teams; so there is no longer any convincing reason for other companies to refuse similar disclosure of de-identified participant data from all past trials.9

The main challenge is to ensure better systems for the future. Because “the optimal systematic review would have complete information about every trial—the full protocol, final study report, raw dataset, and any journal publications and regulatory submissions,”2 10 a prospective system of research governance should insist on nothing less. This may require the global organisation of a suitable shared database for all raw data from human trials—an obvious next step for the World Health Organization after its excellent work on the International Clinical Trials Registry Platform Search Portal. Concealment of data should be regarded as the serious ethical breach that it is, and clinical researchers who fail to disclose data should be subject to disciplinary action by professional organisations. This may achieve quicker results than legislation in individual countries, although this is also desirable.
These changes have been long called for,11 and delay has already caused harm. The evidence we publish shows that the current situation is a disservice to research participants, patients, health systems, and the whole endeavour of clinical medicine.

Notes
Cite this as: BMJ 2012;344:d8158
Footnotes
•   Research, doi:10.1136/bmj.d7202
•   Research Methods and Reporting, doi:10.1136/bmj.d8013
•   Research, doi:10.1136/bmj.d7292
•   Research, doi:10.1136/bmj.d7373
•   Research, doi:10.1136/bmj.d8141
•   Research, doi:10.1136/bmj.d7501
•   Research, doi:10.1136/bmj.d7762
•   Competing interests: Both authors have completed the ICMJE uniform disclosure form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declare: no support from any organisation for the submitted work; no financial relationships with any organisations that might have an interest in the submitted work in the previous three years; no other relationships or activities that could appear to have influenced the submitted work.
•   Provenance and peer review: Commissioned; not externally peer reviewed.

Submit Your Video Now! Last Call for Entries to Neuro Film Festival

2012-01-07T01:54:00.000-08:00

We Need Your Story! Submit Your Video Now

The American Academy of Neurology Foundation is reminding everyone affected by brain disease tosubmit a short video to its 2012 Neuro Film Festival, telling your story about why more research is needed to cure brain disease. Winners could receive up to $1,000 and a trip to New Orleans.
Deadline to enter is January 31, 2012.

Submit Your Video Now.
The third annual Neuro Film Festival aims to raise awareness about the need to donate money for research into finding a cure for brain diseases, such as Alzheimer’s disease, stroke, autism, Parkinson’s disease and multiple sclerosis. Learn more!

Another xenotropic virus that can infect humans has been found by Dr Sandra Ruscetti in a Lung cancer cell line

2012-01-05T11:05:00.000-08:00

Viruses 2011, 3(12), 2442-2461:

The Human Lung Adenocarcinoma Cell Line EKVX Produces an Infectious Xenotropic Murine Leukemia Virus

Joan L. Cmarik * , Jami A. Troxler, Charlotte A. Hanson, Xiang Zhang and Sandra K. Ruscetti

Laboratory of Cancer Prevention, National Cancer Institute-Frederick, Frederick, MD 21702, USA

* Author to whom correspondence should be addressed.

Received: 26 October 2011; in revised form: 22 November 2011 / Accepted: 9 December 2011 / Published: 19 December 2011

Download PDF Full-Text [619 KB, uploaded 19 December 2011 11:55 CET]

Abstract: The cell lines of the NCI-60 panel represent different cancer types and have been widely utilized for drug screening and molecular target identification. Screening these cell lines for envelope proteins or gene sequences related to xenotropic murine leukemia viruses (X-MLVs) revealed that one cell line, EKVX, was a candidate for production of an infectious gammaretrovirus. The presence of a retrovirus infectious to human cells was confirmed by the cell-free transmission of infection to the human prostate cancer cell line LNCaP. Amplification and sequencing of additional proviral sequences from EKVX confirmed a high degree of similarity to X-MLV. The cell line EKVX was established following passage of the original tumor cells through nude mice, providing a possible source of the X-MLV found in the EKVX cells.

Keywords: EKVX; NCI-60; human cell line; xenotropic murine leukemia virus; gammaretrovirus

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Cite This Article

MDPI and ACS Style

Cmarik, J.L.; Troxler, J.A.; Hanson, C.A.; Zhang, X.; Ruscetti, S.K. The Human Lung Adenocarcinoma Cell Line EKVX Produces an Infectious Xenotropic Murine Leukemia Virus. Viruses 2011, 3, 2442-2461.

AMA Style

Cmarik J.L., Troxler J.A., Hanson C.A., Zhang X., Ruscetti S.K. The Human Lung Adenocarcinoma Cell Line EKVX Produces an Infectious Xenotropic Murine Leukemia Virus. Viruses. 2011; 3(12):2442-2461.

