The Guardian's Scott Jordan Harris: How many more people have to die before 'chronic fatigue syndrome' merits properly funded biomedical research?

Scott Jordan Harris guardian.co.uk, Friday 30 March 2012: On Sunday 18 March, Emily Collingridge, a beautiful 30-year-old activist and author, died after she was apparently no longer able to struggle against the chronic illness that had afflicted her since she was six. Major news organisations have all but ignored her death – the death of a noteworthy campaigner while suffering from the very condition she tried to persuade the world actually existed – just as they continually ignore so many important stories about the illness she had.

That illness is a neurological condition called myalgic encephalomyelitis or ME. There are many who think it is not real and many others, even within the medical profession, who think it is a psychological condition best treated with enforced exercise, which only worsens its effects. Even those doctors and lay people who acknowledge the illness often refer to it by the ridiculous name "chronic fatigue syndrome", which is almost as damaging to ME sufferers as the symptoms we suffer.

Fatigue is what a person feels after a hard work day or an intense session at the gym. It is a gentle tiredness that makes the back ache slightly and the eyelids a little heavy. It is cured by a nap or a reviving espresso. Collingridge was beyond bedridden. She was crippled by incessant agony and dependent on morphine. She was fed through a tube and her body couldn't cope with noise, light or movement. She was doubly incontinent and experienced periods of both blindness and paralysis.

Around a year ago, she wrote, "I have come very close to dying on more than one occasion. If you met me you may well think I was about to die now." She is now dead. To call the illness that savaged her "chronic fatigue syndrome" is like calling stomach cancer "chronic upset tummy".

Remarkably, she was – in her healthier periods – able to write a book called Severe ME/CFS: A Guide to Living, which is an invaluable text for many ME sufferers. It is published by AYME, the Association for Young People with ME, of which Collingridge was a prominent member. Her most important work, though, was her appeal for adequate biomedical research into ME.

I recently wrote a piece for the website of the Chicago Sun-Times, discussing both my history of ME and my reactions to the new documentary Voices from the Shadows. For anyone who wishes to understand the agony ME can inflict, and the dangerous ignorance endured by many who have it, the film is a must-see. One of the ME sufferers it profiles is Sophia Mirza, the first person in Britain whose death was officially listed as being caused by chronic fatigue syndrome. Another is my late friend, Lynn Gilderdale, whose mother assisted in her suicide after Lynn's condition became unendurable.

Both Mirza and Gilderdale suffered – and perhaps died – because of the unforgivable actions, and also the unforgivable inaction, of members of the medical profession. Mirza was committed to a mental institution to treat an illness that was purely physical and never recovered from the damage that did. Gilderdale, too, was referred to a psychiatrist when she needed physicians working from the results of cutting-edge studies. The question we must ask is obvious: how many young people like them, and like Collingridge, have to die before their illness is taken seriously and huge, well-focused efforts are made to cure it through properly funded biomedical research?

Collingridge was a great light for thousands of victims of severe ME whose lives pass in almost total darkness. It is essential that her tragedy is not overlooked. We must all understand that the cause she championed in life – the urgent need for proper recognition of, and research into, ME – is made even more urgent by her death.

The Sun's Lynsey Haywood: ME – sometimes called Chronic Fatigue Syndrome – is a severely debilitating illness

LYNSEY HAYWOOD speaks to three people who tell us why these two illnesses are far more serious than most people realise.




SOPHIE ELLIS has suffered from ME since she was nine. She can't even watch TV or send a text and is fed through a tube.

She has not been downstairs in her house in Banbury, Oxon, for more than a year.

She lives with dad Mark Ellis, 52, a financial adviser, and mum Karen, 52, her full-time carer. Mark says:

When Sophie was nine she got a fairly typical virus which lasted two to three weeks.

But she never really recovered.

She suffered crippling gastric problems, heartburn and acid reflux, as well as a general lack of energy.

The GPs we saw tried to deal with the symptoms rather than the root cause.

As parents we had no knowledge of ME, so while seeing countless consultants we never thought to ask about it.

We simply thought it was something people got in the Eighties and it made you feel like you had flu.

We certainly didn't know you could treat it.

Sophie was getting worse and worse to the point where she couldn't eat and was increasingly bedbound.

Then, about two years ago, one consultant suggested ME and, after researching it ourselves, it all made sense.


