Friday, September 14, 2007
About Disability Assistance
and Other Advocacy Issues
SAN DIEGO, CALIFORNIA
September 04, 2007
(PRLEAP.COM) SAN DIEGO — SEPTEMBER 2007 —
Nearly one in two people in the USA live with chronic
illness. Although medical professionals do their best
to address the health concerns of the chronically ill,
those who live with illness must learn to be a good
advocate for their healthcare and a victorious
National Invisible Chronic Illness Awareness Week,
September 10-16, 2007, is featuring four of twenty
free online chat workshops at
www.invisibleillness.com that specifically address
ways to be a good health advocate.
* "Increasing Your Odds in Receiving Disability
Assistance" is being presented by Attorney, Scott E.
Davis, one of the nation's legal specialists in
representing clients who are disabled due to
fibromyalgia or chronic fatigue immune dysfunction
syndrome. He wins chronic pain and fatigue Social
Security disability cases over 90% of the time, more
than double the success rate of Social Security
claimants who are not represented.
* "Taking a Stand: How to Avoid Medical Mistakes" is
a workshop led by Janet Lynn Mitchell, author of
"Taking a Stand." Janet Lynn was a senior in high
school, when she lost the use of her legs following
surgery. She later learned she had been a victim of
medical negligence, fraud and concealment
undergoing additional surgeries in doctor's attempts
to correct the mistakes. Assembly Bill 2571, borne
out of her misfortunes, unanimously passed both the
California Assembly and the Senate and was signed
into state law on August 31, 2000.
* "What Everybody Ought to Know About
Magnesium" is the topic of Patrick Sullivan, Jr.,
co-founder and president of Jigsaw Health. According
to Sullivan, up to 80% of Americans are deficient in
this essential macro mineral that is involved in over
325 known biochemical reactions and tied to body
aches, muscle twitches, spasms and cramps, low
energy, headaches and more
* "How to Shamelessly Get What You Want When No
One Seems to Care" will be led by Carmen Leal,
author and founder of Someone Cares Christian
Caregiver Conference. This workshop will focus on
creative and positive ways to cut through the red
tape facing caregivers and their families. It will help
families understand how to effectively interact with
church, social services agencies, and medical
decision makers to get what they need to provide
the best level of care for their loved ones.
Workshops are free chat sessions, Sept 10-14, 2007.
See dates and times at www.invisibleillness.com .
Guests will present for about forty minutes and then
accept questions from attendees. Transcripts will be
available in October. Many guests are donating free
items or services.
National Invisible Chronic Illness Awareness Week
was founded in 2002 by Lisa Copen, author of
"Beyond Casseroles: 505 Ways to Encourage a
Chronically Ill Friend." It is held annually in
September and is sponsored by HopeKeepers
Magazine and Rest Ministries, Inc.
The 2007 theme is "Invisible Illness is a roller
coaster. Help a friend hold on!" T-shirts, silicone
bracelets and more awareness items are available.
See http://www.invisibleillness.com for more info.
Chronique Couture, www.chroniquecouture.com , a
company that has stylish items such as whimsical
walker bags or sharps containers, is an additional
sponsor for 2007.
Thursday, September 13, 2007
The American Academy of Sleep Medicine recommends seeking medical advice if sleep deprivation has compromised your daytime functioning for more than a month.
You shouldn't hesitate to ask for help when you're sleeping badly following a death in the family or some other stressful event. A physician may suggest the short-term use of a sedative to help you sleep at night and thus cope better during the day and prevent development of a long-term sleep disorder.
|A sample sleep history questionnaire
Your physician may ask you some of the following questions during an evaluation for a sleep problem. You may find it helpful to write down your answers to these questions and bring the completed questionnaire to the exam so you and your doctor can discuss it.
It's not always easy for people to get evaluation and treatment for a sleep problem. Doctors trained in the United States receive less than two hours of instruction on this topic during four years of medical school. According to a survey conducted by the National Sleep Foundation, most primary care physicians do not routinely ask their patients about sleep. And while most of the physicians who took part in the survey admitted they had limited knowledge about sleep-related matters, more than half did not consult with an expert in sleep medicine. This puts the responsibility on you to seek out the help you need.
* * *
I reported to one of my doctors that I collapsed into bed at 5 PM, too exhausted to function any longer, but didn't fall asleep till 5 AM. Then I forced myself to get up at 7 AM (the time I had always had to get up to go to work), so that I wouldn't get out of the habit of getting up on time for when I returned to work. He didn't consult an expert in sleep, he didn't hear the part about "tossing and turning in pain", the only thing that registered with him was that I went to bed at 5 and got up at 7, which he interpreted as "sleeping too much".
I never got a sleep study to document how little I was sleeping and how poor the quality of that sleep was. As a result, I didn't get anything to treat either the sleep disturbance or the pain that was keeping me awake.
Eventually, I got to a doctor who was trained better about sleep disturbance. He had me keep a sleep diary: when I went to bed, how long I was awake before I fell asleep, how many times I woke up during the night, how long I was awake before I fell back to sleep. He diagnosed "SEVERE sleep disturbance" where the prior doctors had been convinced that I had no sleep disturbance at all. When I got effective sleep medication, I slept through the night, my immune system revved up enough to fight off the virus, I lost 30 pounds...
Clete Kushida, MD, PhD, head of Stanford University Center for Sleep Research, says "Sleep deprivation puts a strain on the heart and the brain and can have an effect on glucose metabolism". In other words, lack of sleep can cause you to gain weight. Inadequate sleep can also affect production of the stress hormone cortisol, "which can have a detrimental effect on nearly all systems of the body".