Chicago/Turabian Style

Cmarik, Joan L.; Troxler, Jami A.; Hanson, Charlotte A.; Zhang, Xiang; Ruscetti, Sandra K. 2011. "The Human Lung Adenocarcinoma Cell Line EKVX Produces an Infectious Xenotropic Murine Leukemia Virus." Viruses 3, no. 12: 2442-2461.

Dr. Andrew Wakefield is suing the BMJ, Brian Deer & Dr. Fiona Godlee (Editor of the BMJ)

2012-01-05T07:02:00.000-08:00

Dr. Andrew Wakefield is suing the BMJ, Brian Deer & Dr. Fiona Godlee (Editor of the BMJ) courthousenews.com/2012/01/04/BritMedJ.pdf

Epstein-Barr virus tricks the immune system into triggering inflammation and nerve cell damage which is known to cause MS and ? ME

2012-01-05T05:06:00.000-08:00

healthcanal.com, 05/01/2012 :

A new study from researchers at Queen Mary, University of London shows how a particular virus tricks the immune system into triggering inflammation and nerve cell damage in the brain, which is known to cause MS.

Previous research has suggested a link between the Epstein-Barr virus (EBV) and multiple sclerosis but the research has remained controversial since scientists have so far failed to substantiate the link.

The new study proves the virus is involved in a manner more sophisticated and subtle than previously imagined, and may offer new ways to treat or prevent the disease.

MS is a neurological condition that affects around 100,000 people in the UK. It can cause vision problems, difficulties with walking and fatigue, and tends to strike mainly young and middle-aged women.

Its causes are not completely understood but both genes and environment are known to play a role.

Some previous research has suggested that EBV triggers MS but subsequent studies have failed to find the connection.

The new research, which is published in the journal Neurology, looked at post mortem brains of MS patients, examining areas where neurological damage had recently occurred.

Lead researcher, Dr Ute-Christiane Meier explained: “EBV is quite a clever virus; when it’s not growing and spreading it can hide away in our immune cells.

“In this study we used a different technique which allowed us to detect the virus in the brains of some people affected by MS, even when it was hiding away in the cells.”

Dr Meier and her team of collaborators found that, although the virus was not actively spreading, it was releasing a chemical message into areas of the brain nearby. This chemical message - made up of small RNA molecules - was activating the body’s immune system, causing inflammation. This damages nerve cells in the brain and causes MS symptoms.

Dr Meier continued: “We have to be careful and have to study more MS brains but this is potentially very exciting research. Now we understand how EBV gets smuggled into the brain by cells of the immune system and that it is found at the crime scene, right where the attack on our nervous system occurs. Now we know this, we may have a number of new ways of treating or even preventing the disease.”

One possibility is the widely-used cancer treatment Rituximab; a drug which is known to kill the cells of the immune system in which the virus hides. It is now being trialed as a treatment for MS.

Another possible approach, using anti-viral treatment, will be tested in clinical trials currently in preparation by Professor Gavin Giovannoni and colleagues, also at Queen Mary.

“If we can pinpoint EBV as a trigger, it’s possible that we could alter the course of MS or potentially even prevent the condition by treating the virus,” Dr Meier added.

“MS so often strikes young women and its unpredictable nature makes it an incredibly difficult disease to live with. We desperately need better ways to tackle the condition.”

Interestingly, the research also hinted that infection with EBV and its action on the immune system could also be playing a role in other brain diseases such as cancer and stroke.

This research was supported by the Medical Research Council and MS charities, Roan Charitable Trust and Aims2Cure.
For media information, contact:Alex FernandesDeputy Head of CommunicationsQueen Mary,
University of London
email: a.fernandes@qmul.ac.uk

=====================================================================

neurology.org/content/78/1/15.abstract:

Articles

Association of innate immune activation with latent Epstein-Barr virus in active MS lesions

+Author Affiliations

From the Department of Neuropathology (J.S.T.), John Radcliffe Hospital, University of Oxford, UK; Department of Biochemistry (J.S.T.), Hellenic Pasteur Institute, Athens, Greece; Faculty of Medicine and Health Sciences (G.K.), Department of Microbiology and Immunology, United Arab Emirates University, Al-Ain, UAE; Institute of Cell and Molecular Sciences, Neuroimmunology Group, Neuroscience Centre (U.C.M., G.G., E.S.), and Centre for Infectious Disease (A.V.), Queen Mary University of London, UK; Biotherapeutics (A.M.), National Institute for Biological Standards and Control, Health Protection Agency, South Mimms, Potters Bar, UK; St George's (A.E.), University of London, Basic Medical Sciences, of London, UK; Department of Biochemistry (J.S.T.), Hellenic Pasteur Institute, Athens, Greece; VU University Medical Centre (J.M.), Amsterdam, the Netherlands; Department of Chemistry & Biochemistry (M.C.), School of Life Sciences, University of Sussex, Brighton, UK; Section of Virology (P.F.), Imperial College Faculty of Medicine, London, UK; Department of Surgical Pathology (S.L.), University of Brescia, Italy; and Instituto de Medicina Molecular Aplicada (M.C.S.), University San Pablo, Madrid, Spain.