Sensitive to light ... Sophie lies in a darkened room
It took up to six years to get an accurate diagnosis but sadly, by then, having pushed herself so hard for six years, Sophie's batteries were completely run down.

It felt like we'd missed our window of opportunity when we could have done something.

Now, Karen has given up her job as a shelf-stacker at Sainsbury's to be her full-time carer.

The slightest thing exhausts Sophie and because it's neurological, it affects every part of her body.

She can't watch TV or use a laptop because she's light intolerant. It makes her dizzy or ill.

She can't read more than a couple of times a day and she hasn't been downstairs for more than a year.

We can't speak to her for more than a few minutes at a time because it drains her energy.

Her room has to be dark and she needs help getting to the loo as she's too wobbly on her feet.

She can read texts but can't type herself because her brain can't co-ordinate her fingers.

Eating and chewing is now almost impossible for her, so she has a tube which feeds liquidised food through her nose, but she can drink herself.

We're trying to step up the little achievements she can manage each day – exposing her to a little more light, getting her to eat a little food herself.

But if we push her too hard she relapses badly and we're back at square one.

We can't have visitors to the house at all now because of any potential disruption. The best Karen and I can hope for in terms of our own lives is a walk and a coffee when Sophie's brother Matt, who is 29, comes round.

This makes Sophie feel terribly guilty too – ME impacts hugely on everyone.

But throughout Sophie's been bright and cheerful, always with a smile on her face.

University of Zurich: It is relatively certain that MS is an autoimmune disease in which the body’s own defense cells attack the myelin in the brain and spinal cord

healthcanal.com, 27/02/2012: Damaged myelin in the brain and spinal cord does not cause the autoimmune disease Multiple sclerosis (MS), neuroimmunologists from the University of Zurich have now demonstrated in collaboration with researchers from Berlin, Leipzig, Mainz and Munich.

In the current issue of Nature Neuroscience, they therefore rule out a popular hypothesis on the origins of MS. The scientists are now primarily looking for the cause of the development of MS in the immune system instead of the central nervous system.

Millions of adults suffer from the incurable disease multiple sclerosis (MS). It is relatively certain that MS is an autoimmune disease in which the body’s own defense cells attack the myelin in the brain and spinal cord. Myelin enwraps the nerve cells and is important for their function of transmitting stimuli as electrical signals. There are numerous unconfirmed hypotheses on the development of MS, one of which has now been refuted by the neuroimmunologists in their current research: The death of oligodendrocytes, as the cells that produce the myelin sheath are called, does not trigger MS.

Neurodegenerative hypothesis obsolete
With their research, the scientists disprove the so-called “neurodegenerative hypothesis”, which was based on observations that certain patients exhibited characteristic myelin damage without a discernable immune attack. In the popular hypothesis, the scientists assume that MS-triggering myelin damage occurs without the involvement of the immune system. In this scenario, the immune response against myelin would be the result – and not the cause – of this pathogenic process.

The aim of the research project was to confirm or disprove this hypothesis based on a new mouse model. Using genetic tricks, they induced myelin defects without alerting the immune defense. “At the beginning of our study, we found myelin damage that strongly resembled the previous observations in MS patients,” explains Burkhard Becher, a professor at the University of Zurich. “However, not once were we able to observe an MS-like autoimmune disease.” In order to ascertain whether an active immune defense causes the disease based on a combination of an infection and myelin damage, the researchers conducted a variety of further experiments – without success. “We were unable to detect an MS-like disease – no matter how intensely we stimulated the immune system," says Ari Waisman, a professor from the University Medical Center Mainz. “We therefore consider the neurodegenerative hypothesis obsolete.”

Focus on immune system
The teams involved in the study want to continue researching the cause and origins of MS. “In light of these and other new findings, research on the pathogenesis of MS is bound to concentrate less on the brain and more on the immune system in future,” says Professor Thorsten Buch from the Technischen Universität München.

Literature:
Giuseppe Locatelli, Simone Wörtge, Thorsten Buch, Barbara Ingold, Friederike Frommer, Bettina Sobottka, Martin Krueger, Khalad Karram, Claudia Bühlmann, Ingo Bechmann, Frank L. Heppner, Ari Waisman and Burkhard Becher. Primary oligodendrocyte death does not elicit anti-CNS immunity. Nature Neuroscience. 26 February, 2012. Doi: 10.1038/nn.3062

University of Zurich

Dr. Fry Finds Protozoa in People with CFS (and FM, MS, ALS & RA)

betterhealthguy.com

Dr. Fry is doing some exciting work on a new biofilm-forming protozoan previously referred to as FL1953 and only recently renamed to Protomyxzoa rheumatica, a highly immunosuppressive microorganism. He refers to it as the premier pathogen.

