Saturday, May 31, 2008

NYTimes: CFS no longer seen as Yuppie Flu

http://health.nytimes.com/ref/health/healthguide/esn-chronicfatigue-ess.html?ref=health

Chronic Fatigue Syndrome No Longer Seen as ‘Yuppie Flu’

By DAVID TULLER

For decades, people suffering from chronic fatigue syndrome have struggled to convince doctors, employers, friends and even family members that they were not imagining their debilitating symptoms. Skeptics called the illness "yuppie flu" and "shirker syndrome."

But the syndrome is now finally gaining some official respect. The Centers for Disease Control and Prevention, which in 1999 acknowledged that it had diverted millions of dollars allocated by Congress for chronic fatigue syndrome research to other programs, has released studies that linked the condition to genetic mutations and abnormalities in gene expression involved in key physiological processes.

The agency has also sponsored a $6 million public awareness campaign about the illness.

And last year, it released survey data suggesting that the prevalence of the syndrome is far higher than previously thought, although these findings have stirred controversy among patients and scientists. Some scientists and many patients remain highly critical of the C.D.C.’s record on chronic fatigue syndrome. But nearly everyone now agrees that the syndrome is real.

"People with C.F.S. are as sick and as functionally impaired as someone with AIDS, with breast cancer, with chronic obstructive pulmonary disease," said Dr. William Reeves, the lead expert on the illness at the disease control agency, who helped expose its misuse of chronic fatigue financing.

Chronic fatigue syndrome was first identified as a distinct entity in the 1980s. (A virtually identical illness had been identified in Britain three decades earlier and called myalgic encephalomyelitis.) The illness, which afflicts more women than men, causes overwhelming fatigue, sleep disorders and other severe symptoms. No consistent biomarkers have been identified and no treatments have been approved for addressing the underlying causes, although some medications provide symptomatic relief.

Patients say the word "fatigue" does not begin to describe their condition. Donna Flowers of Los Gatos, Calif., a physical therapist and former professional figure skater, said the profound exhaustion was unlike anything she had ever experienced. "I slept for 12 to 14 hours a day but still felt sleep-deprived," said Ms. Flowers, 51, who fell ill several years ago after a bout of mononucleosis. "I had what we call ‘brain fog.’ I couldn’t think straight, and I could barely read. I couldn’t get the energy to go out of the door. I thought I was doomed. I wanted to die."

Studies have shown that people with the syndrome experience abnormalities in the central and autonomic nervous systems, the immune system, cognitive functions, the stress response pathways and other major biological functions.

Researchers believe the illness will ultimately prove to have multiple causes, including genetic predisposition and exposure to microbial agents, toxins and other physical and emotional traumas. Studies have linked the onset of chronic fatigue syndrome with an acute bout of Lyme disease, Q fever, Ross River virus, parvovirus, mononucleosis and other infectious diseases.

"It’s unlikely that this big cluster of people who fit the symptoms all have the same triggers," said Kimberly McCleary, president of the Chronic Fatigue and Immune Dysfunction Syndrome Association of America, the advocacy group in charge of the C.D.C.-sponsored awareness campaign. "You’re looking not just at apples and oranges but pineapples, hot dogs and skateboards, too."

Under the most widely used case definition, a diagnosis of chronic fatigue syndrome requires six months of unexplained fatigue as well as four of eight other persistent symptoms: impaired memory and concentration, sore throat, tender lymph nodes, muscle pain, joint pain, headaches, disturbed sleeping patterns and feelings of malaise after exertion.

The broadness of the definition has led to varying estimates of the syndrome’s prevalence. Based on previous surveys, the C.D.C. has estimated that more than a million Americans have the illness. Last month, however, the agency reported that a randomized telephone survey in Georgia, using a less restrictive methodology to identify cases, found that about one in 40 adults ages 18 to 59 met the diagnostic criteria -- an estimate 6 to 10 times higher than previously reported rates. Many patients and researchers fear that the expanded prevalence rate could complicate the search for consistent findings across patient cohorts. These critics say the new figures are greatly inflated and include many people who are likely to be suffering not from chronic fatigue syndrome but from psychiatric illnesses.

"There are many, many conditions that are psychological in nature that share symptoms with this illness but do not share much of the underlying biology," said John Herd, 55, a former medical illustrator and a C.F.S. patient for two decades.

Researchers and patient advocates have faulted other aspects of the C.D.C.’s research. Dr. Jonathan Kerr, a microbiologist and chronic fatigue expert at St. George’s University of London, said the agency’s gene expression findings last year were "rather meaningless" because they were not confirmed through more advanced laboratory techniques.

Kristin Loomis, executive director of the HHV-6 Foundation, a research advocacy group for a form of herpes virus that has been linked to C.F.S., said studying subsets of patients with similar profiles was more likely to generate useful findings than Dr. Reeves’s population-based approach. Dr. Reeves responded that understanding of the disease and of some newer research technologies is still in its infancy, so methodological disagreements were to be expected. He defended the population-based approach as necessary for obtaining a broad picture and replicable results. "To me, this is the usual scientific dialogue," he said.

Dr. Jose G. Montoya, a Stanford infectious disease specialist pursuing the kind of research favored by Ms. Loomis, caused a buzz last December when he reported remarkable improvement in 9 out of 12 patients given a powerful antiviral medication, valganciclovir. Dr. Montoya has recently completed a randomized controlled trial of the drug, which is approved for other uses, but the findings have not been released. Dr. Montoya said some cases of the syndrome were caused when an acute infection set off a recurrence of latent infections of Epstein Barr virus and HHV-6, two pathogens that most people are exposed to in childhood. Ms. Flowers, the former figure skater, had high levels of antibodies to both viruses and was one of Dr. Montoya’s initial C.F.S. patients. Six months after starting treatment, Ms. Flowers said, she was able to go snowboarding and take yoga and ballet classes. "Now I pace myself, but I’m probably 75 percent of normal," she said.

Many patients point to another problem with chronic fatigue syndrome: the name itself, which they say trivializes their condition and has discouraged researchers, drug companies and government agencies from taking it seriously. Many patients prefer the older British term, myalgic encephalomyelitis, which means "muscle pain with inflammation of the brain and spinal cord," or a more generic term, myalgic encephalopathy.

"You can change people’s attributions of the seriousness of the illness if you have a more medical-sounding name," said Dr. Leonard Jason, a professor of community psychology at DePaul University in Chicago.

Updated from an article that originally appeared in The New York Times on July 17, 2007.

* * *

If the only two medications proven to work on CFS are Ampligen and Valganciclovir -- both anti-virals -- and anti-depressants are proven useless against post-viral CFS, then it should be obvious that CFS has a viral origin and is not a psychiatric problem.

It should be recalled that when the AIDS epidemic started, there was no blood test for that virus, either.  So just because all tests are normal does not mean that the patient doesn't have a virus ... it only means that the patient doesn't have one of the viruses tested for.  My tests for specific viruses don't reveal anything to be concerned about, but when I was given a non-specific test for signs of infection/inflammation, the results were "off the charts".  Clearly, there's something very wrong, even if no one has yet identified the exact virus causing my problems.

CFS costs this country about $25B per year in lost productivity.  A mere 1% of that annual loss, if poured into medical research that would get us back to work, would amount to exponentially more than the total spent on CFS research by CDC in the quarter-century since the first cases were identified.  Yet, that amount would be repaid in taxes in a matter of weeks if all the patients and their caregivers could get back to full productivity.

This patient alone, over my lifetime, will cost the economy over $1M in lost earnings.  Many years, that's been around 15% of the total CDC research budget for CFS.  Yes, you read that right -- getting 7 people like me back to our old jobs would produce more than the amount CDC spends to get us back to work.  If you accept CDC's prevalence numbers of 4M patients, they're spending just over $1 per patient per year on research!  Shameful.

"The incidence of CFIDS is now higher than that of lung cancer, breast cancer or HIV infection in women."  How much per patient is spent on researching those diseases?  What will it take for CFS to achieve parity with them?

At the very least, they need to make as much effort to publicize in the media (not with feel-good photo displays that are seen by only a few people) that CFS is real, as they have previously invested in portraying it as "depression", "psychosomatic" and other disparaging remarks.  Go on TV with CNN's Dr. Gupta, with NBC's Dr. Snyderman, with Oprah, with Dr. Phil, and recant the previous claims, stating flat out that CFS has been proven to have biological underpinnings, and spelling out that it is not depression, because it has these signs and symptoms that are not seen in primary depression.  (It is possible to have depression which is caused by the CFS, just as cancer patients can become depressed over their health problems, but depression doesn't cause the initial disease process, it results from the disease robbing the patient of their former lifestyle.)

Every media outlet which previously broadcast or published derisive stories claiming CFS is all in our heads should be required to devote as much air time or page space to stories enlightening their listeners/readers to the false statements made previously, and what the proven facts are about CFS.

ME/CFS Expert Leonard Jason's New York Times Q&A

 ME/CFS Expert Leonard Jason's New York Times Q&A.
What’s strikingly different about this illness is that the majority of people not only have to deal with a particularly debilitating health problem, they also have to deal with the stigma and societal reaction and disbelief and illegitimacy and that is crushing. The epidemiology done by the CDC was atrocious. The prevalence research was very poorly done. The tests they were using were inappropriate and had a real bias for psychiatric morbidity.
David Tuller/Leonard A Jason, The New York Times
Information Provided:

*
Problems with the New CDC CFS Prevalence Estimates
Leonard A Jason
*
Chronic Fatigue Syndrome No Longer Seen as ‘Yuppie Flu’
The New York Times
Reporter's File
David Tuller

Ellen Goudsmit's Letter in "The Psychologist"

 Letter in the Psychologist, June 2008. Response to Deary.


The Psychologist, 2008, 21, 6, 549.

Letter.

I was interested to read in the 'Out now in BPS Journals' section of the
Psychologist (April 2008) that patients with chronic fatigue syndrome  (CFS)
cope with their illness by operating "within a narrow energy budget, which
ultimately becomes self-defeating". As a specialist in this field, I accept
that most patients try to control their fatigue by restricting their activity levels. However, I am yet to be persuaded that this is maladaptive
and I’m concerned that the item may have given readers a distorted  view of this disabling condition.