Correspondence & reprint requests to Dr. Meier: u.meier@qmul.ac.uk

ABSTRACT

Objective: To determine whether the activation of innate immune responses, which can be elicited by pathogenic and endogenous triggers, is associated with the presence of Epstein-Barr virus (EBV) infection in the multiple sclerosis (MS) brain.

Methods: White matter postmortem MS (n = 10) and control tissue (n = 11) was analyzed for the expression of the proinflammatory cytokine interferon α (IFNα) by immunohistochemistry and for EBV by using the highly sensitive method of EBV-encoded RNA (EBER) in situ hybridization.

Results: We detected overexpression of IFNα in active areas of white matter MS lesions but not in inactive MS lesions, normal-appearing white matter, or normal brains. The presence of IFNα in macrophages and microglia (expressing human leukocyte antigen class II) is suggestive of local production as part of an acute inflammatory process. Interestingly, EBERs were also specifically detected in areas where IFNα was overexpressed in these preselected active MS lesions. EBER+ cells were also found in CNS lymphoma and stroke cases, but were absent in other control brains. We next addressed a potential mechanism, e.g., the role of EBERs in eliciting IFNα production, and transfected EBERs into human embryonic kidney (HEK) cells. We used HEK cells that stably expressed Toll-like receptor-3, which recognizes double-stranded RNAs, associated with many viral infections. EBERs elicited IFNα production in vitro.

Conclusion: These findings suggest that latent EBV infection may contribute to the inflammatory milieu in active MS lesions by activating innate immune responses, e.g., IFNα production. Unraveling the underlying mechanisms may help in uncovering causal pathways and developing better treatment strategies for MS and other neuroinflammatory diseases.

FOOTNOTES

Study funding: AIMS2CURE (G.G., U.M.), Roan Charitable Trust (U.M., G.G.), MRC grant (G.G.), UAEU FMHS Project Grant (G.K.), Wellcome Trust grant no. WT082609MA (M.C.)

Why staying positive WON'T speed your recovery

2012-01-04T03:08:00.001-08:00

By SIMON CROMPTONLast updated at 10:30 PM on 2nd January 2012:

Try to stay positive . . . it’s become a common call to those who are ill as the belief has grown that having a positive attitude will not only help you get through illness, but make you better quicker.

But is it true? In fact, there’s no evidence that teaching yourself to have a positive attitude makes you physically healthier. A recent study of cancer patients in Finland and Sweden found no association between survival rates and whether people were positive or negative in their outlook.

The study, in the American Journal Of Epidemiology, looked at 4,600 people with cancer over 30 years, and found that whether they were extrovert or neurotic, their attitude to life had no relationship with how long they survived their illness.

It’s not an isolated finding. An analysis of research by Dr James Coyne, professor of psychology at the University of Pennsylvania School of Medicine, found that there were no good quality studies showing that ‘positive psychology’ had any effect on physical health.

In one of his own large studies, he found that the sense of emotional wellbeing of cancer patients had no effect on how long they lived.

British researchers and health staff are becoming concerned that American lifestyle gurus who urge us to ‘be positive and live longer’ may be doing more harm than good. Read more>>

New for 2012, Dr. Speedy's MRC

2012-01-02T10:21:00.000-08:00

Dr. Speedy's MRC.pdf

Happy New Year

2012-01-01T07:27:00.000-08:00

Professor Simon Wessely once again attempts to defend the indefensible

2011-12-30T10:57:00.000-08:00

Margaret Williams, meactionuk.org.uk:

Defending the indefensible?

Margaret Williams 27^th December 2011

Professor Simon Wessely once again attempts to defend what has already been shown to be indefensible, namely his own beliefs about the nature of ME/CFS, including his belief that graded exercise therapy (GET) has “an impeccable safety record” (Simon Wessely; Health in mind and body; The Journal of the Foundation for Science and Technology: 2011:20:7: 9 –11).

The article contains so many insupportable assertions that it cannot go unchallenged.

In his article, although he does not mention ME as such, Wessely refers to Chronic Fatigue Syndrome (CFS), but in countless articles published in medical journals, reports from official bodies such as the Joint Royal Colleges, in medical textbooks and in the media, as well as in the PACE Trial literature itself, the Wessely School insist that ME and CFS are synonymous.