I recently had the opportunity to attend a lecture by Dr. Stephen Fry MD as part of Dr. Klinghardt's recent "Beyond Lyme" conference. I'm still working on my notes from that event and will post them soon. In the meantime, I just listened to a radio interview from Dr. Fry which can be found here.

Some of the key points from the the radio interview:

FL1953 is a new, unique protozoan organism that is found in people with CFS, Fibromyalgia, Multiple Sclerosis, ALS, and Rheumatoid Arthritis.

People with Morgellon's also have evidence of the organism. In Morgellon's, Dr. Fry talked about this new protozoan possibly suppressing the immune system such that a fungal/mycelial condition then develops leading to the symptoms of Morgellons.
Dr. Fry discussed the use of Tetracyclines, Zithromax, Plaquenil and other options, but more interesting were his other recommendations. One of the future projects his lab is working on is to complete sensitivity testing of various therapies for this new protozoan.
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ME vs CFS: More than just a name

Posted on February 27, 2012 by The M.E. Closet

ME vs CFS: More than just a name

For the first decade of my illness, I thought ME and CFS were different names for the same thing. I belonged to an online community of people with chronic illnesses, and CFS and ME were always lumped together into the same category. The Brits in the community were usually diagnosed with ME; the Americans with CFS. I assumed that CFS was the American term for ME.

When the term CFS began to be adopted in the UK, I was angry that such an inaccurate, trivial sounding name was being slapped on such a serious illness. I still, however, believed that ME and CFS were one and the same.

Then I started hearing that ME and CFS are two different things, and I became very confused. I have a diagnosis of ME, while my American partner was diagnosed with CFS two decades ago. We share many of the same symptoms, neurological abnormalities, and illness patterns. Do we have the same illness?

I started to do my own research, and that’s when I learned what each of these diagnoses truly means.

ME is a very specific neurological disease – ‘myalgic’ meaning ‘muscle pain’, and ‘encephalomyelitis’ meaning ‘inflammation of the brain and spinal cord’. ME is characterised by scientifically measurable damage to the brain stem initiated by a viral infection. It has many similarities to both MS and non-paralytic polio.

CFS is a term coined in the USA, which covers a whole spectrum of disorders, including ME. It is a wastebasket diagnosis for any illness involving a long period of “medically unexplained fatigue”. (Of course, ‘medically unexplained’ doesn’t mean anything if the correct diagnostic tests have not been performed. Most fatigue can be explained if you look hard enough for its cause.) A significant proportion of people with a CFS diagnosis do indeed have ME, but the CFS criteria are so broad that people with post viral fatigue syndrome, depression, nutrient deficiencies, or even undetected cancers will fall into this category.

The term CFS essentially means: ‘We don’t know what’s wrong with you, and we can’t be bothered to find out. Here’s a label to keep you quiet.’

CFS screws everybody except medical insurance companies, for whom it protects against expensive disability claims. Being diagnosed with CFS is like being thrown in the trash. How many people with treatable illnesses are tossed into the CFS bin, losing years of their lives to an ailment that could be cured? Nobody knows. How many cancer patients become terminally ill, after doctors slap a CFS diagnosis on them and stop looking for what’s actually wrong? Again, nobody knows. How many people with severe depression are left without the right support, after being thrown into the CFS wastebasket? I could go on and on.

Most of all, the term CFS screws people with ME.

When a study is done on ‘CFS patients’, it is entirely possible (and likely) that not a single patient in that study actually has ME. However, the results are then applied to ME as if the two were synonymous, often with devastating consequences. For example, a researcher could cherry-pick people with depression from the CFS wastebasket, treat them with graded exercise therapy (GET), get good results, and then declare exercise as a viable treatment for ME. GET might be a valid treatment for depression or post-viral fatigue, but it can cause severe and permanent damage to ME patients.