The claims made by the author seem to be based on a number of assumptions. The first is that all patients respond to their symptoms in the same way, i.e. fear, avoidance and misattribution.  However, studies have shown that the majority of people with CFS use a range of coping strategies, that most remain ambulant, and I’ve seen no evidence yet that this illness is linked to a general ‘fear of fatigue’ (Lovell, 1999). Moreover, it is difficult to reconcile theories focused on challenging somatic attributions when research has identified abnormalities in the cerebrospinal fluid, brain, muscle and
immune system
(Goudsmit & Howes, 2008).

However, the author’s  main assumption is that his approach to the
management of CFS  is superior to strategies such as pacing, where patients
conserve energy to avoid exertion-related fatigue.  In the case of graded
exercise, the effects tend to be modest, and studies using objective
measures have not found significant or sustained increases in activity
levels. The second alternative is mindfulness. This has been tested in three
small studies, and while it reduced fatigue, only the uncontrolled trial on
9 patients found a significant improvement in physical functioning (Surawy,
Roberts & Silver, 2005). Most notably, the author recommends that patients
adopt a  third approach: to accept the “symptoms and distress”. Firstly,
this implies that  the first two interventions don’t work. Secondly, given
the severity of the illness, is this best practice? Thirdly, the paper
challenges homeostasis, yet we are asked to encourage acceptance. Isn’t that
homeostasis?

The essence of the author’s argument is that pacing is associated with a
poor outcome. However, this is speculation and there is no evidence from
trials or surveys to support this negative view.  A summary of  the
literature relating to pacing, plus a discussion of the abnormalities
referred to above, can be found in the current issue of Health Psychology
Update, also published by the BPS.


Goudsmit, E. & Howes, S. (2008). Pacing: A strategy to improve energy
management in chronic fatigue syndrome. Health Psychology Update, 17, 1,
46-52.

Lovell, DM. (1999). Chronic fatigue syndrome among overseas development
workers: a qualitative study. Journal of Travel Medicine, 6, 16-23.

Surawy, C., Roberts, J. & Silver, A. (2005). The effect of mindfulness
training on mood and measures of fatigue, activity, and quality of life in
patients with chronic fatigue syndrome on a hospital waiting list: a series
of exploratory studies.  Behavioural and Cognitive Psychotherapy, 33,
103-109.
  ---------------------------------------------------------------------- 
Ellen M. Goudsmit PhD CPsychol CSci AFBPsS

For information on ME and CFS,
see: http://freespace.virgin.net/david.axford/melist.htm  

* * *

A friend who is a trained counselor has often pointed out to me the differences between "irrational fear" and "reasonable concern".  For someone who has repeatedly gotten worse by exceeding her limits, it's not an "irrational fear" to think that doing too much will lead to getting worse ... it's something that's been proven via experimentation to be fact.

Unfortunately, those who are dead-set on believing that CFS is a psychological problem won't accept either my experience or the mounds of clinical evidence proving there are biological abnormalities as proof that this is not an irrational fear.  The real "misattribution" isn't in my mind, but in theirs.

FACT: I was happy and healthy until I had a 105 fever for several days.  Psychological problems do not start with a virus.

FACT: I was happy after the fever, but my health never fully returned.

FACT: I went back to work a few days after the fever broke, and remained at work full-time for another 13 years -- this isn't a case of laziness or unwillingness to work, because I perservered at working against the odds.  I'm still working part-time.

FACT: No trained counselor, psychologist or psychiatrist has ever found anything they felt required counseling.  Only people who are not trained/licensed to make psych diagnoses have tried to affix a psych label to me.  The psych experts recognize that some symptoms of physical illness (fatigue, sleeping, inability to concentrate, etc.) are similar to some symptoms of psych problems, and that I lack the necessary emotional components to warrant a psych diagnosis.

FACT: There are symptoms of CFS which are not symptoms of depression.  Depression does not cause fever, swollen glands, abnormal blood tests, viral damage to the heart and brain, etc.

We often see in other people what exists in ourselves: people who would gladly fake an illness in order to quit work will assume that everyone would do the same.  People who get married so they won't have to work any more will assume that this is everyone's goal in getting married.  People who are looking for a psychiatric reason for symptoms can find it in anything, even claiming that fever can be psychosomatically induced.

Before casting aspersions on the character of a CFS patient, look inside yourself.  How much are you projecting your own character flaws onto someone else?  People are different -- there are those who live to work, those who work to live, and those who will do absolutely anything so they'll never have to work again.  But someone with a lifelong reputation as a hard worker does not magically become lazy overnight -- it took a serious virus and severe symptoms to make me stop working full-time, and despite a specialist's assessment that I will never work full-time again, my goal is to prove him wrong.  However, getting there requires doing something out of character for me: resting enough to get well, rather than pushing my limits every day and getting steadily worse because I'm not being patient and waiting to get better before I start running full-tilt again.

Dr. Murphree www.DrRodger.com says that for each year of deterioration, it takes at least one year of recuperation.  Which means that the soonestthat I can expect to reach maximum improvement is 2010-2011. 

Since I was half-dead from sleep deprivation before that problem was finally addressed, it may take longer: the specialist was clear that I was allowed to deteriorate too far without proper medication, and some of the damage would be permanent as a result of the doctors' refusal to prescribe what's appropriate for my actual diagnosis, instead of incorrectly changing my diagnosis to something they know how to treat.  (One of the doctors who preferred a different diagnosis couldn't explain WHY he changed it, what symptoms told him it was That rather than This.  If he doesn't know how to differentiate the two, then how does he know the specialist was wrong?)

Pacing works for me.  If restricting activity now means that I can go back to work full-time later, I'll do it.  But that doesn't necessarily mean that I've got activity-phobia ... it may just mean that I'm following the advice of the experts, which I've proven through trial and error to be what keeps me healthiest.

Friday, May 30, 2008

Britain's Pathway to Work program

[Permission to Repost].

NEW-LABOUR'S FLAWED 'PATHWAY TO WORK': M.E. PATIENTS IN A CORPORATE-SKEWED DRIFT NET.

Anglia ME Action. May 2008. www.angliameaction.org.uk

There are many well-documented reasons to be cynical about the UK New-Labour Government's snowballing Pathways to Work policy - favourably portrayed in the BBC 1 Panorama TV programme entitled Britain on the Sick[1] on May 19th and featuring Professor Mansel Aylward of the Unum Provident Centre for Psychosocial and Disability Research at Cardiff University. For sure, there is no doubt that there are indeed a number of long-term sickness benefit claimants that would, if they could indeed work, be generally better off in employment even if they were not better off financially as a result of the change. The social and self-esteem benefits of this are obvious PROVIDED the employment is suitable and not exploitative. For sure too, there is some fraction of this number that are likely to be actually capable or, with the right sensitive and encouraging support, have the potential to be rendered capable of at least some part-time work. Indeed, anyone in the UK who is politically aware and old enough to remember the nightmare monetarist policies[2] of the 1980s (that even Milton Friedman condemned as excessive) will know only too well that many victims of mass forced redundancy were spuriously swept up in the sickness benefit register at the time (and some have faced long-term negative consequences as a result). In some cases this was partly for short-term personal gain to the claimants themselves but, crucially, it was tolerated and even encouraged by more than a few intellectually dishonest politicians: a political class that cared more about keeping official unemployment figures artificially low and massaging politically embarrassing statistics than it cared for the recipients or victims of its social policy. Now the policy fashion and the political expediencies it serves have reversed but, in spite of this reversal, in overall terms, it still manages to generate a sense of déjà-vu in those who look beyond the spin to examine the fine detail of yet another new policy initiative. Ditto in those who care about the impending unintended (or arguably perversely intended in some cases) effects upon some of society's most vulnerable individuals.

Even if you were to give New-Labour Ministers the benefit of the doubt and assume that their primary intention in the policy change was to compassionately assist patients who are needlessly trapped on benefits (as opposed to reducing DWP budgets and appeasing powerful corporate lobbies - more on this aspect below), it is clear that such policy is based upon some highly questionable premises. For a start, in the BBC Panorama programme, ex Department of Work & Pensions advisor Professor Mansel Aylward (who left the DWP to receive a large salary cheque from multinational health & welfare insurer Unum Provident) reiterated the claim that a major barrier to people leaving sickness benefits and returning to work was that they would be no financially better off. This is what labour-market economists describe as a problematic 'replacement-ratio' - which usually carries with it the questionable assumption that welfare benefits are too high as opposed to wages being too low. Such claims as trotted out by Professor Aylward and his ilk more often than not come from those who have never themselves had to live on long-term benefits and simply do not fully understand how impoverishing, socially debilitating and unwanted such a predicament is for the overwhelming majority. The prejudiced assumption that many claimants prefer life on benefits is often augmented by very spurious 'research' that, with loaded questions and similar devices, narrowly sets out to over-highlight such a factor from the start: and thereby skews its own findings.

Such contentious studies tend to over-focus on monetary issues and leave out the fact that many patients value and greatly miss other aspects of a lost career that has been forcibly denied them by illness. Similarly an irresponsible media can all too readily find a few benefit claimants that clearly should be otherwise occupied and spuriously represent these as the norm to the fertile and prejudiced minds of overburdened taxpayers that are themselves fortunate not to have the tragedy of serious illness within their own family. What is often missed in such caricatures however is that genuine claimants very much want to work if they can (as indicated by the large number that attempt to do a little therapeutic voluntary work when able) but are simply incapable of SUSTAINING regular full-time or even part-time work over the medium or long-term without health deterioration. What is essentially wrong with the crude instrument that is the 'pathways' policy is that, in weedingout misguided or feckless claimants, those that are genuinely ill will experience increased and substantial suffering in the process. This will be particularly problematic for ME patients given the relapsing nature of the illness and the controversy surrounding diagnosis, treatment and disability assessment (more of which below). Such matters have received erudite and sensible social scientists' comment from the likes of Professor Alison Ravetz[3] at Leeds Metropolitan University for example. Moreover, there is growing anecdotal evidence that some patients who are genuinely incapable of sustained gainful full or part-time employment are now increasingly eschewing occasional and beneficial light voluntary or social activities for fear of this being spuriously used as 'evidence' that they can do more. This is an utterly perverse state of affairs that can only harm individuals' prognosis and increase long-term welfare dependency.