In this latest article (the publishing of which is perhaps surprising, given his frequent assertions that he has relinquished his work on ME/CFS and that he no longer feels safe publishing about the disorder because of the death threats he has received, and that he now feels safer in Afghanistan), Wessely conforms to his track record of appearing to form his conclusions before he has generated the data to support his conclusions (he often states his assumptions and beliefs as though they are established fact, for example, he has asserted that people with ME benefit from “adopting the sick role” and from “secondary gain”, and that what “precipitates” ME is not what “perpetuates” it, all of which are supposition not supported by data; a further illustration is to be seen in his study of Vitamin B status in just 12 CFS patients in which he found evidence of reduced functional vitamin B status but concluded: “clearly, many patients with CFS are currently taking vitamin B…with little evidence of benefit”, yet nowhere does he provide any evidence that “many” patients are taking supplements with little evidence of benefit and his final conclusion again fails to follow from his data: JRSM 1999:92:183-185).

Wessely’s assertions in his current article are of particular interest because they provide such clear illustration of his cognitive biases, for example:

“CFS illustrates the gap that lies between physical health/illness on the one hand and mental health/illness on the other”: all life-destroying diseases affect both physical and mental health, not just ME/CFS.

“CFS is a multi-factorial illness”: Wessely does not know this, since the cause remains unknown.

“To understand why some people do not get better as the months and years go by, one has to look at behavioural and psychological factors”: this is nothing more than Wessely’s assumption; people do not recover from multiple sclerosis or from motor neurone disease, so it is telling that he makes an exception only in the case of one particular classified neurological disorder (ME/CFS): why do so, unless it is as a face-saving measure because for the last 25 years the Wessely School have rigidly and unscientifically conflated psychiatric fatigue with ME/CFS?

“The illness is then a complicated mixture of predisposition, precipitation, and perpetuation”: Wessely states this as though it were proven fact, but it is unproven and his inability to recognise this demonstrates a fundamental misunderstanding of the nature of scientific knowledge.

“A landmark trial on the management of CFS, known as the PACE Trial, was published recently in The Lancet….Two treatments, graded exercise and CBT, clearly made a difference, although they were certainly not ‘magic bullets’: not only were the interventions used in the PACE Trial very far from being magic bullets, the Chief Principal Investigator himself described them as being “only moderately effective”.

“For those who appreciate these things, the trial is a thing of beauty”: for those who appreciate these things, the PACE Trial -- which cost £5 million -- has been described as a travesty of science and a tragedy for patients; the conclusions were flawed; the primary outcome measures were dropped; ratings that would qualify a participant as sufficiently impaired to enter the trial were deemed by the Principal Investigators (PIs) to be “within the normal range” when recorded on completion of the trial; there were significant conflicts of interest in that all three PIs work for the insurance industry (whose managers insist that claimants undertake a course of CBT and GET -- called “rehabilitation” -- which, if people are too ill to do so or if they know from their own experience that it makes worse and therefore decline, payments are stopped on the basis that claimants do not to want to get better); the PIs intentionally studied a heterogeneous population and it was conceded only after publication of the results in The Lancet that the Investigators did not purport to be studying ME; there was a failure to control the trial; there was downgrading of what constituted serious adverse events; there were many changes to the entry criteria; data was not reported and objective outcome measures were dropped; methods of scoring were changed so as to produce minimally better results, and the results were blatantly misreported in The Lancet (see http://www.meactionuk.org.uk/COMPLAINT-to-Lancet-re-PACE.htm and see also http://www.meactionuk.org.uk/Normal-fatigue.htm ).

“We now have two treatments that we can recommend with confidence to our patients. However, the story does not quite end there. Patient groups rejected the trial out of hand, and the internet was abuzz with abuse and allegations. The main reason for this depressing reaction was the stigma that attaches to disorders perceived (rightly or wrongly) to be psychiatric in origin”: the reason people with ME/CFS reject CBT and GET is because they do not work, but Wessely refuses to accept this, so he here provides an explanation already shown by his own research to be incorrect.

He has previously written: “CFS sufferers are also usually portrayed as hostile to psychological explanation, mental illness, and psychiatry in general….This study aims to investigate attitudes of CFS patients to psychiatric illness (and) a comparison group of patients with rheumatoid arthritis (RA) was chosen….We began with the following hypotheses: CFS patients have more negative attitudes to mental illness…(represented by the perceived stigma of psychiatric illness)…(and) failure to identify emotional states (alexithymia) contributes to denial of the role of psychiatric disorders in the aetiology of CFS….Contrary to our hypotheses and the media accounts of CFS, we found no evidence that CFS patients are characterized by particularly hostile attitudes to mental distress….Our study also failed to demonstrate any overall differences in personality traits that may underlie negative attitudes to mental illness or psychiatry….The… alexithymia scores found in the CFS compared with the RA patients were contrary to our original hypothesis….There was no difference between CFS and RA patients in hostility to mental illness….This study provides no evidence to support the anti-psychiatry tone that is so striking in the popular literature on CFS” (Personality and Social Attitudes in Chronic Fatigue Syndrome. Barbara Wood and Simon Wessely; J Psychsom Res 1999:47:4:385-397).