The Rite Health Journal observes "Sustained sleep deprivation -- on the order of getting only four hours of shut-eye a night over 12 consecutive nights -- is associated with significant increases in pain". At the time I finally got sleeping pills, I'd been averaging 2 hours a night for 3 YEARS.
There is research showing that fibromyalgia-like symptoms can be created in healthy volunteers simply by depriving them of sleep, and those symptoms go away when they are allowed to return to normal sleep patterns. Yet, even the doctors who diagnosed fibromyalgia never considered that sleeping pills might fix that problem; apparently, they were completely unfamiliar with that research.
First, a CFS expert told me to take 5HTP (see www.DrRodger.com) to improve the quality of my sleep (you'll have to play with the dosage to find the one that puts you to sleep; my case of insomnia was too stubborn for just one capsule). Then I got a Sleep Number bed -- you can try one for 30 days and if you don't like it, return it owing only the delivery fee. After one week on the Sleep Number bed, I considered my fibromyalgia a thing of the past -- although I still have pain at the test points when the doctor presses on them, the 24/7 pain just from existing is gone. When I finally got pain pills this spring after 7 years of begging for them, I had the last piece of the puzzle, and am starting to improve.
The simple fact is, I asked for sleeping pills and pain pills at my first doctor appointment in 2000, based on the recommendation of the virologist who diagnosed me in 1988. I improved when I finally got them. The only possible conclusion is that if I'd gotten what I asked for when I first asked for them, I would've been back to work in a couple months. Instead, I've been told by a specialist that I deteriorated too far and will never return to full-time work again.
Although insomnia does not "cause" true CFS, treating the pain/sleep disturbance so the patient can sleep 8 hours a night will allow the body to start healing itself. Quite a few of my symptoms are significantly reduced now that I'm sleeping better.
Researchers John and Andrew Chia report today in the Journal of Clinical Pathology that endoscopy and stomach biopsy revealed evidence of enteroviral infection in 80 percent of 165 CFS patients tested and just 20 percent of 34 control subjects. This study was also presented in January at the 8th International Association for CFS/ME conference. As the authors state, more study is needed to confirm these findings, but this reports adds weight to a growing body of evidence that infections can trigger or perpetuate CFS in at least a subset of cases.
Media outlets in England have picked up the story and coverage in the U.S. is anticipated given media calls to the CFIDS Association.
The press release and a link to the paper is copied below.
JOURNAL OF CLINICAL PATHOLOGY
Chronic fatigue syndrome linked to stomach virus
[Chronic fatigue syndrome is associated with chronic enterovirus infection of the stomach Online First J Clin Pathol 2007; doi: 10.1136/jcp.2007.050054]
Chronic fatigue syndrome, also known as ME (myalgic encephalitis), is linked to a stomach virus, suggests research published ahead of print in Journal of Clinical Pathology.
The researchers base their findings on 165 patients with ME, all of whom were subjected to endoscopy because of longstanding gut complaints.
Endoscopy involves the threading of a long tube with a camera on the tip through the gullet into the stomach.
Specimens of stomach tissue were also taken to search for viral proteins and compared with specimens taken from healthy people and patients with other gut diseases none of whom had been diagnosed with ME.
Patients with ME often have intermittent or persistent gut problems, including indigestion and irritable bowel syndrome.
And viral infections, such as Epstein Barr virus (glandular fever), cytomegalovirus, and parvovirus, among others, produce many of the symptoms associated with chronic fatigue syndrome.
Enteroviruses, which infect the bowel, cause severe but short lasting respiratory and gut infections.
There are more than 70 different types, and they head for the central nervous system, heart and muscles.
Most of the biopsy specimens from patients with gut problems showed evidence of mild long term inflammation, although few were infected with Helicobacter pylori, a common bacterial infection associated with inflammation.
But more than 80% of the specimens from the ME patients tested positive for enteroviral particles compared with only seven of the 34 specimens from healthy people.
In a significant proportion of patients, the initial infection had occurred many years earlier.
Click here to view the paper in full: http://press.psprings.co.uk/jcp/september/cp50054.pdf
Wednesday, September 12, 2007
NIMEA Medical Conference,
Lisburn, Co. Antrim,
8th September 2007.
The Northern Ireland ME Association held a successful medical conference on
8th September. Present were paediatricians, GPs, hospital consultants,
nurses, O.T.s, representatives from the Health and Education boards - and
Delegates were welcomed to Lisburn's riverside Civic Centre by the Lord
Mayor - who has staff and family members affected by ME and Fibromyalgia.
Doctors and visiting speakers got on famously. Generous catering was
supplied ensuite, and attendees didn't leave the function room all day.
Terry Kelly, NIMEA's benefits officer, was in demand, explaining the
intricacies of DLA.
First speaker was Dr. Larry Martel, paediatrician at the Ulster Hospital,
Dundonald. "I do not believe that ME is a psychiatric condition", he
declared. "It is a physical illness". That set the tone for the rest of the
day. There was no hard-sell of CBT and GET; no-one blamed the patients for
being ill. Instead the conference got down to the serious business of what
could and should be done for ME patients.