Worse, the diagnostic criteria for CFS states that symptoms have to be present for six months before a diagnosis can be given. If the brain stem damage in ME patients is caused by a ‘hit and run’ virus (and given the similarities between ME and non-paralytic polio, and the rise of ME coinciding with the distribution of the polio vaccine, it seems likely), then at six months, you are three months beyond the latest date that the virus is still present in the body. ME can be diagnosed in weeks, if the correct tests are carried out. By making ME patients wait six months for a diagnosis, you lose that precious window of time in which researchers could identify the infectious agent that triggers ME, and potentially find a cure. Could anti-viral drugs, prescribed early enough, limit further brain stem damage and give ME patients a better quality of life? As long as the six month rule is adhered to, we will never know.

If you’re not angry about the invention of CFS as a diagnostic wastebasket, you should be. It’s not just the human cost. Even if you’re completely unaffected by CFS or ME, the cost to the state is screwing you, too. Your tax money is paying for pseudo research that is of no real benefit to patients, and that could ultimately make patients sicker and more costly to the state.

(Just to muddy things further, in the UK, ‘ME’ has now been tacked onto ‘CFS’ to form ‘ME/CFS’. This is as unhelpful and nonsensical as calling it ‘Parkinson’s/CFS’ or ‘Cancer/CFS’. Now sufferers of myalgic encephalomyelitis are forced to use the term ‘Neuro ME’ to try and differentiate this specific neurological illness from other disorders covered by the woolly ME/CFS criteria. ‘ME’ has become a meaningless acronym.)

I was taken in by this scam for many years. Although my official diagnosis is ME (and was later amended by an infectious diseases specialist to ‘post encephalitic damage caused by a polio vaccination’), I was led to believe that CFS and ME were interchangeable. I always disliked the term ‘CFS’ because it had so little relevance to my illness. Now I know that the problem is far more extensive than an inappropriate name. That’s just the tip of the iceberg. You could call ME ‘Arsewipe Disease’ and it would still be the same illness. The bigger problem is that a distinct, measurable, physiological disease is being lumped together with a vast spectrum of different disorders, that happen to fit a huge, muddy criteria. This is what CFS is, and it is screwing us all.

dorsal root ganglia channelopathie associated with severe fibromyalgia

http://www.biomedcentral.com/1471-2474/13/23/abstract

A SCN9A gene-encoded dorsal root ganglia sodium channel polymorphism associated with severe fibromyalgia

Gilberto Vargas-Alarcon, Edith Alvarez-Leon, Jose-Manuel Fragoso, Angelica Vargas, Aline Martinez, Maite Vallejo and Manuel Martinez-Lavin

• 
  

For all author emails, please log on.

BMC Musculoskeletal Disorders 2012, 13:23 doi:10.1186/1471-2474-13-23

Published: 20 February 2012

Abstract (provisional)

Background

A consistent line of investigation suggests that autonomic nervous system dysfunction may explain the multi-system features of fibromyalgia (FM); and that FM is a sympathetically maintained neuropathic pain syndrome. Dorsal root ganglia (DRG) are key sympathetic-nociceptive short-circuit sites. Sodium channels located in DRG (particularly Nav1.7) act as molecular gatekeepers for pain detection. Nav1.7 is encoded in gene SCN9A of chromosome 2q24.3 and is predominantly expressed in the DRG pain-sensing neurons and sympathetic ganglia neurons. Several SCN9A sodium channelopathies have been recognized as the cause of rare painful dysautonomic syndromes such as paroxysmal extreme pain disorder and primary erythromelalgia. The aim of this study was to search for an association between fibromyalgia and several SCN9A sodium channels gene polymorphisms.

Methods

We studied 73 Mexican women suffering from FM and 48 age-matched women who considered themselves healthy. All participants filled out the Fibromyalgia Impact Questionnaire (FIQ). Genomic DNA from whole blood containing EDTA was extracted by standard techniques. The following SCN9A single-nucleotide polymorphisms (SNP) were determined by 5' exonuclease TaqMan assays: rs4371369; rs4387806; rs4453709; rs4597545; rs6746030; rs6754031; rs7607967; rs12620053; rs12994338; and rs13017637.

Results

The frequency of the rs6754031 polymorphism was significantly different in both groups (P = 0.036) mostly due to an absence of the GG genotype in controls. Interestingly; patients with this rs6754031 GG genotype had higher FIQ scores (median = 80; percentile 25/75 = 69/88) than patients with the GT genotype (median = 63; percentile 25/75 = 58/73; P = 0.002) and the TT genotype (median = 71; percentile 25/75 = 64/77; P = 0.001).