Exaggerated numbers of patients allegedly capable of being transferred from sickness benefits into work are effectively pulled out of the air by those with a clear vested interest in matters and are very much at odds with estimates from social policy experts like Professor Ravetz that have no financial axe to grind. They are also at odds with views of most patients' own GPs and specialist Hospital Consultants. It is therefore very telling that wealthy corporate merchant banker and government welfare policy adviser David Freud, amongst others, has called for such qualified professionals (who possess actual long-term detailed knowledge of the individual patients concerned) to be further removed from the benefits decision-making process[4]. Whilst it would be foolish to deny that an unknown fraction of patients are capable of doing some work, it is far from guaranteed that most employers will want to employ them and more likely that benefit cuts will lead patients into the exploitative low-wage sector or to a never-ending treadmill of fruitless interviews - where many will face poverty, exhaustion, further declining health or worse.

Indeed, if a true and rigorous econometric cost-benefit analysis of the pathways to work programme were undertaken it would more likely conclude that the public purse would gain nothing in the long-run overall: due to relapse, worsening prognosis, personal stress, family break-up, increased child-poverty, increased welfare dependency and desperation-driven suicide, black-market activity and even crime. What is certain however, is that the private sector agencies and corporations running the show and providing the highly questionable sausage-factory CBT services[5] will be banking copious amounts of taxpayers' money in fee and consultancy payments - whatever the effects upon patients. It is also clear that tightening up of benefits access, whose gateway is guarded with 'incentivised' private sector therapists and employment 'counsellors', will result in many thousands of ill and disabled patients that are genuinely too ill to work being constantly harassed, facing reduced benefit levels and driven into poverty and worsening health as a direct result. Some of society's most vulnerable people will live in a climate of fear, suspicion and derision.

The notion that great public savings are to be had from such a policy is grossly over-egged: Britain already has one of the highest adult employment rates in the western world and the likelihood that this can be significantly increased by targeting the sick is statistically flawed as well as conceptually so[6]. Moreover, the burden of sickness benefit upon the exchequer is widely exaggerated and misrepresented. To quote Professor Ravetz:

"Incapacity benefit has become one of this year's favourite scare stories. Hardly a day passes without a new headline deploring its soaring costs and the rising numbers of claimants who get "something for nothing", at the expense of decent, hardworking taxpayers. We are told that we are footing an outrageously escalating bill for 2.4 million people, a million of whom shouldn't be on the benefit at all, and each successive work and pensions minister vows to be more ruthless than the last. The true picture is somewhat different. The unreported version, which can be culled from Department for Work and Pensions (DWP) data, is that only 1.4 of the 2.4 million actually receive any payment, the rest get national insurance credits only, and numbers have been falling since 2003."[7]

In fact, UK sickness benefits claimants do not get "something for nothing" when they are unfortunate enough to have to request state help: most of them have for years been paying National Insurance contributions for this exact purpose. It seems clear however that, increasingly, the UK political class is intent upon wriggling out of this paid-for 'social contract' - just as private insurance companies do allthey can to avoid paying out to policy-holders. Indeed, since Peter Lilley (Margaret Thatcher's Social Security Minister) first began to significantly open the public policy-making doors to the likes of Unum Provident, we have already had over a decade of extremely stringent sickness benefit claim reforms: Including rolling downgrades of a patient's own physicians in the decision making process and replacement with agency practitioners possessing little knowledge of the patient but wielding increasingly arbitrary power. Such agency doctors are to be further incentivised/pressured to withhold benefits in what is regarded by many as a disgraceful and unethical conflict of interest. It is in fact now already extremely difficult to obtain sickness benefits without a major struggle and this is particularly well illustrated by the enormous proportion of DLA (Disability Living Allowance) claimants who are forced to successfully fight their claim via the appeals process.

Indeed, many have argued that instead of looking at the supply-side equation of why sickness benefits claims persist, government should, for a refreshing change, make an honest and broad-ranging demand-side inquiry that examines why people get ill and stay ill. Such an inquiry would need to be conducted by a properly independent/objective panel of doctors and research scientists and not dominated by those with clear vested interests in outcomes: such as the various psychiatrists and physicians linked to Unum Provident - as in the case of Professor Aylward. The inquiry would do well to focus on why, for example, in our ever increasingly toxic environment, degenerative nervous and other illnesses - including Myalgic Encephalomyelitis or ME[8] - have occurred in such large numbers of late. The recent Cross-Party Gibson Group of inquiry from both UK Houses of Parliament made precisely this point in regard to ME patients (that have been so roundly misrepresented as primarily suffering from mere behavioural illness by certain doctors linked to Unum Provident)[9]: "In Britain, there has been a clear historical bias towards research into the psychosocial explanations of CFS/ME. This is despite Parliament recognizing ME as a physical illness in a Private Members Bill, the ME Sufferers Bill, in 1988."[10]

"The Group was very interested in the international evidence submitted and concerned as to why this evidence has not been seriously examined in the UK. The Group calls for a further Inquiry into the Scientific Evidence for CFS/ME by the appropriately qualified professionals. This Inquiry should be commissioned by government undertaken by an independent panel of scientific and medical experts, including virologists, immunologists, biochemists etc who can objectively assess the relevance and importance of the international scientific data."[11]

"An independent scientific committee must examine the wealth of international research data. To exclude it from the debate is a great injustice to patients."[12]

"There is a need to undertake further research of post viral infective cause in carefully controlled studies."[13]

"The evidence for a toxin aetiology requires critical and controlled studies. This includes research into possible causes, like pesticides."[14]

With regard to the question of corporate influence upon government policy and conflicts of illness generally, and more specifically in relation to Professor Aylward's particular association with both the Department for Work & Pensions and Unum Provident, the group sates bluntly:

"There have been numerous cases where advisors to the DWP have also had consultancy roles in medical insurance companies. Particularly the Company UNUM Provident. Given the vested interest private medical insurance companies have in ensuring CFS/ME remain classified as a psychosocial illness there is blatant conflict of interest here. The Group find this to be an area for serious concern and recommends a full investigation of this possibility by the appropriate standards body."[15]

Moreover, in the case of ME patients in particular, concern was expressed that such factors would improperly and adversely affect patients' assessment for and entitlement to sickness and disability benefits:

"It may even be that assessment by a medical 'expert' in a field of high controversy requires a different methodology of benefit assessment."[16]

In spite of calls from the Gibson Group of Parliamentarians (backed up by numerous doctors, scientists, patients, carers and concerned members of the public) that the government should not primarily rely on the views of doctors linked to Unum Provident, that conflicts of interest should be thoroughly examined, that the facts of the disease should be independently assessed and that ME patients require a more appropriate means of benefits assessment than the one on offer, not one of these justified recommendations has been taken up by an increasingly dictatorial and corporate-influenced New-Labour Government. Such privileged access to the process of public policy formation that is granted to multinational corporations, in stark contrast to ignored voices of informed and concerned parliamentarians, doctors, scientists, patients, carers and concerned citizens can be, and has been, summed up as 'corporate capture' of New-Labour welfare policy. Such disgraceful bias is eruditely and extensively illustrated in the document entitled 'Corporate Collusion', by Professor Malcolm Hooper et al[17] and elsewhere. These well referenced concerns are particularly worrying in a democracy governed by a so-called 'Labour' party that claims it represents the interests of ordinary voters. Neither are such concerns confined to benefits issues: as the Guardian Newspaper's Seumas Milne commented with regard to health policy:

"It beggars belief that US health privateers straight out of Michael Moore's Sicko are being lined up to run core NHS services. Only dogma and corporate capture can explain this."[18]

And as Privy Councillor and former Liberal Democrat Leader Sir Menzies Campbell put it:

"the public no longer has any influence on the way decisions are taken and has become alienated from the democratic process."[19]

Whilst it cannot be denied that some/unknown fraction of sickness benefit claimants are capable of work and would benefit from working, it is already clear that the world inhabited by those who are genuinely too ill to undertake sustainable work will be increasingly extremely difficult as a direct result of the new 'pathways' policy. The declining public sympathy for sick and disabled people in this country, as a result of widespread over-simplifying sound bite descriptions in the press, is already distinctly apparent.

In some quarters this has amounted to outright demonization and is an utter disgrace in a supposedly modern civilised democracy. This whole misconceived New-Labour policy can be likened to the cruel and all-encompassing giant drift nets of the mechanised fishing industry: that impact upon a whole gamut of precious marine life (notably including dolphins) and not just the intended catch: with the former simply discarded in their droves as collateral damage. Out of sight is out of mind? Times ahead will be increasingly tough for most genuine sickness benefit claimants but the greatest victims of all in this disgracefully skewed and malign 'welfare' juggernaut will of course be ME patients that are genuinely unable to sustain gainful work. No other group has suffered such a long history of denigration, misrepresentation as mere psychiatric fatigue sufferers and portrayal as outright malingerers[20]. All in spite of the long-standing recognition of physical/neurological disease by the World Health Organisation[21] and the large and growing volume of biomedical research findings[22]. For ME patients; the ground for mistreatment and benefits reduction at the hands of the DWP and their privateers has been long and well prepared. [23] Truly unjust and dire times lie ahead.

The supreme and heartrending irony of all of this is that research-led mitochondrial[24], antiviral[25] and other biomedical therapies that are denied ME patients by the NICE (for reasons other than good science [26]) are now being developed, privately accessed and beginning to yield tangible results that may one day see many patients able to return to a better level of functioning and, in some cases, employment! That is precisely what ALL ME patients would want. Being on long-term benefits and burdened with a difficult illness that attracts horrendous neglect, mistreatment and abuse is not something most ME patients would wish on their worst enemy. It does not take a Nobel Laureate to work out that ME patients who are beginning to improve on such biomedical therapies will be forced into relapse as a result of harassment, premature enforced entry into the labour market and poverty arising from benefit cuts: all due to the crude sad joke of a welfare policy that is 'pathways to work'. Genuine ME patients, as distinct from those with psychiatric 'fatigue' (with whom ME patients are all too often confused - sometimes deliberately[27]), will be forced into a no-win situation by a blunt and blundering policy that in reality will be a one way street to relapse, poorer prognosis and, inevitably, more patient deaths[28].