Second was Horace Reid of NIMEA, who since 22nd August had distilled 317
pages of new NICE guidelines into a 50-minute Powerpoint. These guidelines
are not the mixture as before. The authors were practitioners rather than
well-known ME researchers. NICE had its own definition of CBT, much of it
good old-fashioned common sense, and none of it about "dictation of illness
beliefs". The NICE brand of GET is not an imposed rigid schedule; it had
built-in rest periods; and it comes with explicit warnings of adverse
effects. NICE asserted that in ME as in other conditions, the patient's
rights to consent and choice of treatment were paramount, and
non-negotiable. NICE takes the view that manifold psychiatric hypotheses -
The audience rapidly warmed to Dr. William Weir, famous for his amusing
presentation to Dr. Ian Gibson's parliamentarians, and respected for his
long experience treating ME. Willy has a streak of Boris Johnston in him:
shrewd, robust, and unfailingly polite. He cocked a satirical snook at the
philosophical pretensions of the bio-psycho-social camp. "Postmodernism and
Cartesian Dualism? It's all fiddlesticks." (He used a saltier phrase). "This
stuff has no relevance to the real world!" Conference had already come to
the same conclusion, and delegates now fell about laughing. Dr. Weir
considers that the guiding principle of managing ME is common sense, and
treatment can be left in the hands of a competent GP. "It's not rocket
Jonathan Kerr was to have been first speaker after lunch. But he came down
with a last-minute bug, and was unable to travel. Instead he entrusted
presentation of his latest research to Dr. Weir, one of his many
collaborators. His findings, soon to be published, confirm abnormal
immunological activation in ME patients. An array of genes governing immune
responses are abnormally "switched on". Better than that, he has now
identified a number of clinically separate ME subgroups, each with its own
Dr. Noel Scott, liason psychiatrist in charge of the CFS Clinic at Belfast
City Hospital, commented on preceding speakers. He echoed one of the key
NICE findings - patients and doctors should stop quarrelling about
imponderables, and concentrate on what could be achieved here and now. Dr.
Scott's clinic is seriously under-resourced. His own role is unfunded, and
his O.T. works part-time. Since April 2007 he has been unable to accept
regional referrals from outside the Belfast area.
He was followed by Jayne Perkes, his Senior Occupational Therapist, who
conducts group classes spread over 8 weeks. She prefers Graded Activity to
GET. A survey of 33 patients in 2005-6 gave her a 90% satisfaction rating.
To wind up, NIMEA president Sylvia Bolton engaged delegates in a
brainstorming session. Split into groups of three, they were asked for
suggestions. One paediatrician took a supportive, rather than macho approach
to the severely affected. Another was unimpressed with the efficacy of
recommended treatments. The psychiatric delegation reflected on the damaging
effects of mental health stigma. A DLA representative regretted the divide
between ME doctors and patients.
Everyone deplored the lack of treatment provision. O.T.s said they were
interested, but as things stood, there was no hope of them taking on this
time-consuming condition. Two ME mothers, who were also NHS nurses, had
come. Both had severely affected teenagers, and found NHS support was nil.
NIMEA identified many gaps in provision - for children, for the severely
affected, and for patients distant from Belfast. NIMEA has long suspected
that many of the severely-affected are not in touch either with the NHS or
charities. They were dismayed to have this situation confirmed on Saturday.
A health board member had strong words of advice for the ME world - NHS
provision would not increase until local MPs were alerted to the current
parlous situation in Northern Ireland.
Around four pm delegates dispersed into the autumn sunshine. Dr. Willy Weir
was last seen settling in front of a Rugby World Cup match, before his
flight back to London.
Tuesday, September 11, 2007
Let’s talk a little about a paragraph in Cort’s comments:
Even in this severe outbreak, though, almost half the patients (49%) were able, despite their fatigue, to fulfill "all work or home responsibilities"(but with nothing left over). (This explodes the myth that all or even most CFS/ME patients are "disabled". While a significant number of CFS/ME are disabled substantial numbers of CFS/ME patients are able to work. Rates of employment in CFS studies have varied dramatically from study to study (32% to 73%) with an average employment rate probably around 50%).
It also explodes the myth that slackers claim to have CFS so that they can give up their jobs. No one whose ultimate goal was to stop working would have put up with the "no quality of life" that I had for much of the dozen years that I was working after receiving the diagnosis. They would’ve quit as soon as they realized that continuing to work required jettisoning the things that made life fun.
I was one of that 49% who managed to take care of the work and home responsibilities, but had little energy left for anything else. My co-workers would babble happily about spending the weekend jet-skiing; my plans were to go home and lie on the couch so I could make it through the next week of work. When they got a three-day weekend, they’d plan on a mini-vacation out of town; I’d thank God that the third day of rest would give me a little extra boost to make it through to the next three-day weekend. Without those extra rest days in there, I would’ve been even more exhausted.
I went to a doctor while I was struggling to continue working even part-time, and was accused of wanting to quit my job. I didn’t want to quit – I wanted to get healthy enough to work full-time. The stereotype blinded him, and he refused to consider that my goal was to continue working; in fact, I had not stopped working. As soon as I could drag myself out of bed for a short time, I was back at my desk. My job was in jeopardy because I wasn't able to do the work properly (although my employer could see how hard I was trying, they couldn't take the chance that I would cause them to commit malpractice). That didn’t square with what he wanted to hear, so he tuned it out. I don’t think it ever registered with him that I was still working despite the obstacles.
Just as it doesn’t register with some of the commenters in this blog that I am working; I own my own business independently, and am in partnership in two other businesses. I actually work a higher percentage of my functional hours than most healthy people, which means that I spend a much lower percentage of my time doing fun things like going out with friends, going to concerts, reading, stitching, etc. Some weeks, the percentage of time I spend doing something fun is precisely zero.
But because that doesn’t fit the stereotype of CFS patients as being lazy, it will never be acknowledged how many CFS patients struggle mightily to continue working as many hours as they can, until (in most cases) their employer makes the decision that they are no longer employable. Very rarely have I heard a patient say they quit voluntarily; either they were fired or they were pressured to resign.
[Ed. Note: Since the artificial construct of CFS was created in 1988, it has been essentially impossible to get a diagnosis of ME in the US, although ME is still diagnosed in other countries. These three articles represent the quest to return to the historic name, or at least, some less derogatory name, so that patients can receive the respect and treatment they deserve. When CDC made the CFS name mandatory, my original diagnosis was changed, even though the virologist didn't agree with the new name; if he had stubbornly refused to change the diagnosis, there was no code for the old one on the insurance forms, which would've made getting treatment paid for difficult.]