“If one obtained identical results to the PACE trial, but this time with anti-viral drugs, the reaction would have been totally different. This is exactly what did happen when a very small trial of a drug that modulates the immune system (and which has some nasty side effects) was greeted with acclaim from the same sources that tried to discredit the PACE trial, which tested interventions with an impeccable safety record”: GET for people with ME does not have an impeccable safety record. Indeed, there is abundant evidence from numerous surveys by ME/CFS charities of almost 5,000 patients that in such patients CBT is ineffective and that GET is unacceptable and sometimes positively harmful.

Those surveys include one sponsored jointly by the ME Association and Action for ME (“Report on a Survey of Members of Local ME Groups”. Dr Lesley Cooper, 2000). Cooper found that “Graded exercise was felt to be the treatment that made more people worse than any other” and that it had actually harmed patients

(http://www.afme.org.uk/res/img/resources/Group%20Survey%20Lesley%20Cooper.pdf).

Another survey of 2,338 ME/CFS sufferers (“Severely Neglected: M.E. in the UK”) was carried out in 2001 by Action for ME; its preliminary report stated: “Graded exercise was reported to be the treatment that had made most people worse”; in the final report, this was changed to stating that graded exercise had made 50% of patients worse

(http://www.afme.org.uk/res/img/resources/Severely%20Neglected.pdf).

The 25% ME Group for the Severely Affected carried out a further survey in 2004 which found that 93% of respondents found GET to be unhelpful, with 82% reporting that their condition was made worse (http://www.25megroup.org/Group%20Leaflets/Group%20reports/March%202004%20Severe%20ME%20Analysis%20Report.doc).

In 2005, a report (“Our Needs, Our Lives”) published by The Young ME Sufferers Trust found that 88% had been made worse by exercise (http://www.tymestrust.org/pdfs/ourneedsourlives.pdf).

In June 2007, through Section 16b funding from the Scottish Government, Action for ME produced a report “Scotland ME/CFS Scoping Exercise Report”, which found that 74.42% were made worse by GET.

In 2008, Action for ME published another survey of over 2,760 patients (“M.E. 2008: What progress?”) which found that one third had been made worse by GET and that at their worst, 88% were bed/housebound, being unable to shower, bathe or wash themselves, and that 15% were unable to eat unaided. The Press Release of 12^th May was unambiguous: “Survey finds recommended treatment makes one in three people worse” (http://www.afme.org.uk/news.asp?newsid=355).

In 2009, the Norfolk and Suffolk ME Patient Survey of 225 respondents stated: “Respondents found the least helpful and most harmful interventions were Graded Exercise Therapy and Cognitive Behavioural Therapy” (http://www.norfolkandsuffolk.me.uk/surveylink.html ).

The International Association of CFS/ME recently published an article by Tom Kindlon (Bulletin of the IACFS/ME: 2011:19(2):59-111: Reporting Harms Associated with Graded Exercise Therapy and Cognitive Behavioural Therapy in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome) that details the high rates of adverse reactions to exercise, as well as dissecting the PACE Trial in relation to the heterogeneity of subjects, the tracking of adverse events and the lack of objective outcome measures.

As Ed Lewisohn correctly points out in correspondence relating to the Frenchay Hospital’s clinic at Bristol: “You refer to ‘Frenchay Hospital’s specialist chronic fatigue, or ME clinic’, but ME is an incurable neurological condition and cannot be synonymous with chronic fatigue. Chronic fatigue syndrome is treated by psychiatrists with graded exercise therapy, but if exercise makes (it) better, then that condition is not ME….But many patients with ME are also sent to chronic fatigue centres and receive the same treatment: they are then, shockingly, made more ill” (http://www.thisisbristol.co.uk/chronic-fatigue-syndrome/story-14243686-detail/story.html ).

There is thus an abundance of empirical evidence that GET can result in high rates of adverse effects.

Why is it that the Wessely School, who claim to be so committed to evidence-based medicine (EBM), are permitted to continue to disregard the evidence that proves them to be wrong about the nature of ME and about the efficacy of GET in those suffering from it?

The answer may be because, like so many of the Wessely School myths, EBM does not actually exist.