In five years time this will be patently obvious to all. By then however the architects of this skewed experiment upon the sick will have moved on: leaving ME patients, their families and genuine science-based doctors to pick up the pieces. God help such maligned, abused, neglected, physically ill and incapacitated patients. Such a 'welfare' policy of course also needs to be viewed against the "Labour" Government's complicity in the tax-avoidance strategies of the super-rich: the real "something for nothing" burden upon the exchequer. Add this disgraceful corporate-capture welfare policy to that of state 'CFS/ME' policy generally, deceitful military adventurism, broken manifesto promises on 'ethical' foreign-policy, broken manifesto promises on top-up loans, broken manifesto promises on a European-referendum and you have just a few reasons why this, and many other decidedly EX-Labour voters will be doing everything they can to call these politicians to account. Woe betide many current New-Labour MPs at the next UK general election: soon after, along with many of the sick and disabled, they too will be forced into job-seeking activities.

M. C. Tully. May 2008.

Anglia ME Action. [email protected]

[Permission to Repost].

THIS DOCUMENT IS AVAILABLE FOR ONLINE DOWNLOAD AT: http://angliameaction.org.uk/docs/corporate-drift-net.pdf

Pathway to Work Endnotes (1) & Commentary

Speaking from personal experience, on dozens of occasions, as soon as I mentioned to an interviewer that I would need to lie down during the day and/or occasionally work from home, the interview ended; there were healthier applicants who would not need those accommodations, and despite my qualifications and experience, I was no longer the best candidate for the job. The only way for a disabled person to get a job is to go through State VocRehab, which deals with employers who have previously been willing to accommodate the disabled. Unfortunately, State VocRehab requires that your health be sufficiently stable to commit to a set work schedule, and will not waste their time trying to place a patient who cannot predict when they will feel well enough to work.

As much as I want to work, I simply cannot find anyone willing to hire me because my symptoms are too severe. I can’t hide them during a job interview, and they’re asked about. I also can’t work enough hours to be employable without making myself sicker – 12 hours in one week landed me back in bed, and it was a month before I got back to baseline. There’s simply no point in working more hours if that makes me sicker and unable to work.

It is easy for those who "see" me only through my writings to convince themselves that I need only a little push to be able to work successfully, but a former State VocRehab counselor who has seen me in person says otherwise: State VocRehab would tell me to go home and get well because they couldn’t place me in my current condition. The SSDI VocRehab experts are unanimous that I cannot work; the judge may imagine that there’s a job somewhere that I could do, but the Ph.D.s say no such job exists and have the statistics to prove it. One was quite clear that fewer than 1% of paralegal jobs in California are part-time, and there are essentially none that are less than half-time; the doctor was theorizing I could work 12-15 hours, but from experience, I knew that was too much – either way, it was a lot fewer hours than would be required to make me employable, and I make significantly more per hour freelancing than I would as a part-time employee.

From your vantage point as a reader, you don’t see that I do most of my writing lying down, and some with my eyes closed (thankfully, I’m a touch-typist); you simply imagine that I use my computer sitting at a desk as you do. And you don’t see that sometimes it takes days (or even weeks) for severely-affectedCFS patients to write something, with substantial editing by other people who can guess at what word was meant when the author wrote [thing] in the middle of a sentence, before it’s actually put out for the public. There’s no employer who would accept that amount of lag time between an assignment and a finished product.

Come to my house and observe me, rather than pre-judging based on your notion of what CFS is, and you’ll change your mind about my ability to hold down a real job without getting fired for not meeting the employer’s standards for attendance, appearance and productivity.

* * *

ENDNOTES:

[1] Panorama: Britain on the Sick. BBC 1. Screened on Monday 19 May 2008. The programme covered what was portrayed as New Labour's 'Pathway to Work' programme when in reality the chief policy architect is Unum Provident: with the policy being facilitated by Labour's 2007 Welfare Reform Act. The BBC programme was conspicuous by the relative lack of expert voices questioning the Government's policy. See: http://news.bbc.co.uk/1/hi/programmes/panorama/7409927.stm

[2] Contrary to much popular belief, monetarist economic policies were first adopted in the UK by Labour Chancellor Dennis Healey. They were subsequently taken to such extremes by the Thatcher government that they were even condemned by former Tory PM Edward Heath - as well as the said US Monetarist architect Milton Friedman. The results were the widely held needless decimation of a large proportion of British manufacturing industry, poor export performance and ultimately a major crash in sterling, along with mass unemployment (in excess of 4 million and which cost the exchequer the equivalent of a decade's North Sea oil revenues ) and community breakdown that is still reverberating to this day.

[3] See for example the New Statesman article by Professor Ravetz of Leeds Metropolitan University on 1 May 2008 entitled: Is Labour Abolishing Illness? Viewable online at: http://www.newstatesman.com/200805010024

[4] David Freud: Interviewed on the BBC Radio 4 'PM' programme on February 2nd 2008. See: http://news.bbc.co.uk/go/pr/fr/-/1/hi/uk_politics/7223687.stm  http://news.bbc.co.uk/1/hi/uk_politics/7223687.stm

[5] CBT (Cognitive Behavioural Therapy) is far from recognised as the panacea it is made out to be and there is much evidence and professional opinion that person-centred counselling is a superior mechanism for addressing long-term emotional and social problems. Such factors are discussed for example in the paper entitled: Inadequacy of the York (2005) Systematic Review of the CFS/ME Medical Evidence Base. Comment on Section 3 of: The diagnosis, treatment and management of chronic fatigue syndrome (CFS)/(ME) in adults and children, Work to support the NICE Guidelines... Anne-Marie Bagnall, et al, Centre for Reviews and Dissemination, University of York. 2005. Professor Malcolm Hooper & Horace Reid, January 2006. From: www.meactionuk.org.uk/FINAL_on_NICE_for_Gibson.html

[6] See for example the New Statesman article (op cit) by Professor Ravetz of Leeds Metropolitan University on 1 May 2008 entitled: Is Labour Abolishing Illness? Viewable online at: http://www.newstatesman.com/200805010024

[7] See the New Statesman article by Professor Ravetz of Leeds Metropolitan University on 1 May 2008 entitled: Is Labour Abolishing Illness? Viewable online at: http://www.newstatesman.com/200805010024

[8] See: M.E. (Myalgic Encephalomyelitis) BASIC INFORMATION. Anglia ME Action. April 2008. At: http://www.meactionuk.org.uk/ME_BASIC_INFORMATION_-_Anglia_ME_Action_-_April_2008.htm  http://www.meactionuk.org.uk/ME_BASIC_INFORMATION_-_Anglia_ME_Action_-_April_2008.pdf

Also see: What is ME? What is CFS? Information for Clinicians and Lawyers. www.meactionuk.org.uk/What_Is_ME_What_Is_CFS.htm

[9] See: CORPORATE COLLUSION. Professor Malcolm Hooper, Eileen Marshall & Margaret Williams. A MUST READ document available at: www.meactionuk.org.uk/Corporate_Collusion_2.htm

And see: QUOTABLE QUOTES ABOUT ME/CFS. Compiled by Margaret Williams on behalf of the charity Invest in ME. Available online at: http://www.investinme.org/IIME%20ME%20Quotes%20Order%20form.htm

[10] Page 9 of the joint Commons/Lords Gibson Parliamentary Inquiry Group (GSRME) Report into ME/CFS: www.erythos.com/gibsonenquiry/index.html

[11] Page 31 of the joint Commons/Lords Gibson Parliamentary Inquiry Group (GSRME) Report into ME/CFS: www.erythos.com/gibsonenquiry/index.html

[12] Page 33 of the joint Commons/Lords Gibson Parliamentary Inquiry Group (GSRME) Report into ME/CFS: www.erythos.com/gibsonenquiry/index.html

[13] Page 33 of the joint Commons/Lords Gibson Parliamentary Inquiry Group (GSRME) Report into ME/CFS: www.erythos.com/gibsonenquiry/index.html

[14] Page 33 of the joint Commons/Lords Gibson Parliamentary Inquiry Group (GSRME) Report into ME/CFS: www.erythos.com/gibsonenquiry/index.html

[15] Page 30 of the joint Commons/Lords Gibson Parliamentary Inquiry Group (GSRME) Report into ME/CFS: www.erythos.com/gibsonenquiry/index.html

[16] Page 30 of the joint Commons/Lords Gibson Parliamentary Inquiry Group (GSRME) Report into ME/CFS: www.erythos.com/gibsonenquiry/index.html

[17] See: CORPORATE COLLUSION. Professor Malcolm Hooper, Eileen Marshall & Margaret Williams. A MUST READ document available at: www.meactionuk.org.uk/Corporate_Collusion_2.htm

See: Proof Positive? Evidence of the deliberate creation via social constructionism of "psychosocial" illness by cult indoctrination of State agencies, and the impact of this on social and welfare policy. Eileen Marshall, Margaret Williams 30th August 2005. At: www.meactionuk.org.uk/PROOF_POSITIVE.htm

See: Concerns About Commercial Conflict of Interest Underlying the DWP Handbook Entry on ME/CFS. Hooper, Marshall & Williams. www.meactionuk.org.uk/HOOPER_CONCERNS_ABOUT_A_COMMERCIAL_CONFLICT_OF_INTEREST.htm

See: Wessely, Woodstock and Warfare? Margaret Williams. 9th August 2007. At: www.meactionuk.org.uk/Wessely_Woodstock_and_Warfare.htm

See: QUOTABLE QUOTES ABOUT ME/CFS. Compiled by Margaret Williams on behalf of the charity Invest in ME. Available online at: http://www.investinme.org/IIME%20ME%20Quotes%20Order%20form.htm

[18] Seumas Milne. Only Dogma and Corporate Capture can Explain This. Thursday October 18, 2007. The Guardian Newspaper. Available online at: http://www.guardian.co.uk/commentisfree/story/0,,2193518,00.html

[19] Sir Menzies Campbell. BBC Radio 4 Today programme on 3rd July 2007.