CFS, ME and Incline Village
By Cort Johnson
Incline Village is ground zero for the modern era of CFS/ME. It is where
CFS/ME first (re)emerged in a big way and made it onto the national
scene. What a scene it was; we had a bucolic (upper class) community in
a resort town in the Sierra’s beset by a bizarre epidemic. We have the
embattled good guys (our doctors) struggling against their supposed
allies (big, bad government bureaucracy – the CDC) and the rest of the
medical establishment all the while defending their scorned and disabled
patients. What a stirring story it was.
Incline Village is a place where, paradoxically, things went right in a
big way (CFS/ME finally gets attention) and wrong in a big way (CFS/ME
called ‘yuppie disease’.) Not so long after the Incline Outbreak the
name ‘chronic fatigue syndrome’ was coined and down the slippery slope
of ‘fatigue’ this disease slid.
Both ME and CFS advocates claim Incline Village as their own. Some
believe it was our first big chance – perhaps our only chance - to fix
this disease in the research community’s mind before it got tainted by
the fatigue label. The facts were all there they say! All the powers
that be had to do was open their eyes. Instead they turned them away and
we have suffered the consequences ever since.
The CDC, of course, was on the scene early but they weren’t the only
ones. A group of committed CFS researchers/physicians were there also.
This group came to this disease with open eyes and for several of them
it was a career changing event. The pedigree of this group is amazing;
many (Cheney, Peterson, Ablashi, Komaroff, Bastien, Buchwald) will go on
to take central roles in CFS research or treatment. Early on they were
able to garner a series of large NIH grants and over the next six or
seven years they would come to publish at least five studies examining
the Incline Village (and other cohorts).
We know the CDC found nothing interesting but did ‘our side’ say? These
researchers - so passionately struck by their patients suffering - knew
they were facing a real disease. What did they report? What kinds of
patients did they find? Were they CFS patients or ME patients? Were
their conclusions listened to or were they dismissed? What kind of start
did CFS research get off to? Twenty-two years later we take a look at
Incline Village and what it meant and didn’t mean for CFS/ME patients.
The Studies: These were not small efforts. Much of the information in
this paper will be taken from a major paper published in 1992 (Buchwald,
Cheney, Peterson, Ablashi, Komaroff et. al. 1992). It was one of the
first major studies ever done on CFS/ME and it is still one of the
largest. It involved cerebrospinal fluid draws, MRI’s, HHV-6, HTLV and
lymphocyte testing in at least a portion of over 200 patients.
Defining CFS: One of the first problems the investigators of the 1992
study faced was one researchers are still struggling with; how to define
an often debilitating disease that is marked, for the most part, by
rather common symptoms. As most definitions have done, these researchers
focused on the predominating symptom, fatigue. They required each
patient in the study to have at least three months of chronic,
debilitating fatigue with at least two of eight other symptoms (fever,
headache, sore throat, earache, rhinnorhea, cough, diarrhea or muscle pain.
Aside from fatigue the symptom set was somewhat unusual; fever, earache,
post-nasal drip, cough and diarrhea will not appear in the 1994
definition or be prominent in others. Headache, sore throat and muscle
aches will. A perhaps special kind of fatigue – post-exertional fatigue
– that some researchers believe characterizes CFS was not mentioned and
had not yet been delineated. Neither cognitive problems nor joint pains
were part of the definition but both were common (79-88/67-82%) in this
They noted that a ‘few patients’ (8%) developed ‘transient periods’ of
an encephalitis-like symptoms including confusion, gait problems,
paralysis and seizures. These early symptoms are similar to some
described in early ME epidemics. Was this an ‘ME’ subset? Like ME
patients earlier studies described the most severe nervous system
problems (paralysis, seizure) were described as ‘transient’. As the
disease progressed these patients looked more and more like the other
patients and they were not segregated out again.
Acute (infectious) vs. Gradual Onset or Acute and Gradual Onset? Debate
persists in the CFS/ME community whether infectious onset patients are
fundamentally different from non-infectious onset patients. While ME
researchers do not require an infectious onset for ME the presence or
absence of an infectious onset is used by some to differentiate ME from
CFS patients; ME patients tend to have an infectious onset while CFS
patients do not. This has at times morphed into the belief that ME
patients have a real illness while CFS patients have psychological problems.
These two groups of patients were also found in the Incline Village
studies. The acute onset epidemic type patients could not be
distinguished symptomatically or with regard to laboratory tests from
the gradual onset endemic type patients and they were lumped together.
Neither an acute onset nor the presence of flu-like symptoms led to a
more severe illness. In the end the investigators believed it didn’t
matter whether the trigger was an infection or some other event or
nothing visible at all; the patients were essentially, so far as they
could tell, the same. They believed a ‘common pathogenetic pathway’ was
present in all of these patients.
THE PATIENT. As expected about 65% were women. Most were middle-aged
(average age of about 39). About 25% were either bed ridden or shut in.
Even in this severe outbreak, though, almost half the patients (49%)
were able, despite their fatigue, to fulfill ‘all work or home
responsibilities’ (but with nothing left over).
(This explodes the myth that all or even most CFS/ME patients are
‘disabled’. While a significant number of CFS/ME are disabled
substantial numbers of CFS/ME patients are able to work. Rates of
employment in CFS studies have varied dramatically from study to study
(32% to 73%) with an average employment rate probably around 50%).