Conclusion

In this ethnic group; a disabling form of FM is associated to a particular SCN9A sodium channel gene variant. These preliminary results raise the possibility that some patients with severe FM may have a dorsal root ganglia sodium channelopathy.

Lois Owen, another ME patient who has died because CBT psychiatrists have blocked proper research and treatment for ME

Derby Telegraph, Monday, February 27, 2012:

"SIX words and she would be exhausted."

That was how Roger Owen explained his daughter's reluctance to be visited by doctors.

"She just couldn't cope with any more information than that," he said. "Even her lunch took four hours to eat because chewing used up energy."

University graduate Lois Owen, 34, died after her weight plummeted to just 3st 2lbs (20kg), leaving her exhausted and barely able to move.

She had battled for years with chronic fatigue syndrome and medics said she also had anorexia.

Neither Mr Owen or his wife could face sitting through the inquest held into her death. Mr Owen attended only to give evidence.

He told the hearing that those involved in Lois's care were "powerless" as everything they tried – from home visits to admitting her to hospital – made her condition worse.

Even Lois's GP said the best course of action was to allow her to remain bed-bound, at home with a team of carers.

Chronic fatigue syndrome is a disorder that affects one in 250,000 people in the UK and results in extreme tiredness. The cause is not known and there is no cure

Treating Autism With Antibiotics (France 3 TV, Feb 17, 2012)

Dr William Weir on UTV: irrefutable evidence of immunological dysfunction in ME

Christopher R. Snell: it is only a matter of time before biomarkers are identified, etiologies understood, and remedies devised for ME/CFS

http://www.intechweb.org/books/show/title/an-international-perspective-on-the-future-of-research-in-chronic-fatigue-syndrome

An International Perspective on the Future of Research in Chronic Fatigue Syndrome

Edited By: Christopher R. Snell

ISBN 978-953-51-0072-0, Hard cover, 104 pages
Publisher: InTech
Publication date: February 2012
Subject: Medical Genetics, Immunology, Allergology and Rheumatology

While the chapters in this book are a long way from solving the enigma that is CFS, they do represent important attempts to understand this complex and perplexing disease. A common theme in them all is CFS as a multisystem disease with the possibility of more than one cause and influenced by a variety of interacting factors. Further, they acknowledge the reality of CFS for persons with this disease and the importance of finding causes, treatments and ultimately a cure. As advanced biomedical research techniques are increasingly applied to the study of CFS, it is surely only a matter of time before biomarkers are identified, etiologies understood, and remedies devised.

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

British Journal of Cancer February 2012: involvement of XMRV in the pathogenesis of MCC and prostate carcinomas remains unclear

British Journal of Cancer , (16 February 2012) | doi:10.1038/bjc.2012.51

http://www.nature.com/bjc/journal/vaop/ncurrent/full/bjc201251a.html

No evidence for the involvement of XMRV or MCV in the pathogenesis of breast cancer

G Khan, P S Philip, M Naase and K M I Al Zarouni

Abstract
Background:

The aetiology of breast cancer remains elusive. A viral aetiology has been proposed, but to date no virus has been conclusively demonstrated to be involved. Recently, two new viruses, namely Merkel cell polyomavirus (MCV) and xenotropic murine leukaemia virus-related virus (XMRV) have been identified and implicated in the pathogenesis of Merkel cell carcinoma (MCC) and familial form of prostate cancer, respectively.

Methods:

We examined 204 samples from 58 different cases of breast cancer for presence of MCV or XMRV by PCR. Samples consisted of both malignant and non-malignant tissues. Additionally, we included 6 cases of MCC and 12 cases of prostate cancer as potential controls for MCV and XMRV, respectively.

Results:

All of the breast cancer samples examined were negative for both MCV and XMRV. However, 4/6 MCC and 2/12 prostate cancer samples were found to be positive for MCV and XMRV, respectively. Sequence analysis of the amplified products confirmed that these sequences belonged to MCV and XMRV.

Conclusion:

We conclude that there is no evidence for the involvement of MCV or XMRV in the pathogenesis of breast cancer. What role these viruses have in the pathogenesis of MCC and prostate carcinomas remains to be demonstrated.