[20] See CORPORATE COLLUSION. Professor Malcolm Hooper, Eileen Marshall & Margaret Williams. Document available at: www.meactionuk.org.uk/Corporate_Collusion_2.htm

And also see: The Mental Health Movement: Persecution of Patients? A Consideration of the Role of Professor Simon Wessely and Other Members of the "Wessely School" in the Perception of Myalgic Encephalomyelitis (ME) in the UK. Background Briefing for the House of Commons Select Health Committee. Professor Malcolm Hooper. At: www.meactionuk.org.uk/SELECT_CTTEE_FINAL_VERSION.htm

And see: QUOTABLE QUOTES ABOUT ME/CFS. Compiled by Margaret Williams on behalf of the charity Invest in ME. Available online at: http://www.investinme.org/IIME%20ME%20Quotes%20Order%20form.htm

[21] Myalgic Encephalomyelitis or M.E. (myalgic= muscle-pain, encephalo= brain, myelitis= spinal-cord, encephalomyelitis= inflammation of brain & spinal-cord) is a long-term organic/biomedical illness and is NOT the same thing as 'Chronic Fatigue', short-term post viral syndrome or 'myalgic encephalopathy' and it is NOT a psychiatric or behavioral illness. ME has been in the medical literature since the 1930s and classed as a physical disease by the WHO (World Health Organisation) International Classification of Diseases (ICD) since 1969 - currently listed at WHO ICD-10-G93.3 as a Multi-System organic/physical NEUROLOGICAL Disorder with similarities to Multiple-Sclerosis and Post-Polio-Syndrome. Documented clinical/research abnormalitie include: immune system/infectious; cardiovascular, endocrine and digestive systems; muscle, cellular, mitochondrial and genetic function and integrity; oxidative stress; central nervous system - including brain and spinal cord; end organs. See: http://meactionuk.org.uk/G93-3-ICD-10-compilation.jpg  http://meactionuk.org.uk/G93-3-ICD-10-index-closeup.jpg  www.who.int/classifications/icd/en/

Pathway to Work ENDNOTES (2)

[22] To Quote Harvard's Professor Anthony Komaroff:

"there are now over 4,000 published studies that show underlying biomedical abnormalities in patients with this illness. It's not an illness that people can simply imagine that they have and it's not a psychological illness. In my view, that debate, which has waged for 20 years, should now be over".

[Professor Anthony Komaroff, Harvard Medical School: Speaking at the USA Government CDC (Centers for Disease Control and Prevention) press conference on 3 November 2006.] www.cdc.gov/od/oc/media/transcripts/t061103.htm

For an excellent regularly updated peer-reviewed overview paper - see: Myalgic Encephalomyelitis: a Review With Emphasis on Key Findings in Biomedical Research. Professor M Hooper. J Clin Pathol 2007; 60:466-471. Doi: 10.1136/jcp.2006.042408. http://jcp.bmj.com/cgi/content/abstract/60/5/466

For a biomedical research overview up to 2005 see: Illustrations of Clinical Observations and International Research Findings from 1955 to 2005 that demonstrate the organic aetiology of Myalgic Encephalomyelitis / Chronic Fatigue Syndrome. Malcolm Hooper, Eileen Marshall, Margaret Williams (For Gibson Inquiry): www.meactionuk.org.uk/Organic_evidence_for_Gibson.doc

For updates on ME and related research - including downloadable pdf abstracts/comments on all published papers see: M.E. Research UK (MERUK): A Scotland based biomedical ME research/ information organization led by Dr Vance Spence, Honorary Senior Research Fellow, University of Dundee Medical School: www.meresearch.org.uk/

Also, for international research & ME issues updates see Co-Cure at: www.co-cure.org/

Seven Genomic Subtypes of Chronic Fatigue Syndrome / Myalgic Encephalomyelitis (CFS/ME): a detailed analysis of gene networks and clinical phenotypes. Jonathan Kerr et al. Journal of Clinical Pathology. 5 Dec 2007. Doi: 10.1136/jcp.2007.053553. http://jcp.bmj.com/cgi/content/abstract/jcp.2007.053553v1

Review: Chronic Fatigue Syndrome. L D Devanur & J R Kerr. Journal of Clinical Virology xxx (2006) xxx-xxx; JCV-1120; doi:10.1016/j.jcv.2006.08.013. www.cfids-cab.org/rc/Devanur.pdf

Abnormal impedance cardiography predicts symptom severity in chronic fatigue syndrome of disease. Peckerman A, Lamanca JJ, Dahl KA, et al. Am J Med Sci. 2003; 326:55-60. www.cfids-cab.org/MESA/Peckerman.pdf

CFS: The Heart of the Matter - 2006 Dr Paul Cheney Seminar DVD www.dfwcfids.org/videos/video200609cheney_about.shtml  Overview document of Dr Cheney's DVD presentation: www.dfwcfids.org/medical/cheney/heart04.part1a.htm

CFS is Low Output Heart Failure Secondary to Mitochondrial Failure. Dr Sarah Myhill www.drmyhill.co.uk/article.cfm?id=381

Oxidative Stress Levels are Raised in Chronic Fatigue Syndrome and are Associated with Clinical Symptoms. Gwen Kennedy, Vance Spence et al. Free Radical Biology & Medicine: 39 (2005) 584-589. DOI: 10.1016/j.freeradbiomed.2005.04.020. www.cfids-cab.org/rc/Kennedy.pdf

Nitric Oxide Synthase Partial Uncoupling as a Key Switching Mechanism for the NO/ONOO- Cycle. Professor Martin Pall. Medical Hypotheses (2007) 69, 821-825. Doi: 10.1016/j.mehy.2007.01.070. www.cfids-cab.org/rc/Pall-1.pdf

Book: Explaining "Unexplained Illnesses". Prof. Martin Pall. ISBN: 978-0-7890-2389-6: www.haworthpress.com/store/PDFFiles/ForReps/Pall-Unexplained.pdf

Chronic Fatigue syndrome is Associated with Chronic Enterovirus Infection of the Stomach. John K S Chia & Andrew Y Chia. Journal of Clinical Pathology 2007, 0:1-6. DOI: 10.1136/jcp.2007.050054. http://press.psprings.co.uk/jcp/september/cp50054.pdf

Use of Valganciclovir in Patients with Elevated Antibody Titres against Human Herpesvirus-6 (HHV-6) and Epstein-Barr Virus (EBV) who were experiencing central nervous system dysfunction including long-standing fatigue. Jose G Montoya et al. Journal of Clinical Virology; 37 Suppl. 1 (2006) S33-S38. www.cfids-cab.org/rc/Kogelnik.pdf

Chronic fatigue Syndrome: The Need for Subtypes. Professor Leonard A Jason et al. Neuropsychology Review, Vol. 15, No.1, March 2005. DOI:10.1007/s11065-005-3588-2. http://condor.depaul.edu/~ljason/

Functional neuroimaging correlates of mental fatigue induced by cognition among chronic fatigue syndrome patients and controls. Dane B. Cook, Patrick J. O'Connor, Gudrun Lange, Jason Steffener. PII: S1053-8119(07)00127-9. DOI: 10.1016/j.neuroimage.2007.02.033. Reference: YNIMG 4490. NeuroImage: 2007. www.cfids-cab.org/rc/Cook-2.pdf

And see MERUK article: Non-invasive structural and functional neuroimaging in ME/CFS at: www.meresearch.org.uk/research/projects/neuroimage.html

Causes of Death Among Patients With Chronic Fatigue Syndrome. Leonard A. Jason, Karina Corradi, Sara Gress, Sarah Williams, and Susan Torres-Harding. DePaul University, Chicago, Illinois, USA Health Care for Women International, 27:615-626, 2006. Routledge. Copyright ©© Taylor & Francis Group, LLC. ISSN: 0739-9332 print / 1096-4665 online: DOI: 10.1080/07399330600803766 www.ingentaconnect.com/content/routledg/uhcw/2006/00000027/00000007/art00005?crawler=true

The Complexities of Diagnosis. Byron Hyde. In: Handbook of Chronic Fatigue Syndrome. Leonard A Jason et al. John Wiley & Sons, Inc. 2003. www.nightingale.ca/documents/ComplexitiesofDiagnosis.pdf

The Clinical and Scientific Basis of Myalgic Encephalomyelitis / Chronic Fatigue Syndrome. Byron Marshall Hyde M.D. et al. The Nightingale Research Foundation. ISBN: 0-9695662-0-4. www.nightingale.ca/index.php?target=bookoffer

Book: Enteroviral and Toxin Mediated Myalgic Encephalomyelitis / Chronic Fatigue Syndrome and Other Organ Pathologies. Dr John Richardson. Haworth Press, 2001. ISBN: 0-7890-1128-X. http://www.haworthpress.com/books/default.asp

[23] See CORPORATE COLLUSION. Professor Malcolm Hooper, Eileen Marshall & Margaret Williams. Document available at: www.meactionuk.org.uk/Corporate_Collusion_2.htm  And also see: The Mental Health Movement: Persecution of Patients? A Consideration of the Role of Professor Simon Wessely and Other Members of the "Wessely School" in the Perception of Myalgic Encephalomyelitis (ME) in the UK. Background Briefing for the House of Commons Select Health Committee. Professor Malcolm Hooper. At: www.meactionuk.org.uk/SELECT_CTTEE_FINAL_VERSION.htm

[24] CFS is Low Output Heart Failure Secondary to Mitochondrial Failure. Dr Sarah Myhill www.drmyhill.co.uk/article.cfm?id=381

Oxidative Stress Levels are Raised in Chronic Fatigue Syndrome and are Associated with Clinical Symptoms. Gwen Kennedy, Vance Spence et al. Free Radical Biology & Medicine: 39 (2005) 584-589. DOI: 10.1016/j.freeradbiomed.2005.04.020. www.cfids-cab.org/rc/Kennedy.pdf

Nitric Oxide Synthase Partial Uncoupling as a Key Switching Mechanism for the NO/ONOO- Cycle. Professor Martin Pall. Medical Hypotheses (2007) 69, 821-825. Doi: 10.1016/j.mehy.2007.01.070. www.cfids-cab.org/rc/Pall-1.pdf

Book: Explaining "Unexplained Illnesses". Professor Martin Pall. ISBN: 978-0-7890-2389-6: www.haworthpress.com/store/PDFFiles/ForReps/Pall-Unexplained.pdf

CFS: The Heart of the Matter - 2006 Dr Paul Cheney Seminar DVD www.dfwcfids.org/videos/video200609cheney_about.shtml Overview document of Dr Cheney's DVD presentation: www.dfwcfids.org/medical/cheney/heart04.part1a.htm

[25] Use of Valganciclovir in Patients with Elevated Antibody Titres against Human Herpesvirus-6 (HHV-6) and Epstein-Barr Virus (EBV) who were experiencing central nervous system dysfunction including long-standing fatigue. Jose G Montoya et al. Journal of Clinical Virology; 37 Suppl. 1 (2006) S33-S38. www.cfids-cab.org/rc/Kogelnik.pdf

Chronic Fatigue syndrome is Associated with Chronic Enterovirus Infection of the Stomach. John K S Chia & Andrew Y Chia. Journal of Clinical Pathology 2007, 0:1-6. DOI: 10.1136/jcp.2007.050054. http://press.psprings.co.uk/jcp/september/cp50054.pdf

[26] On the highly questionable behavioural approach to ME (now officially adopted by NICE and others in the UK); Dr Bruce Carruthers, Senior Fellow of the Canadian Royal College and principle lead of the international expert team that produced the highly respected ME Clinical Case Definition, states: "Supporters suggest that 'ideally general practitioners should diagnose CFS and refer patients to psychotherapists for CBT without detours to medical specialists as in other functional somatic syndromes'. Proponents ignore the documented pathophysiology of ME/CFS, disregard the reality of patient's symptoms, blame them for their illness and withhold medical treatment. Their studies have often included patients who have chronic fatigue but excluded more severe cases as well as those who have other symptoms that are part of the clinical criteria of ME/CFS."