A large 1993 follow up study found that most patients got better over
time; the researchers, in fact, stated that ‘the overall prognosis of
chronic fatigue syndrome is usually favorable.’(!) and that ‘After 3
years of follow-up, almost all study subjects were able to return to
pre-illness activity’ (!). While most apparently got well a subset of
these patients had “More-serious and longer-lasting neurologic
impairments, including seizures, psychosis, and dementia”.
LABORATORY FINDINGS – Were these CFS researchers findings taken
seriously? Were they on the right track? Let’s find out.
MRI BRAIN SCANS. The MRI findings have been described as objective
evidence of central nervous system damage, something that only an agency
determined to subvert CFS patients could ignore. Indeed the researchers
‘frequently saw areas of abnormal signal intensity in the white matter
of the central nervous system” of CFS patients. The meaning of those
abnormal signal intensities were, however, unclear. In a few patients
they were able to correlate problems in, say, vision with abnormalities
in the visual cortex but in most they were not. The fact that ‘similar
white matter changes were found in many disease and conditions (multiple
sclerosis, Alzheimer’s, metastatic disease, post- chemotherapy, trauma,
viral infection, etc.)’ suggested some pathology was at work but left
the cause of it unclear.
Problematically while significantly more CFS patients demonstrated these
abnormalities than the healthy controls a significant percentage (20%)
of the healthy controls had them as well. The researchers noted that
this was not unexpected stating “such..areas..can also be seen in
apparently health people of all ages”.
A further problem involved linking these areas to the actual disease
since they occurred in different areas in different patients. While they
suggested that at least some patients were ‘experiencing a genuine but
as yet undefined pathologic process” they concluded that the
significance of these ‘incidental’ areas ‘is not known’.
The significance of the MRI findings was muddied by a lower rate of MRI
abnormalities in the New England cohort of patients and by the fact that
they were not found in all the patients. Suggestions that these
abnormalities increased with age did not help clarify matters. Finally,
since the clinical significance of the tests was unclear they did not
recommend the routine use of MRI in CFS patients. It was clear the
authors thought they might be onto something but were unsure what it was.
The Medical Community’s Response. At least nine studies will examine MRI
findings in CFS between 1990 and 2000. All will display variable
findings; a 1993 study found abnormalities in 27% of CFS patients; a1994
study in 50%; another found them in 32% of CFS patients (and a
statistically equal numbers of controls). The inability to find
abnormalities in all or at times in a majority of CFS patients or to
find them in specific areas of the brain will continue to leave the
scientific community unclear as to their significance.
The Present. Things will change for the better around 2000 as
researchers refine their techniques and imaging technology improves. Dr.
Natelson’s finding of increased central nervous system abnormalities in
CFS patients without mood disorders as opposed to those with mood
disorders will help to increase interest in this area. Functional MRI’s
and other brain imaging techniques now consistently show abnormalities
in certain parts of the brains of CFS patients. CFS patients have had to
wait for brain imagining technology to catch up to them before it could
reveal consistent results.
IMMUNE FINDINGS. These researchers concentrated on two herpesviruses,
EBV and HHV-6. Both were relative newcomers to the medical world at that
point. EBV was discovered in 1964 and HHV-6 in 1986. Several of the
Incline Village studies did find evidence of increased EBV and HHV-6
activation in their patients but all were unclear as to their
significance. The 1993 Levine, Cheney, Pocinki, Ablashi, Peterson study
noted that HHV-6 reactivation might either be an epiphenomenon,
secondary to immune dysfunction….or could have no relation to patients
symptoms” or it could be destroying nerve and immune cells. This study
concluded that “None of the viruses evaluated--human T-lymphotropic
viruses I and II, Epstein-Barr virus, or human herpesvirus-6--could be
etiologically linked to these outbreaks”. They postulated that one
outbreak was caused not by HHV-6 or EBV but by giardiasis.
Medical Communities Response. EBV and HHV-6will both be studied
intensively in CFS in the aftermath of Incline Village. Between 1987 and
1996 over twenty studies will examine the relationship between EBV
infection and CFS and between 1990 and 2000 at least 14 studies will
examine the relationship between HHV-6 infection and CFS. At one point,
Dr. Komaroff, now an advocate for HHV-6’s effects in CFS, will co-author
a paper concluding the opposite (Buchwald 1996). This very large study
(548 CF and CFS patients and controls) found no differences in the
levels of 13 viruses in CFS patients relative to the other groups or to
CFS patients with acute onset. (This size study is almost unimaginable
today!) Researchers will end up concluding that increased EBV activation
does not play a role in CFS. A similar but less strong consensus will
emerge concerning HHV-6.
The Present. Again, improved testing and knowledge will re-ignite some
interest in both these pathogens. Dr. Komaroff recently detailed a
series of factors suggesting that HHV-6 reactivation does play a role in
some CFS patients. Dr. Glaser has continued to explore the possibility
that some types of EBV activation are damaging in CFS. While
underfunding is a problem resolving the role these pathogens play in CFS
may await further technological advances. In particular inadequate
testing for HHV-6A virus still limits our understanding of its effects.
CFS and ME and Post-viral Syndrome and. Icelandic Disease and Royal Free
disease, etc. or Not? Debate rages in the CFS/ME communities whether CFS
and ME are similar diseases. The authors of the 1992 paper (Buchwald,
Cheney, Peterson, Ablashi, Gallo, Komaroff, etc.) were faced with a
similar question. Notice that the title of the paper ‘A Chronic
Illness..” doesn’t mention CFS or ME or any other names. Because CFS and
its definition – which differed from the one used – came after the study
began they couldn’t refer to their patients as CFS patients. The most
they could say was that ‘most patients probably would have met the case
definition forchronic fatigue syndrome”
They didn’t refer to their patients as myalgic encephalomyelitis (ME) or
Icelandic disease or Royal Free disease, etc. patients either. Instead
they noted that ‘the illness we have observed shares many features with
entities variably called…“postviral fatigue syndrome, myalgic
encephalomyelitis, Icelandic disease, etc.”
