Tuesday, January 31, 2012

Prof Behan on BBC ALBA: electron microscopy shows abnormal mitochondria in Myalgic Encephalomyelitis, and we have known this since the 1980s

Professor Peter Behan on BBC ALBA. “Electron microscopy shows abnormal mitochondria in Myalgic Encephalomyelitis, and we have known this since the 1980s.

Research money should be spent on biomedical Myalgic Encephalomyelitis research and not on psycho nonsense,” says Dr. Behan, a retired Harvard trained neurologist and psychiatrist who became a world expert on the physiological nature of ME (also known as chronic fatigue syndrome) in his practice at Southern General Hospital in Glasgow.

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

Thursday, January 26, 2012

New Vaccine Tested Against Autoimmune Diseases

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

Wednesday, January 25, 2012

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

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

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

Tuesday, January 24, 2012

I never imagined my sister would die from ME

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.

Friday, January 20, 2012

Cardiac autonomic impairment and chronotropic incompetence in fibromyalgia

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.br Author Affiliations 1 Division of Rheumatology, School of Medicine, University of Sao Paulo, Brazil. Av. Dr. Arnaldo, 455, Cerqueira César, Brazil 2 School of Physical Education and Sport, University of Sao Paulo, Brazil. Av. Prof. Mello Moraes, 65, Butantã, Brazil For 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/R190 Received: 19 May 2011 Revisions received: 25 August 2011 Accepted: 18 November 2011 Published: 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


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).

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.


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.

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.

Wednesday, January 18, 2012

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

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

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:

Lyme Disease as a Cause of Supraspinatus tendinitis

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]:

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


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]

Tuesday, January 17, 2012

For years medics were baffled by her catalogue of problems

By SADIE WHITELOCKS Last 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>>

Monday, January 16, 2012

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

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.

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.

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]

Saturday, January 14, 2012

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

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.


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