In 2009 Bruce Charlton, Professor of Theoretical Medicine at the University of Birmingham, clarified the facts in relation to EBM: “It is obvious that EBM was from its very inception a Zombie science….A Zombie science does not perform any scientific function, so it is invulnerable to scientific critique since it is sustained purely by the continuous pumping of funds….The massive success of EBM is that it has rationalised the takeover of UK clinical medicine by politicians and managers….Zombie science is not driven by the scientific search for truth (and it is) kept moving for so long as it serves the purpose of its funders….EBM embraced a top-down and coercive power structure to impose EBM-defined ‘best evidence’ on clinical practice, whether clinical scientists or doctors agreed that the evidence was best or not….Expertise was arbitrarily redefined (and) virtue redefined as submission to EBM recommendations, so the job of physician was at a stroke transformed into one based upon absolute obedience to the instructions of EBM-utilising managers. Indeed, since too many UK doctors were found to be disobedient to their managers, in the NHS this has led to a progressive long-term strategy of the replacing doctors by more-controllable nurses, who are now the first contact for patients in many primary and specialist health service situations…. EBM was not a real science, indeed, it wasn’t any kind of science at all (and) it was not adopted by scientists but by politicians, government officials, managers, and biostatisticians….When the UK government understood that what was being proposed was a perfect rationale for re-moulding medicine into exactly the shape they had always wanted it, the NHS hierarchy were falling over each other in their haste to establish this new orthodoxy in management, medical education and in founding new government institutions such as NICE….Suddenly, the Zombie science of EBM was everywhere in the UK…unhampered by inconveniences such as truthfulness or integrity…it was being practised by many individuals…who lacked…any training and experience in clinical medicine and who certainly did not provide direct patient care….Here was a doctrine which advocated rejecting and replacing with itself the whole model of medical science and practice of the past. It advocated a new model of health service provision, new principles for research funding, a new basis for medical education. And the evidence for this? Well, none. Not one particle. ‘Evidence-based’ medicine was based on zero evidence (but it) was proclaimed Messiah with the backing of serious amounts of UK state funding…to create a fairly-realsitic Zombie of pseudo-science….Nowadays, EBM means whatever the political and managerial hierarchy of the health service want it to mean for the purpose in hand” (Zombie science of Evidence-Based Medicine. Bruce G Charlton. Journal of Evaluation in Clinical Practice 2009:15:930-934).

EBM, however, has proved invaluable to the Wessely School in the perpetuation of their own myths about and management of ME/CFS, to the advantage of both the state and the insurance industry.

Despite the relentless determination of the Wessely School to claim ME/CFS as a functional somatoform disorder (in his latest article, Wessely reiterates his claim that: “the greater the number of symptoms, the more likely the patient was to develop a mood or anxiety disorder”), medical science is at last ensuring that the Wessely era is coming to an end.

Whilst XMRV is now thought to be a laboratory contaminant (and the triumphant glee of those who rejoiced at this is to be greatly deplored), the role of a retrovirus has not yet been resolved: indeed, Dr Ian Lipkin of Columbia University and chief virus-hunter for the NIH was reported on the Wall Street Journal blog on 27^th December 2011 by Amy Dockser Marcus to have said that all the scientists and doctors involved in the NIH study, including the authors of the retracted PNAS and Science papers, “are committed to completing this study because none of us believes that the issue of retroviral infection in CFS/ME is resolved”.

Retrovirology apart, there is now undeniable evidence of multi-system damage in ME/CFS, including inflammation of the blood vessels, hypoperfusion of the brain, delayed recovery of muscles after exercise, dysfunction of the immune and neuroendocrine systems, and evidence of marked abnormalities in gene expression profiling.

Professor Nancy Klimas is to head a new Institute for Neuroimmune Medicine (specifically ME/CFS) at Nova Southeastern University: she will be providing cutting edge research and education of health care professionals, combined with care of patients; she will focus on systems biology, connecting neuro-imaging experts with scientists researching inflammation and genomics/proteomics, as well as collaborating with experts in neurotoxicology.

There is also the work of Dr Jose Montoya’s Chronic Illness Initiative at Stanford; the husband and wife team of Drs Light at the University of Utah; Dr Derek Enlander’s Chronic Fatigue Initiative with a very large budget for research at Mount Sinai, as well as the Public Health and Neuroimmunology Unit (PHANU) at Bond University in Australia (http://forums.phoenixrising.me/content.php?519), plus the committed work of Professors Mark VanNess and Christopher Snell at the University of the Pacific, all of which disprove the beliefs of the Wessely School that ME/CFS is a behavioural disorder.

Furthermore, the UK Medical Research Council has finally recognised the need for biomedical research into ME/CFS and is funding £1.6 million for research into aspects including autonomic dysfunction, aberrant mitochrondrial and cytokine production in skeletal muscles, and immune system dysfunction.

As clinical psychologist Dr Dorothy Rowe pointed out in 1993: “People who know absolutely that they are right are very dangerous” (The Observer, 14^th November 1993), but who paid any attention? Father Cormac Rigby did: “The greatest enemies of truth are those who think they have a monopoly of truth” (The Lord be with you; Family Publications, Oxford, 2004).