It was clear that seven years after they first encountered these
patients that they felt that their group (still one of the most
intensively studied group of CFS patients ever) was very closely allied
with if not identical with these other groups.
After all this study these researchers felt competent to address some
basic questions regarding not just their group of patients but all this
entire group of patients (CFS/ME/Royal Free, etc.). In the beginning of
the discussion section of the paper they asked whether all these
diseases were each caused by one pathogen, were caused by different
factors, or did they all represent one general illness that could be
triggered in numerous ways?
They came down on the last possibility –the one that prevails in the US
today. In the last paragraph of the paper they stated that ‘we think
that this is probably a heterogeneous illness that can be triggered by
multiple different genetic and environmental factors (including stress,
toxins and exogenous infectious agents)”
Thus while some ME advocates may single out the Incline Village outbreak
as an ME as opposed to a CFS outbreak the researchers and physicians
involved in treating and examining these patients did not. Nor did they
believe that acute infectious onset patients differed from gradual onset
patients. While many point their fingers at the CDC for turning an
infectious illness into a grab bag of undifferentiated and fatiguing
illnesses, they should note that this group, which featured many who
will go on to be outspoken advocates for CFS/ME – will come to much the
same conclusion; CFS/ME is an illness that can be triggered in many
different ways but which reveals itself by a core group of symptoms.
Overall Conclusion. The ‘CFS friendly’ researchers at the Incline
Village outbreak (and elsewhere) raised questions that the scientific
community did look more closely at. EBV and HHV-6, in particular, were
exhaustively researched butsubstantial numbers of MRI studies were done
The progess in unraveling CFS has been slower than one would have hoped.
Much of the blame for this has been laid at the hands of an inattentive
if not biased research community. CFS has certainly never enjoyed the
amount of research funding it deserves but this short survey suggests
that the research community did respond to many of the issues raised.
The blame for the slow progress in understanding CFS can be laid at many
different feet; the bias evoked by the name, the poor performance by the
CDC, the poor leadership at the NIH, an inherent conservatism at
research institutions around the world, an inadequate technology, a lack
of creativity, etc. but a good share of it must be laid at the
complexity of the disease itself. Many of the issues that plague
researchers today such as how to define CFS, the difficulties
replicating study results and the obvious presence of subsets showed up
in these early studies as well. CFS/ME was a puzzle from the beginning –
not only to the research community at large but to those intimately
involved in studying it. Even when they have had adequate resources to
study it CFS/ME has often yielded its insights slowly and grudgingly.
Addendum. Ironically the research community may have been more amenable
to embracing CFS before much was known about it. The search for
pathogens that much early research was focused on is, after all,
something the research community knows well. The large size of several
early studies suggests a commitment to understanding CFS/ME that is not
be present today. Ironically while much more is known about CFS today
and more intriguing research avenues exist than ever before the CFS/ME
research program has been cut back severely at both the NIH and the CDC.
There are many easier diseases to study, many diseases that provide much
better expectations of success for researchers. The difficulty CFS/ME
presents researchers requires that we a) be appreciative of those that
have joined us for this hard slog and b) be vigilant in demanding that
the scientific community commits the resources needed to adequately
Buchwald, D., Cheney, P., Peterson, D., Henry, B., Wormsley, S., Geiger,
A., Ablashi, D., Komaroff, D.etc. 1992. A chronic illness characterized
by fatigue, neurologic and immunologic disorders, and active Human
Herpesvirus Type 6 Infection. Annals of Internal Medicine 1116: 103-13.
Daugherty SA, Henry BE, Peterson DL, Swarts RL, Bastien S, Thomas RS.
Rev Infect Dis. 1991 Jan-Feb;13 Suppl 1:S39-44. Chronic fatigue syndrome
in northern Nevada.
Buchwald D, Ashley RL, Pearlman T, Kith P, Komaroff AL., J Med Virol.
1996 Sep;50(1):25-30.Viral serologies in patients with chronic fatigue
and chronic fatigue syndrome.
Levine PH, Jacobson S, Pocinki AG, Cheney P, Peterson D, Connelly RR,
Weil R, Robinson SM, Ablashi DV, Salahuddin SZ, et al. Arch Intern Med.
1993 Mar 8;153(5):661. Clinical, epidemiologic, and virologic studies in
four clusters of the chronic fatigue syndrome.
I hope my free thoughts in this subject presented below may help getting
some ideas of how to find a suitable name for ME/CFS. The main idea is to
avoid using any medical terms in the name, but instead use a surname for the
disease as for example in "Ménières disease". Let us be creative when
thinking about a new name!
I think ME/CFS should be renamed to a name that does not include anything
about the patho-physiology. That would be the logical thing to for a disease
that has a very complex patho-physiology. The patho-physiology is not known
for the moment and we need a name now, and not in 20 years or so when the
disease is understood in detail. What name could we expect anyhow when the
origin of the diseased is found? Maybe we end up with "high expression of
the CGDT-123 gene coupled with mutations on the DGEE-1 and DETA-5 genes".
That would not be suitable anyway.
The more generic name neuro-endocrine dysfunction, I think is too general to
be used for ME/CFS. I am convinced that in the future a lot of diseases will
be discovered to pertain to the neuro-endocrine system. We already have a
few. So I think neuro-endocrine dysfunction is not suitable for ME/CFS.