Mitochondrial myopathy presenting as fibromyalgia

Mitochondrial myopathy presenting as fibromyalgia: a case report
Mishal Abdullah, Sahana Vishwanath, Amro Elbalkhi and Julian L. Ambrus
http://www.jmedicalcasereports.com/content/6/1/55/abstract
For all author emails, please log on.

MA: mishalabdullah@hotmail.com
SV: sahana_vishwanath@yahoo.com
AE: amrbalkhi@yahoo.com
JLAJr: jambrus@buffalo.edu

Journal of Medical Case Reports 2012, 6:55 doi:10.1186/1752-1947-6-55
Published: 10 February 2012
Abstract (provisional)
Introduction
To the best of our knowledge, we describe for the first time the case of a woman who met the diagnostic criteria for fibromyalgia, did not respond to therapy for that disorder, and was subsequently diagnosed by biochemical and genetic studies with a mitochondrial myopathy. Treatment of the mitochondrial myopathy resulted in resolution of symptoms. This case demonstrates that mitochondrial myopathy may present in an adult with a symptom complex consistent with fibromyalgia.

Case presentation
Our patient was a 41-year-old Caucasian woman with symptoms of fatigue, exercise intolerance, headache, and multiple trigger points. Treatment for fibromyalgia with a wide spectrum of medications including non-steroidal anti-inflammatory drugs, antidepressants, gabapentin and pregabalin had no impact on her symptoms. A six-minute walk study demonstrated an elevated lactic acid level (5mmol/L; normal <2mmol/L). Biochemical and genetic studies from a muscle biopsy revealed a mitochondrial myopathy. Our patient was started on a compound of coenzyme Q10 (ubiquinone) 200mg, creatine 1000mg, carnitine 200mg and folic acid 1mg to be taken four times a day. She gradually showed significant improvement in her symptoms over a course of several months.

Conclusions
This case demonstrates that adults diagnosed with fibromyalgia may have their symptom complex related to an adult onset mitochondrial myopathy. This is an important finding since treatment of mitochondrial myopathy resulted in resolution of symptoms.

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.
_------------------------------------

http://www.jmedicalcasereports.com/content/pdf/1752-1947-6-55.pdf

Discussion
Mitochondrial myopathies are disorders characterized by morphological abnormalities of
muscle mitochondria. Accumulating evidence suggests that mitochondrial disorders are
among the most common inherited metabolic diseases [10]. Similar to fibromyalgia,
patients may present with muscle weakness, pain, fatigue and exercise intolerance that
progressively worsens over time.
Several steps are involved in Adenosine-5'-triphosphate (ATP) generation in the
mitochondria, and defects in any part of the cycle may impair energy production leading
to symptoms [11]. These abnormalities in generation and utilization of ATP can be
assessed by specific tests, which as in our patient pointed towards problems in energy
metabolism [12].

Genetic testing with sequencing of the mitochondrial genome and
chromosomal genes affecting mitochondrial function may also be pursued, as was
performed in our patient. Mutations in POLG1 and several mitochondrial genome
polymorphisms were noted. our patient was started on a regimen of coenzyme Q10 (Co-Q10;
ubiquinone), creatine, carnitine, folic acid and α-lipoic acid. Co-Q10 transports electrons
between complex I and complex III of the mitochondrial respiratory chain and has been
shown to improve mitochondrial function in several studies [13]. Creatine generates
additional ATP through the creatine phosphate shuttle. Carnitine enhances transport of
fatty acids into the mitochondria. Folic acid is a cofactor for several mitochondrial
enzymes, while α-lipoic acid is a strong antioxidant [14]. Although this treatment
regimen was started several years after symptom onset, within the first few months our
patient showed tremendous improvement. With continued therapy, her complaints
dissipated over several months, with a gradual but sustained resolution of all symptoms.

http://www.jmedicalcasereports.com/content/pdf/1752-1947-6-55.pdf

CDC: ME is accompanied by neurologic and muscular signs and has a case definition distinct from that of CFS

‎"The name myalgic encephalomyelitis (ME) was coined in the 1950s to clarify well-documented outbreaks of disease; however, ME is accompanied by neurologic and muscular signs and has a case definition distinct from that of CFS."

http://www.cdc.gov/cfs/education/wb3151/chapter1-1.html

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

a deepening state of apartheid for people with disabilities

Ian Birrell 7 Feb 2012

http://www.thisislondon.co.uk/standard/article-24033624-disabled-are-at-the-mercy-of-ministers-and-media.do

What would you think if you heard the Home Office was colluding with newspapers to fuel hatred against gay people? Or if affable Ken Clarke at the Ministry of Justice fed propaganda to broadcasters designed to disparage ethnic minorities? There would, quite rightly, be an outcry.