A Message from CII Director W. Ian Lipkin Regarding the XMRV/MLV CFS/ME Study

2011-12-29T11:20:00.000-08:00

By W. Ian Lipkin, MDDirector, Center for Infection and Immunity:

Posted 12/28/2011 3:40:37 PM

December 28, 2011

Dear Colleagues and Friends in the CFS/ME Community:

This letter is written to clarify the status of the XMRV/MLV CFS/ME study I am coordinating at the request of the National Institutes of Health. Although frequently described as the “Lipkin Study,” it is in fact the Alter, Bateman, Klimas, Komaroff, Levine, Lo, Mikovits, Montoya, Peterson, Ruscetti, and Switzer study, designed by these 11 investigators to bring their best methods for case ascertainment and characterization and state-of-the-art molecular and serological diagnostic tools to address the question of whether a retrovirus is associated with disease. My role in conjunction with Mady Hornig and Bruce Levin at Columbia University is to ensure that the study represents an appropriately powered, definitive, representative sample of CFS/ME patients across the United States; to receive and distribute samples; and to assess results obtained in individual laboratories for consistency and evidence for or against an association between retroviral signal and disease. I use the term “signal” because any finding related to a retrovirus, whether infectious or noninfectious, genetic material, protein, or antibody, may provide insights into disease or allow development of diagnostic tests even if a causative relationship is not established. My condition on accepting this charge from the NIH and the clinical and laboratory investigators is that each participant agree to unconditionally accept group criteria for defining cases to be used in this study. Laboratory investigators were also required to unequivocally endorse their results at the conclusion of the study. Several months were required to develop clinical criteria for case and control definition and to complete approvals for human subject protection. We encountered additional delays when Dr. Mikovits could no longer pursue her work at the WPI. At that juncture, some parties suggested that the work proceed at WPI without her. However, in my judgment, the value of this study rests in its inclusion of the original investigators who reported the XMRV/MLV findings. Thus, I was grateful when we found a way to fully engage Dr. Mikovits. At the time of this writing we have collected and distributed for laboratory analysis samples from 123 CFS/ME patients and 88 matched control subjects. We intend to complete collection and analysis of samples from 150 patients and 150 controls in early 2012.

There is criticism in some quarters that this study is unnecessary given results obtained by other investigators with other samples. However, the participating clinical and laboratory investigators and our team at Columbia do not agree. We are fully committed to completing the work rapidly and rigorously. For those who continue to express concerns that this study is an inappropriate use of resources in a challenging fiscal environment, please be assured that more than 85% of the funding associated with this initiative is invested in patient recruitment and characterization and sample collection, archiving, and distribution. Thus, irrespective of study outcome there will be unprecedented opportunity to explore hypotheses other than that disease is due to XMRV or MLV infection.

Sincerely yours,

W. Ian Lipkin, MD
Director, Center for Infection and Immunity

Another cracker from the CBT school of denial: “The bastards don’t want to get better”…

2011-12-28T12:12:00.000-08:00

This delightful quote by the way is from page 18, if you're interested, that is.

If you still fancy reading this report, which denies the existence of almost 5000 research papers showing that ME is a physical disease, which was obviously funded by the Medical Research Council, which we all know likes to waste shed loads of money on silly CBT and dangerous GET, but which is so sad and not even beautifully written, that I would advise you to get some anti-sickness tablets from your doctor first before you sit down and puke all over this delightful document.

The bastards don’t want to get better.pdf

PS: this report is so sad and badly researched that the so-called researchers don't even know that ME means Myalgic Encephalomyelitis and not myalgic encephalitis

PS 2: thanks to HP who spotted this very professional remark in this paper, which wasted more than 1 million taxpayers pounds on a therapy which doesn't work for ME, which we have known for decades

See also: Harvard Medical School: EEG spectral coherence data distinguish chronic fatigue syndrome patients from healthy controls and depressed patients
See also: The putative agent of ME/CFS can be transferred to monkeys
See also: Almost 5% of ME/CFS patients contracted ME/CFS from a blood transfusion
See also: Cerebrospinal fluid profiles can differentiate between Lyme disease, ME/CFS and healthy controls
See also: The main characteristic of ME is an abnormally delayed muscle recovery after doing trivial things, if you don't have that, you don't have ME

See also: GET (graded exercise therapy) is torture for ME patients and directly contravenes the do NO Harm principle of the GMC
See also: Harvard Medical School: EEG spectral coherence data distinguish chronic fatigue syndrome patients from healthy controls and depressed patients
See also: Dr. Hilary Jones, When you say, "ME is controversial", did you check that with Alison, Annabel and Sophia? Now, I'm sure you didn't, because all three died of ME. Yes you read that right, …

Dr. Judy Mikovits: Shine's Reader's Choice Woman of the Year 2011

2011-12-28T02:13:00.000-08:00

By Jessica Ashley, Senior Editor, Parenting | Healthy Living – Fri, Dec 16, 2011:

Michelle Obama, Sandra Bullock, Elizabeth Edwards, teen activist Constance McMillen, Chef April Bloomfield, and community member Brett Blumenthal are just a few of the amazing women who have worn a crown as one of Shine's women of the year.