Instead, my suggestion is to rename ME/CFS to "Sisyphus disease". Sisyphus
was a king in Greek mythology that outwit/duped death. As punishment he had
to work in underworld to repeatedly for eternity roll up a rock uphill a
mountain, from where it fell down again. From there, a "Sisyphus work" is a
work that last for ever and never yields no result. This is exactly what it
is like to live with ME/CFS. The inability to finish things. You do a bit
but get tired and have to stop and then you have to start all over again.
You get nowhere and can not go an and pursue your life.
It might be that Sisyphus disease might not be "serious enough" because it
might people laugh when saying that "I have got Sisyphus disease" and think
that you are telling a yoke. If that is the case, then I think that it can
be named with any surname. For instance call it "Ezelius disease".
/Kasper Ezelius, Örebro, Sweden ( http://goto.glocalnet.net/me_cfs )
Background and more thoughts about the name change that I propose:
More about Sisyphus: http://en.wikipedia.org/wiki/Sisyphos
Why the bogus disease category of 'CFS' must be abandoned
Jodi Bassett, September 2007 http://www.ahummingbirdsguide.com/cfsmustbeabandoned.htm
A brief history of Myalgic Encephalomyelitis up to 1988
The illness we now know as Myalgic Encephalomyelitis is not a new illness. M.E. is thought to have existed for centuries. (Hyde 1998, [Online]) (Dowsett 1999a, [Online])
One of the most fundamental facts about M.E. throughout its history is that it occurs in epidemics. This fact conveys, among other things, the infectious and contagious nature of the disease (Hyde 1998, [Online]). The usual incubation period of the virus infection involved is 4-7 days. There is a history of over sixty recorded outbreaks of the illness going back to 1934 when an epidemic of what seemed at first to be poliomyelitis was reported in Los Angeles. As with many of the other M.E. outbreaks the Los Angeles outbreak occurred during a local polio epidemic.
The presenting illness resembled polio and so for some years the illness was considered to be a variant of polio and classified as 'Atypical poliomyelitis' or 'Non-paralytic polio' (TCJRME 2007, [Online]) (Hyde 1998, [Online]) (Hyde 2006, [Online]). Many early outbreaks of M.E. were also individually named for their locations and so we also have outbreaks known as Tapanui flu in New Zealand, Akureyri or Icelandic disease in Iceland, Royal Free Disease in the UK, and so on. M.E. was also known as 'Atypical multiple sclerosis' at one time, because of the similarities between M.E. and MS (TCJRME 2007, [Online]) (Hyde 1998, [Online]).
A review of early M.E. outbreaks found that clinical symptoms were consistent in over sixty recorded epidemics spread all over the world (Hyde 1998, [Online]). Despite the different names being used, these were repeated outbreaks of the same illness. It was also confirmed that the epidemic cases of M.E., and the sporadic cases of M.E. each represented the same illness (Hyde 2006, [Online]) (Dowsett 1999a, [Online]).
In 1956 the name Myalgic Encephalomyelitis was created. The term was invented jointly by Dr A Melvin Ramsay who coined this name in relation to the Royal Free Hospital epidemics that occurred in London in 1955 - 1957 and by Dr John Richardson who observed the same type of illness in his rural practice in Newcastle-upon-Tyne area during the same period. It was obvious to these physicians that they were dealing with the consequences of an epidemic and endemic infectious neurological disease (Hyde 1998, [Online]) (Hyde 2006, [Online]). The term Myalgic Encephalomyelitis means: My = muscle, Algic = pain, Encephalo = brain, Mye = spinal cord, Itis = inflammation (Hyde 2006, [Online]). As M.E. expert Dr Byron Hyde MD writes:
'The reason why these physicians were so sure that they were dealing with an inflammatory illness of the brain is that they examined patients in both epidemic and endemic situations with this curious diffuse brain injury. In the epidemic situation with patients falling acutely ill and in some cases dying, autopsies were performed and the diffuse inflammatory brain changes are on record (2006, [Online]).'
In 1957, the Wallis description of M.E. was created. In 1959 Sir Donald Acheson (a former UK Chief Medical Officer) conducted a major review of M.E. (Hooper et al. 2001, [Online]). In 1959 Dr. Donald Henderson (a CDC epidemiologist) and Dr. Alexis Shelakov (a NIH epidemiologist), published a comprehensive review paper in the New England Journal of Medicine describing several outbreaks. Dr. Henderson noted: 'The pattern of the epidemic, the absence of any common exposure factors and the high incidence among medical and hospital personnel were consistent only with an infectious disease transmitted from person to person' (McLaughlin 2004, [Online]). In 1962 the distinguished neurologist Lord Brain included M.E. in the standard textbook of neurology. In recognition of the large body of compelling research that was available, M.E. was formally classified as an organic disease of the central nervous system in the World Health Organisation's International Classification of Diseases in 1969 with the code G.93.3. In 1978 the Royal Society of Medicine held a symposium on Myalgic Encephalomyelitis at which M.E. was accepted as a distinct entity. The symposium proceedings were published in The Postgraduate Medical Journal later that same year. The Ramsay case description of M.E. was published in 1981 (Hooper et al. 2001, [Online]).
Myalgic Encephalomyelitis from 1988 to the present
Modern technology has now served to confirm and to detail the meticulous clinical and scientific observations made about M.E. before 1988, and the name Myalgic Encephalomyelitis has stood the test of time scientifically for more than 50 years. What we now know about Myalgic encephalomyelitis includesthat;
M.E. is a systemic acutely acquired illness initiated by a virus infection which is characterised by post encephalitic damage to the brain stem; a nerve centre through which many spinal nerve tracts connect with higher centres in the brain in order to control all vital bodily functions - this is always damaged in M.E. (Hence the name Myalgic Encephalomyelitis.) The CNS is diffusely (and MEASURABLY) injured at several levels, these include the cortex, the limbic system, the basal ganglia, the hypothalamus and areas of the spinal cord and its appendages. This persisting multilevel central nervous system (CNS) dysfunction is undoubtedly both the chief cause of disability in M.E. and the most critical in the definition of the entire disease process. Myalgic Encephalomyelitis causes a loss of normal internal homeostasis. The individual can no longer function systemically within normal limits.