[Underline emphasis added. See: SHS Box on page 10 of (and indeed the whole document): Myalgic Encephalomyelitis / Chronic Fatigue Syndrome: A Clinical Case Definition and Guidelines for Medical Practitioners - An Overview of the Canadian Consensus Document by Professor Bruce M Carruthers and Dr Marjorie I Van de Sande. UK - NHS Clinician Endorsed / UK A4 Format - Version]: http://data.eastanglia.me.uk/pdfs/Canadian_ME_Overview_A4.pdf

And the Parliamentary Gibson Group Inquiry Report unequivocally states:

"The Group found that the international criteria paid far greater attention to the symptoms of CFS/ME while the Oxford criteria focus very little on any symptoms other than long term tiredness. There is concern that the broad spectrum of patients who may be included in these criteria may lead to inaccurate results in patient studies of CFS/ME." [Page 12 of the joint Commons/Lords Gibson Parliamentary Inquiry Group (GSRME) Report into ME/CFS: www.erythos.com/gibsonenquiry/index.html ].

AN ABSOLUTE MUST READ document on this matter is: Inadequacy of the York (2005) Systematic Review of the CFS/ME Medical Evidence Base. Comment on Section 3 of: The diagnosis, treatment and management of chronic fatigue syndrome (CFS)/(ME) in adults and children, Work to support the NICE Guidelines... Anne-Marie Bagnall, et al, Centre for Reviews and Dissemination, University of York. 2005. Professor Malcolm Hooper & Horace Reid, January 2006. From: www.meactionuk.org.uk/FINAL_on_NICE_for_Gibson.html

Another MUST READ document is: Some Concerns about the National Institute for Health &Clinical Excellence (NICE) Draft Guideline issued on 29th September 2006 on Diagnosis and Management of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis in Adults and Children. M Williams/25% ME: www.meactionuk.org.uk/Concerns_re_NICE_Draft.pdf

And see: ADDENDUM to Some Concerns about the NICE Draft Guideline on "CFS/ME". Margaret Williams. At: www.meactionuk.org.uk/ADDENDUM_to_Response_to_NICE.htm

[27] There has been a great deal of sloppy science and downright dishonesty when it comes to categorizing and separating true ME patients (recognized as physical/neurological by the WHO at ICD-10-G.93.3) from psychiatric/idiopathic 'fatigue' patients (categorised completely separately by the WHO at ICD-10-F.48). This has led to skewed studies and outrageously misleading comment on patients' illness and disability. See for example: M.E. (Myalgic Encephalomyelitis) BASIC INFORMATION. Anglia ME Action. April 2008. At: http://www.meactionuk.org.uk/ME_BASIC_INFORMATION_-_Anglia_ME_Action_-_April _2008.htm http://www.meactionuk.org.uk/ME_BASIC_INFORMATION_-_Anglia_ME_Action_-_April _2008.pdf

Also see: What is ME? What is CFS? Information for Clinicians and Lawyers. www.meactionuk.org.uk/What_Is_ME_What_Is_CFS.htm

Note also that Dr Bruce Carruthers, Senior Fellow of the Canadian Royal College and principle lead of the international expert team that produced the highly respected ME Clinical Case Definition, states:

"Supporters suggest that 'ideally general practitioners should diagnose CFS and refer patients to psychotherapists for CBT without detours to medical specialists as in other functional somatic syndromes'. Proponents ignore the documented pathophysiology of ME/CFS, disregard the reality of patient's symptoms, blame them for their illness and withhold medical treatment. Their studies have often included patients who have chronic fatigue but excluded more severe cases as well as those who have other symptoms that are part of the clinical criteria of ME/CFS."

[Underline emphasis added. See: SHS Box on page 10 of (and indeed the whole document): Myalgic Encephalomyelitis / Chronic Fatigue Syndrome: A Clinical Case Definition and Guidelines for Medical Practitioners - An Overview of the Canadian Consensus Document by Professor Bruce M Carruthers and Dr Marjorie I Van de Sande. UK - NHS Clinician Endorsed / UK A4 Format - Version]: http://data.eastanglia.me.uk/pdfs/Canadian_ME_Overview_A4.pdf

And the Parliamentary Gibson Group Inquiry Report unequivocally states:

"The Group found that the international criteria paid far greater attention to the symptoms of CFS/ME while the Oxford criteria focus very little on any symptoms other than long term tiredness. There is concern that the broad spectrum of patients who may be included in these criteria may lead to inaccurate results in patient studies of CFS/ME." [Page 12 of the joint Commons/Lords Gibson Parliamentary Inquiry Group (GSRME) Report into ME/CFS: www.erythos.com/gibsonenquiry/index.html ].

AN ABSOLUTE MUST READ document on this matter is: Inadequacy of the York (2005) Systematic Review of the CFS/ME Medical Evidence Base. Comment on Section 3 of: The diagnosis, treatment and management of chronic fatigue syndrome (CFS)/(ME) in adults and children, Work to support the NICE Guidelines... Anne-Marie Bagnall, et al, Centre for Reviews and Dissemination, University of York. 2005. Professor Malcolm Hooper & Horace Reid, January 2006. From: www.meactionuk.org.uk/FINAL_on_NICE_for_Gibson.html

Another MUST READ document is: Some Concerns about the National Institute for Health &Clinical Excellence (NICE) Draft Guideline issued on 29th September 2006 on Diagnosis and Management of Chronic Fatigue Syndrome / Myalgic Encephalomyelitis in Adults and Children. Margaret Williams / 25% ME: www.meactionuk.org.uk/Concerns_re_NICE_Draft.pdf

And see: ADDENDUM to Some Concerns about the NICE Draft Guideline on "CFS/ME". Margaret Williams. At: www.meactionuk.org.uk/ADDENDUM_to_Response_to_NICE.htm And see: See CORPORATE COLLUSION. Professor Malcolm Hooper, Eileen Marshall & Margaret Williams. Document available at: www.meactionuk.org.uk/Corporate_Collusion_2.htm

[28] Consultant Microbiologist & ME specialist Dr Elizabeth Dowsett stated that some 10% of patients die early due to complications from ME - organ failure and other factors*. It is believed that a great number of ME-related early deaths due to end-organ failure etc are not picked up because they are simply put down to heart-failure etc per se and not properly connected with ME as the underlying cause. Moreover, it is arguable the majority of life-long ME patients have some life span reduction due to increased oxidative stress etc.

Professor Leonard Jason studied such factors and also discovered that the largest tragic joint killer was suicide: due to the appalling stress and lack of support such patients experience. Such factors can only increase under New Labour's/Unum Provident's Pathways to Work initiative. See: Professor Leonard Jason's et al paper entitled: Causes of Death Among Patients With Chronic Fatigue Syndrome. DePaul University, Chicago, Illinois, USA Health Care for Women International, 27:615-626, 2006. Routledge. Copyright © Taylor & Francis Group, LLC. ISSN: 0739-9332 print / 1096-4665 online: DOI: 10.1080/07399330600803766 www.ingentaconnect.com/content/routledg/uhcw/2006/00000027/00000007/art00005?crawler=true

Even more alarming was the tragic death by ME of 32 year old Sophia Mirza that was recently recorded by a UK coroner and was the result of organ failure and alleged psychiatric mistreatment/neglect. A large online archive of the papers of this case - including the death certificate - is now available at the following thanks to the courageous work of Sophia's family: The Sophia Mirza Memorial Website - Coroner's Comments/Death Certificate: http://www.sophiaandme.org.uk/index.html

Also see: Inquest Implications: www.meactionuk.org.uk/Inquest_Implications.htm

[* Dr Elizabeth (Betty) Dowsett. Addressing the Spring 2002 Annual General Meeting of ME Support Norfolk (UK). The lecture was filmed and put into the ME Support Norfolk resource library.]

[Permission to Repost].

Wednesday, May 28, 2008

Faculties Failure

Faculties Failure

Margaret Williams

There can be few in the international ME/CFS community, either researchers or sufferers, who are not profoundly dismayed at yet another article co-authored by Professor Simon Wessely that fails to distinguish between patients with chronic fatigue and those with chronic fatigue syndrome.

His article Physical or Psychological a comparative study of causal attribution for chronic fatigue in Brazilian and British primary care patients (Acta Psychiatr Scand May 2008: doi:10.111/j.1600-0447.2008.01200.x) fails to distinguish between chronic fatigue and chronic fatigue syndrome, the latter also being referred to as myalgic encephalomyelitis.

For peer-reviewers of a highly-rated journal such as Acta Psychiatrica Scandinavica (which has an impact factor of 3.857, this being a high score, since 90% of journals score less than 1 on impact rating) to have allowed such blatant misrepresentation to have escaped censure is alarming.

It is a matter of record that when serious errors and misrepresentations in his published articles (which, when challenged, even Wessely himself cannot rationally condone) have been pointed out to him and to Editors, Wessely blames his peer-reviewers. One instance of this occurred in 1997 in relation to his article in the Quarterly Journal of Medicine (The prognosis of chronic fatigue and chronic fatigue syndrome: a systematic review. Joyce J, Hotopf M, Wessely S. Q J Med 1997:90:223-233), the many flaws of which were exposed by Dr Terry Hedrick (a research methodologist) in a bullet-proof analysis that was published in Q J Med 1997:90:723-725. To quote Hedrick: Patients beliefs in organic bases for their illnesses may be more accurate than anything else we have to offer at this time. Not only did the Joyce et al article fail to summarize the psychiatric literature accurately, it omitted discussion of the many avenues now being explored on the organic underpinnings of (ME)CFS.