This is the issue confronting another minority - and one far more ostracised in society. Ministers at the Department for Work and Pensions, desperate to force through cuts to their budgets, have demonised disabled people with smears designed to give the impression that many are cheats and scroungers.

Daily life is already tough enough for the disabled. A majority of Britons believe most people see them as being inferior. Little wonder they find it harder to get a job, are more likely to live in poverty and, increasingly, are victims of hate crime.

Typical is a case heard last week when a teenager attacked a man walking along the street, shouting: "He's disabled. He deserves everything he gets."

The charity Scope has revealed increasing antagonism towards disabled people, with two-thirds saying they have experienced recent abuse.
This dark new mood is terrifying for people who struggle to access things the rest of us take for granted: not just jobs but public transport or a meal out. It destroys confidence and makes people change behaviour; I know one man who barely left home after being targeted and others who always ensure they are back before dark.

This is shocking enough. But what is so scandalous is that a government department - run by ministers calling themselves compassionate Conservatives - has fuelled this disturbing new climate. It distorts data, manipulates facts and misuses statistics to feed a false media narrative that scapegoats the vulnerable.

So they give the impression that fraud is commonplace, conflate benefits designed to support people in jobs with those supporting people unable to work, and encourage the idea that filling in a simple form is the passport to a life of luxury at taxpayers' expense. Oh yes, with an expensive car thrown in, even if your child just has mild behavioural issues.

The facts are very different: levels of fraud for disability benefits are significantly lower than for other benefits, with more money wasted by officials making errors. Not that we hear much about maladministration, do we? Nor that taxpayers save more by disabled people not claiming than is spent on overpayments.

Instead there is a spate of drip-fed stories about "scroungers" and a decline in sympathetic articles - not just in tabloids but in broadsheets and on the BBC. Columnists talk about the "fake" disabled, or think it witty to say we should all pretend to be disabled to get lucrative handouts.

The legacy of such negative stereotyping is more hostility, more attacks, more fear and a deepening state of apartheid for people with disabilities.

Perversely, this comes as Mr Clarke extends hate crime laws to ensure tougher penalties for those attacking the disabled.

There is nothing wrong in stopping fraud or imposing cuts at a time of austerity. But it is revolting to see politicians and the media collude to target people who just want to join society. Or do we want to live in a world in which people with disabilities are driven further into the shadows?

Experts now generally believe that infectious agents set off a persistent, hyperactive immune response that causes chronic fatigue syndrome

By DAVID TULLER Published: February 6, 2012: An estimated one million people in the United States suffer from chronic fatigue syndrome, which is characterized by profound exhaustion, a prolonged loss of energy following minimal exertion, swollen lymph nodes, sore throat, cognitive dysfunction and other symptoms. Experts now generally believe that one or more infectious agents, or perhaps exposure to toxins, set off a persistent, hyperactive immune response — the likely cause of many of the symptoms.


¶ The events of the past couple of years, though disheartening to chronic fatigue syndrome patients, may have a silver lining: Research into the disease, much of it privately financed, is ratcheting up.

¶ A new research and treatment center has been created at Mount Sinai Hospital in New York. The Hutchins Family Foundation is investing $10 million in the Chronic Fatigue Initiative, an effort to find causes and treatments that has recruited top researchers from Columbia, Harvard, Duke and other institutions.

¶ “The disease had languished in the background at N.I.H. and C.D.C., and other scientists had not been paying much attention to it,” said John Coffin, a professor of molecular biology at Tufts University. “This has brought it back into attention.”

¶ Dr. Coffin, who at first supported the mouse retrovirus theory but later disputed it, noted that the illness “does seem to have characteristics that would suggest infectious origins” and that other retroviruses could be involved.

¶ Despite the personal and professional setbacks for Dr. Mikovits, many patients, like Ms. Solomon, continue to believe that a retrovirus is causing their illness.

¶ “But even if the retroviral research does not pan out, her work, and the publicity it has brought to our illness, has forever changed the landscape,” said Ms. Solomon.

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