While our editors throw out many names and list off the accomplishments and awards that make celebrities, politicians, activists, and real, hard-working women stand out in their efforts to make all of our lives better, there's always one lady who...well, shines brightest.

Judy Mikovits- Shine's Reader's Choice Woman of the Year 2011 Winner: Researcher Judy Mikovits. Her breakthrough studies of chronic fatigue syndrome made her a hero to many. But her firing and felony arrests late this year cast her in a suspicious and controversial light. Shine readers rallied around her, making Mikovits your overwhelming winner.

Read more>>

See also: A big thank you to Dr. Judy Mikovits

Rumours have it that the Lancet is about to retract the ME/CFS PACE trial

2011-12-27T09:39:00.000-08:00

A controversial study published in the Lancet by CBT psychiatrists which used the Oxford criteria to make sure that no one with ME/CFS was included in the ME/CFS PACE trial, might be retracted if rumours circulating on the Internet are correct.

A source very close to the powers that be at the Lancet has issued the following statement:

“It is our current view that the PACE trial has not withstood the test of independent verification and proper peer review and that this paper, although beautifully written, should be retracted and shredded come the New Year.”

See also: The main characteristic of ME is an abnormally delayed muscle recovery after doing trivial things, if you don't have that, you don't have ME
See also: GET (graded exercise therapy) is torture for ME patients and directly contravenes the do NO Harm principle of the GMC
See also: Harvard Medical School: EEG spectral coherence data distinguish chronic fatigue syndrome patients from healthy controls and depressed patients

See also: Post-exercise acid exposure 50 times higher in ME/CFS patients vs healthy controls, with no reduction with repeat exercise
See also: Jan 2011, Spanish study shows that CBT and GET make things WORSE in ME/CFS !!!
See also: Journal for Psychotherapy 2011: CBT and GET are ineffective and potentially harmful for many ME/CFS patients

See also: Pacific Labs in California (Snell, Stevens et al): it is dangerous to put patients with M.E. through a graded exercise program
See also: Tom Kindlon's paper: "Reporting of Harms Associated with Graded Exercise Therapy and Cognitive Behavioural Therapy in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome"
See also: World exclusive: Prof Wessely admits in the BMJ that there were no ME/CFS patients in the ME/CFS PACE trial

Prof Wessely continues to promote graded exercise therapy despite all the evidence against its use in ME because of the detrimental effects it has on the health of ME patients

2011-12-26T12:12:00.000-08:00

If you fancy to read his delightful comments about the ME/ CFS PACE trial that deliberately used the Oxford criteria

to exclude the patients that were supposed to be in the trial, then scroll to page 10, but make sure you've got a bucket ready.

See also: Cerebrospinal fluid profiles can differentiate between Lyme disease, ME/CFS and healthy controls
See also: The main characteristic of ME is an abnormally delayed muscle recovery after doing trivial things, if you don't have that, you don't have ME
See also: GET (graded exercise therapy) is torture for ME patients and directly contravenes the do NO Harm principle of the GMC
See also: Harvard Medical School: EEG spectral coherence data distinguish chronic fatigue syndrome patients from healthy controls and depressed patients

See also: Post-exercise acid exposure 50 times higher in ME/CFS patients vs healthy controls, with no reduction with repeat exercise
See also: Jan 2011, Spanish study shows that CBT and GET make things WORSE in ME/CFS !!!

See also: Journal for Psychotherapy 2011: CBT and GET are ineffective and potentially harmful for many ME/CFS patients

See also: Tom Kindlon's paper: "Reporting of Harms Associated with Graded Exercise Therapy and Cognitive Behavioural Therapy in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome"

See also: Pacific Labs in California (Snell, Stevens et al): it is dangerous to put patients with M.E. through a graded exercise program

Merry Christmas !!

2011-12-23T03:38:00.000-08:00

MRC misuse ME funding for other diseases

2011-12-22T03:41:00.000-08:00

Medical Research Council announces ME/CFS research projects worth £1.6m: "Summary:

Researchers will analyse the immune systems of more than 500 patients with primary Sjögren syndrome"

Read more>>

See also: The main characteristic of ME is an abnormally delayed muscle recovery after doing trivial things, if you don't have that, you don't have ME

See also: Harvard Medical School: EEG spectral coherence data distinguish chronic fatigue syndrome patients from healthy controls and depressed patients
See also: The putative agent of ME/CFS can be transferred to monkeys
See also: Almost 5% of ME/CFS patients contracted ME/CFS from a blood transfusion
See also: Cerebrospinal fluid profiles can differentiate between Lyme disease, ME/CFS and healthy controls
See also: The main characteristic of ME is an abnormally delayed muscle recovery after doing trivial things, if you don't have that, you don't have ME