This is not an isolated example of Wessely blaming his peer-reviewers. There have been others, for example, when UK medical statistician Professor Martin Bland from St Georges Hospital Medical School, London, pointed out significant statistical errors in a paper by Wessely and Trudie Chalder, saying that Wesselys findings were clearly impossible, Wessely absolved himself from any blame.

Bland was robust: Potentiallyincorrect conclusions, based on faulty analysis, should not be allowed to remain in the literature to be cited uncritically by others (Fatigue and psychological distress. BMJ: 19th February 2000:320:515-516). Wessely was compelled to acknowledge on published record that his figures were incorrect: We have been attacked by gremlins. We find it hard to believe that the usually infallible statistical reviewers at the BMJ could have overlooked this and wonder, totally ungallantly, if we can transfer the blame to the production side.

Will Wessely once again try to blame his peer-reviewers for this latest confusion and absolve himself from any blame? By what mental mechanism does he continue to dissociate himself from the fact that his personal belief that ME/CFS is a behavioural disorder is unsupported by hard evidence? Is he unmoved by the body of irrefutable evidence that has shown him to be wrong? That body of evidence is not going to go away. Why does he continue to deny it?

How often must it be pointed out that it was in 1990 that the American Medical Association made it plain that chronic fatigue and chronic fatigue syndrome are not the same? The AMA statement said: A news release in the July 4 packet confused chronic fatigue with chronic fatigue syndrome; the two are not the same. We regret the error and any confusion it may have caused.

And yet --- eighteen years later --- here we have Wessely and his co-authors still using the terms chronic fatigue and chronic fatigue syndrome and myalgic encephalomyelitis synonymously.

Does this not amount to scientific misconduct?

The title and the abstract of his latest paper refer to chronic fatigue but the text refers to chronic fatigue syndrome and ME.

Given the fact that chronic fatigue is not synonymous with ME/CFS, the authors cannot possibly be talking about patients with ME/CFS, yet they claim to be doing so: Chronic fatigue syndrome (CFS), sometimes also known as myalgic encephalomyelitis (ME)..

Once again, this is in rank defiance of the World Health Organisations International Classification of Diseases (ICD-10, 1992), which classifies fatigue quite separately from ME/CFS; moreover, the WHO has provided written clarification that it is not permitted for the same disorder to be classified to more than one rubric. Fatigue is classified as a mental disorder whilst ME/CFS is classified as a neurological disorder.

Why isWessely continually permitted to defy such international taxonomic principles?

Unsurprisingly, this latest paper is replete with self-references.

In it, Wessely states emphatically: British primary care patients with unexplained chronic fatigue were more likely to attribute their fatigue to physical causes than their Brazilian counterparts.

Wessely acknowledges that: The study participants were not randomly selected representative samples from the healthcare seeking population yet his conclusion is categoric: Causal attribution influences symptom experience, help-seeking behaviour and prognosis in chronic fatigue syndrome.

Wessely states: Less explored is a possible variation in causal attribution between sociocultural settings and to what extent physical attribution consistently associated with a poor prognosis of CFS is enhanced by sociocultural variables more frequently observed in Western affluent countries such as the UK. These include the sociopolitical debate about the nosological status of CFS in general and for disability benefits in particular.

Somewhat unexpectedly, Wessely concedes that CFS is officially endorsed as a medical condition in the UK, citing A report of the CFS/ME working group: report to the Chief Medical Officer of an independent working group. Hutchinson A. cited 2007 September 23 (i.e. the Report to the CMO). This is notable, given that the original report of 11th January 2002 specifically omitted to accept the WHO classification of ME/CFS as a neurological disorder.

If Wessely concedes that CFS is officially endorsed as a medical condition in the UK, why does he refer to it as unexplained chronic fatigue (UCF), which is a WHO classified mental disorder?

It is a straight-forward enough concept, so once again it has to be asked what is it about this concept that Wessely seems so continually unable or unwilling to understand?

In this latest paper, patients in the study with unexplained chronic fatigue were identified using the Chalder Fatigue Questionnaire, which is said to identify substantial chronic fatigue lasting six months or more. How this matches the criteria for ME/CFS such as the 2003 Canadian definition by Carruthers et al is not explained. The authors state: The questionnaires were read out to illiterate (Brazillian) participants. Those who fulfilled criteria for CFS were then asked to answer questions on causal attribution, duration of fatigue, and the Centre for Disease Control and Prevention (CDC) 1994 case definition of CFS.

Furthermore, the authors state that they relied upon an estimated prevalence of chronic fatigue and on an assumed prevalence of UCF.

Despite a study cohort that seems to be a conglomeration of ill-defined participants, Wessely et al state: More widespread awareness of CFS/ME in the UK may lead to a greater likelihood of British patients viewing their fatigue via a biomedical perspective than their counterparts in Brazil. In the UK, most media and self-help material provided by patient organisations are more likely to promote physical rather than psychological explanations (and) the health care system, which labels fatigue as a medical condition, may further reinforce this tendency.

No reference is provided to support the assertion that the UK health care system labels fatigue as a medical condition.

The authors state: Social support provided in a way which fosters dependency can help maintain chronic fatigue (and) there is an association between secondary gain and health outcomes (in) functional somatic syndromes.

Wessely et al supply no references to support their claim, and seem to ignore the fact that both the Canadian and Australian guidelines reject such a notion.

Despite Wesselys acknowledgement that there was a high non-response rate in the UK (Approximately 30% of the eligible patients in the UK did not complete phase 2 in comparison with only 6% in Brazil), the conclusion is that The higher availability of sick leave / sickness benefit because of CFS in the UK may both contribute to and reflect the greater legitimsiation of chronic fatigue as a medical disorder. The findings of this study lend some support to the evidence on the important role of sociocultural factors in shaping illness attribution and perception around chronic fatigue and chronic fatigue syndrome.

It cannot be emphasised enough that unexplained chronic fatigue is not the same as ME/CFS.

At the Second World Congress on CFS and related disorders held in September 1999 in Brussels, Dr Daniel Peterson from the US said that ten years ago (i.e. in 1989), he believed that (ME)CFS would be resolved by science, but that he had now changed his mind and believed that it could only be resolved by politics.

It is politicians whom Wessely advises on CFS/ME and it is politicians who implement his advice, without seeming either to be aware of or to care about the enormous body of scientific evidence demonstrating that Wessely is simply wrong to lump chronic fatigue with ME/CFS as a single entity.

Can it be right that politicians should now control the science of medicine?

Wessely seems to think so. His latest paper seems to be saying that if Social Security benefits are stopped, patients will stop having ME/CFS.

This contradicts the NICE Guideline on CFS/ME that was published in August 2007, which clearly said that it was the doctors job to support CFS/ME patients in obtaining benefits.

 

 

It seems that Wessely disagrees.

 

* * *

Misinformation is the biggest problem with CFS.

The name Chronic Fatigue Syndrome was intentionally selected by CDC because of the ease with which it could be confused with mere "fatigue". Psychobabblers like Wessely took that ball and ran with it. As intended.

Hillary J. Johnson, author of Osler's Web, commented that the name "Chronic Fatigue Syndrome" was selected "by a small group of politically motivated and/or poorly informed scientists and doctors who were vastly more concerned about costs to insurance companies and the Social Security Administration than about public health. Their deliberate intention – based on the correspondence they exchanged over a period of months – was to obfuscate the nature of the disease by placing it in the realm of the psychiatric rather than the organic. The harm they have caused is surely one of the great tragedies of medicine." Chronic Fatigue Syndrome, Fibromyalgia, and Other Invisible Illnesses, Katrina Berne, Ph.D., page 10

In fact, CFS also occurs in Third World countries where there are no government disability benefits, and in people whose only choice is "work or starve".

Granted, there are shiftless people who claim to have CFS because it’s an easy way to avoid having to get a job (though they manage to do everything else in life and are never too tired to go out partying, whereas a True CFS patient will spend most of her time resting), True CFS is caused by a virus, not by an ulterior motive. There’s no secondary gain: SSDI benefits are about 1/3 of the person’s usual salary, not to mention that I now have to pay for my own health insurance and my own pension plan, since I no longer have an employer to take care of those expenses – I’m losing thousands of dollars per month by being too sick to work, and my Social Security retirement benefit is going down, not up, because what should be my peak earning years are being wasted earning below the poverty level. Withdrawing disability benefits will not result in a miraculous recovery, the only effect will be in the number of people who can no longer afford to live independently and apply for Medicaid-paid nursing home care (at a far greater cost than their disability benefits).

There are tests which show abnormalities in CFS, but they are rarely ordered because only specialists are aware of them. It’s already possible to weed out those who are claiming to have CFS because they think there’s no way to disprove their claim; the correct tests just need to be ordered. The same tests can differentiate between CFS and depression. I have an "off the charts" result on one of those blood tests (normal should be 3, on the first test I had 28 and on the re-test I had 30), proving that I am physically sick, not a malingerer. And proving, as I’ve said from the beginning, that mine is not a borderline case of disability – it’s not something where a little extra effort on my part or some minimal accommodations by an employer would get me back to work – with test results 10x what they should be, it’s clear that I’m seriously ill.

HAPPY BIRTHDAY TO ME!

My birthday wish is that by my next birthday we can have a magic pill for CFS, like fibromyalgia has just gotten.

I want to be able to go out to birthday dinner without worrying how many days I'm going to spend in bed as a result of the outing.

And I want respect for this disease on a par with its lookalikes, MS and post-polio.

Fibromyalgia: A disease of amplified pain

http://www.immunesupport.com/library/showarticle.cfm?id=8892&T=CFIDS_FM&B1=EM052808F&LN=1

Fibromyalgia - Ultimately a Disease of Amplified Pain


by Mark J. Pellegrino, MD
ImmuneSupport.com


05-26-2008
Excerpted with permission from Chapter 9 of Dr. Mark Pellegrino’s very popular book, Fibromyalgia: Up Close and Personal.* Dr. Pellegrino has seen more than 20,000 FM patients in his practice at the Ohio Rehab Center, and has been a Fibromyalgia patient himself since childhood.

Many conditions can lead to permanent changes in the pain transmission mechanism and result in chronic pain that overwhelms the body’s pain defense mechanisms. One such condition is Fibromyalgia.

Fibromyalgia may not cause destruction along the pain pathways as other conditions I have mentioned can [rheumatoid arthritis, carpal tunnel syndrome, shingles, multiple sclerosis, for example]. However, Fibromyalgia does cause chronic abnormal changes along all the pathway components and this results in chronic pain via both peripheral (from skin, muscles and nerves) and central (from spinal cord and brain) neurological mechanisms.

The end result of Fibromyalgia’s abnormal changes appears to be a state of pain amplification that cause severe generalized pain. Fibromyalgia is ultimately a disease of amplified pain.

Dr. Robert Bennett has written and presented excellent information that explains why we hurt with Fibromyalgia (e.g., “Emerging Concepts in the Neurobiology of Chronic Pain: Evidence of Abnormal Sensory Processing in Fibromyalgia,” Mayo Clinic Proceedings). If we trace the pain signals through the various parts of the pain pathway (from the nociceptors - or specialized pain nerve endings – to the nerves to the spinal cord to the brain) in people with Fibromyalgia, we find various abnormalities along the way. Many studies have shed light on different points along the complete pain pathway.

I want to briefly summarize some of these different abnormalities and possible problems encountered by Fibromyalgia pain signals on the path to the brain.

NOCICEPTORS - Pain originates from the nociceptors

Trauma is a common trigger of Fibromyalgia. Tissue injury - damage to the muscles and soft tissues – activates the nociceptors. Some studies have suggested that microscopic injury occurs in specific parts of the muscles (for those who want the medical names: muscle spindles, intrafusal fibers, and calcium pumps).

Localized tissue injury probably activates arachidonic acid (a biological protein), which turns into “bad” prostaglandans (called Cox-II prostaglandins), and cause inflammation and pain.

In addition to trauma, autoimmune factors may be another pain nerve activator. Perhaps autoimmune processes create compounds which act as irritants and activate the nociceptors chronically to the point where they become “permanently” sensitized and irritated. As a result, biochemical, hormonal, and red blood cell changes occur that interfere with the cells’ ability to receive adequate supplies of oxygen, glucose, and other nutrients. Blood flow, energy formation, and the cells’ electrical and neurological harmonies are all disrupted.

Since the nociceptors remain “faulty,” the electrical and neurological balance remains abnormal, and nociceptors continue to be activated. Pain-producing neurotransmitters are released and accumulate as long as the nociceptors stay activated at the peripheral level (skin and muscles, especially).

These persistent pain signals we experience may be interpreted as an itching, burning, swelling, or tingling at one end of the spectrum, or – at the other end – knife-stabbing, burning, or throbbing. One nociceptor can signal different pain signals and sensations depending on its level of irritation – the more irritated it is, the more severe the pain.

These changes can become permanent and cause the nerves to become sensitized to the point where they are easily activated to send pain, even in the absence of any noxious stimulus.

In other words, persistent pain signals can spontaneously arise from peripheral nerve endings and bombard the rest of the pain pathway. So, instead of waiting for outside stimulation such as trauma, pressure, temperature, or touch to signal the nociceptors, these nociceptors send pain signals on their own, without any outside help. This “spontaneous” pain is what we complain about the most!

NERVES

The nerves, especially the sensory nerves and the autonomic nerves, “wonder what is happening” because they are getting bombarded by all of these signals from the nociceptors. At first, they try to diminish these painful signals by using accommodation and gate mechanisms.

However, the signals persist and they, too, undergo a sensitization process. They become hypersensitized and react with an exaggerated response instead of a normal or diminishing response (accommodation). Now we get even more pain, numbness, swelling, burning, and other sensations.

Some of the hypersensitization may be mediated by nerve growth factor, which has been found in higher levels in Fibromyalgia. A high nerve growth factor may indicate the nerves are trying to regenerate or repair themselves. But instead of repairing the nerves so they act normal again, the opposite seems to happen. Nerve growth factor is probably enhancing the nerves’ abilities to transmit pain to the spinal cord. More pain results, not less.

SPINAL CORD – Amplification, wind-up, allodynia, Substance P, generalization

At the spinal cord level, the Fibromyalgia begins to take control.

It is here that additional changes occur to perpetuate the pain and spread it to different levels. When pain generators first start firing, the spinal cord pain processing centers may act at first like a dry sponge and easily soak up all the signals. Our bodies may have many pain generators at any given time, but if they are slowly and intermittently firing, drug sponges can soak up the signals and not cause any bothersome symptoms.

From time to time there may be an acute exacerbation of a problem leading to a lot of pain signals being generated, and if a lot of pain signals are dumped at once into the spinal cord sponge, only a little bit gets absorbed and a lot gets passed through and perceived as acute pain.

In Fibromyalgia, however, the different pain generators continue to send signals and eventually the dry sponges becomes a wet sponge and it can’t soak up any more. The additional oncoming continuous signals will spill over the wet sponge, and this leads to persistent pain.

The two main changes that occur at the spinal cord include:

  • Pain amplification (by specialized nerves called NMDA receptors)

  • And loss of pain filtering (by the diffuse noxious inhibitory control system).

Spinal cord nerves are bombarded by continuous stimulation from the peripheral nerves, causing a progressive increase in electrical signals to be sent up to the brain. This phenomenon is called “wind-up,” and is the neurological mechanism for the amplification of pain.

Once this wind-up phenomenon occurs, a central sensitization results in which various types of sensory signals - not just pain - will arrive in the spinal cord, become amplified, and be sent to the brain as pain. The spinal cord becomes more sensitized to sending pain, lots of it. Once this happens, the spinal cord is not able to properly sort out and filter various sensory signals.

As a result, different sensory signals such as touch, pressure, temperature, and joint movement all become amplified and sent up the pain pathways, resulting in pain signals instead of the appropriate touch, pressure, temperature, or joint motion signals.

This defect in pain transmission where there is increased sensitivity to all stimuli – even those which normally do not evoke pain – is called allodynia. Unfortunately for the person with Fibromyalgia, the spinal cord is now “wired” to interpret nearly all sensory signals as pain – severe pain! We can still appreciate touch, pressure, temperature, joint movement, and other non-pain signals, but pain contaminates these signals, and we feel the pain.

Another key change at the spinal cord level is an increased formation of Substance P and other neurotransmitters.

Substance P’s primary role at the spinal cord level is to transmit pain signals and to sensitize the spinal cord so it is readily available to transmit pain. When Substance P reaches high concentrations (as it does in Fibromyalgia), it can migrate up and down the spinal cord, away from the initial location of the pain signal. As a result, multiple levels of the spinal cord undergo sensitization and send increased pain signals, leading to a “generalization” of the Fibromyalgia.

This spreading of pain explains how one can develop generalized Fibromyalgia from an initial regional area of pain. A common example of this occurs following a motor vehicle accident where a particular body part, such as the neck, was injured. Over time, the pain begins to involve the mid-back, low back, and ultimately the whole body, even though these areas were never injured. The Substance P-induced spinal cord changes can explain this migration of pain from the neck to the entire body.

BRAIN

Our poor brains have no chance, do they? Any pain memory stored in the past will be re-awakened by this process. Fibromyalgia is notorious for causing previously injured areas to hurt more once it develops. This previously injured area may have settled down and become essentially pain-free, but the pain memories remained, although inactive. Thanks to the Fibromyalgia pain amplification process, the inactive memories are reactivated.

The pain centers of our brain, the limbic system and the cerebral cortex, are continuously fed these amplified signals from the spinal cord. Changes occur:

  • Serotonin levels decrease,
  • Brain waves change,
  • Sleep stages are affected,
  • Blood flow and glucose [blood sugar] metabolism are affected.

The brain gets overwhelmed with these pain signals and spends a lot of attention and energy monitoring the pain. Fibrofog occurs. Emotional components are “attached” to pain, including fear, depression, anxiety, anger, hopelessness, and helplessness, which can further amplify the pain.

In patients with Fibromyalgia, functional reorganization (brain plasticity) in both sensory and motor portions of the brain has been observed, and appears directly related to the chronicity of the pain (Dr. H. Flor, 2003). These brain changes may be viewed as pain memories that influence how painful and non-painful signals affect the body’s sensory and motor responses. The brain makes these changes to enhance its ability to perceive pain – brain amplified pain.

This type of abnormal brain plasticity can be measured. Doctors Richard H. Gracely, Richard A. Harris, Daniel J. Clauw, et al. at the University of Michigan Chronic Pain and Fatigue Research Center have published studies which demonstrated abnormal “hyperactive” areas of the brains and abnormal “quiet” areas of the brains in Fibromyalgia test subjects who underwent functional MRIs. This provides objective evidence to support brain plasticity with both hypersensitive amplified pain, and turning off the ability to inhibit pain.

FIBROMYALGIA PAIN SUMMARY

To summarize, Fibromyalgia changes our pain pathways. It may start off as a peripheral irritant, but eventually it becomes a self-perpetuating process that affects the entire pathway from the nociceptors to the brain. The main problem, in a nutshell, is amplified pain.

The amplified pain is the result of our nervous system gaining the ability to magnify pain and losing the ability to inhibit pain. What comes in at a signal of a “1” does not end up in the brain as a signal of a “1” as it would in people without Fibromyalgia. Our pain signal of a “1” gets amplified and magnified, and by the time it reaches our brain, it is a “10”!

Other non-painful signals get thrown into this pain amplification pathway and arrive at our brain as pain signals. Even tiny subconscious pain signals can get amplified, or the nerve pathways can automatically “fire away” without any obvious noxious stimulus to cause spontaneous pain.

These are not your everyday aches and pains, these are severe pains that cannot be ignored. This severe, chronic pain can completely disrupt one’s life. And by the way, while all of this is happening, we continue to look completely normal on the outside.

___
* Reproduced with permission from Fibromyalgia: Up Close & Personal by Mark J. Pellegrino, MD. © Anadem Publishing, Inc. (www.anadem.com) and Mark Pellegrino, MD, 2005, all rights reserved. This book may be purchased for $24.50 plus S&H from Dr. Mark J. Pellegrino at the Ohio Rehab Center (phone 330/498-9865 or fax 330/498-9869).

Note: This information has not been evaluated by the FDA. It is not meant to prevent, diagnose, treat, or cure any illness or disease. It is very important that you make no change in your personal healthcare plan or health support regimen without researching and discussing it in collaboration with your professional healthcare team.