M.E. is primarily neurological, but because the brain controls all vital bodily functions virtually every bodily system can be affected by M.E. Again, although M.E. is primarily neurological it is also known that the vascular and cardiac dysfunctions seen in M.E. are also the cause of many of the symptoms and much of the disability associated with M.E. - and that the well-documented mitochondrial abnormalities present in M.E. significantly contribute to both of these pathologies. There is also multi-system involvement of cardiac and skeletal muscle, liver, lymphoid and endocrine organs in M.E. Some individuals also have damage to skeletal and heart muscle. Thus M.E. symptoms are manifested by virtually all bodily systems including: cognitive, cardiac, cardiovascular, immunological, endocrinological, respiratory, hormonal, gastrointestinal and musculo-skeletal dysfunctions and damage.
M.E. is an infectious neurological disease and represents a major attack on the central nervous system (CNS) - and an associated injury of the immune system - by the chronic effects of a viral infection. M.E. affects the body systemically. Even minor levels of physical and cognitive activity, sensory input and orthostatic stress beyond a M.E. patient's individual post-illness limits causes a worsening of the severity of the illness (and of symptoms) which can persist for days, weeks or months or longer. In addition to the risk of relapse, repeated or severe overexertion can also cause permanent damage (eg. to the heart), disease progression and/or death in M.E.
M.E. is a distinct, recognisable disease entity that is not difficult to diagnose and can in fact be diagnosed relatively early in the course of the disease (within just a few weeks) - providing that the physician has some experience with the illness. Although there is as yet no single test which can be used to diagnose M.E. there are a series of tests which can confirm a suspected M.E. diagnosis. Virtually every M.E. patient will also have various abnormalities visible on physical exam. If all tests are normal, if specific abnormalities are not seen on certain of these tests (eg. brain scans), then a diagnosis of M.E. cannot be correct. M.E. is similar in a number of significant ways to multiple sclerosis, Lupus and poliomyelitis (polio). There is good evidence to suggest that M.E. is caused by an enterovirus; the same type of virus which causes polio (Bassett 2007, [Online]).
This is not simply theory, but is based upon an enormous body of mutually supportive clinical information which has been published in prestigious peer-reviewed journals all over the world and spans over 70 years, Confirmation of this hypothesis is now supported by electrical tests of muscle and of brain function (CT, MRI, SPECT and PET scans) and by biochemical and hormonal assays, and so on (Chabursky et al. 1992 p. 20) (Hyde 2007, [Online]) (Hyde 2006, [Online]) (Hyde 2003, [Online]) (Dowsett 2001a, [Online]) (Dowsett 2000, [Online]) (Dowsett 1999a, 1999b, [Online]) (Hyde 1992 pp. x-xxi) (Hyde & Jain 1992 pp. 38 - 43) (Hyde et al. 1992, pp. 25-37) (Dowsett et al. 1990, pp. 285-291) (Ramsay 1986, [Online]) (Dowsett & Ramsay n.d., pp. 81-84) (Richardson n.d., pp. 85-92).
But despite the long history of M.E., and the overwhelming irrefutable evidence that M.E. a distinct organic neurological disease, the perception and treatment of M.E. by the public, the medical profession, the government and the media has changed profoundly since 1988.
It is common to read written material on M.E. in the media and produced by government etc. which does not include even one legitimate fact about the illness and is made up entirely of myths and propaganda.
People with the symptom of chronic fatigue and those with authentic neurological Myalgic Encephalomyelitis share few if any similarities.
The new name CFS and the CFS casedefinition was created by the CDC in the US in 1988 by a board of eighteen members (many of them psychiatrists); few of which had studied either an epidemic of M.E., or any patients with the illness. This new criteria failed to select patients using any past or current relevant research or lab work, excluded the cardinal symptoms and signs of M.E. and instead focused almost entirely on 'fatigued persons.'
CFS was created in a response to an outbreak of what was unmistakably M.E., but this new name and definition did not describe the known signs, symptoms, history and pathology of M.E. It described a disease process that did not, and could not exist. The three more experienced members of the board refused to sign the final document and withdrew themselves from the (CDC) definitional committee because the proposed new name and definition for the illness were just too different from the M.E. with which they were so familiar (Hooper et al. 2001 [Online]).
In the two most commonly used definitions of CFS - the US 1994 Fukada (or CDC) definition and the 1991 UK Oxford definition - the only essential symptom required for the diagnosis of CFS to be made is 'chronic fatigue.'
Despite the fact that it was an outbreak of M.E. which these CFS definitions were created to define the vast majority (an estimated 95% at least) of the research and articles available today which use the term CFS are not in any way concerned with, or relevant to, Myalgic Encephalomyelitis patients - yet these 'CFS' studies are what is used to determine the treatments that people with M.E. are recommended, or forced, to participate in. The small amount of research done under the name CFS which does relate to M.E. is also virtually always tainted by CFS propaganda. The creation of 'CFS' is an abuse of basic science. Despite the high level of disability and the vast number of patients involved, governments around the world are currently spending $0 a year on M.E. research.
So why were a group of psychiatrists allowed to redefine a disease of infectious origin?
Professor Malcolm Hooper explains:
'In the 1980s in the US (where there is no NHS and most of the costs of health care are borne by insurance companies), the incidence of ME escalated rapidly, so a political decision was taken to rename M.E. as "chronic fatigue syndrome", the cardinal feature of which was to be chronic or on going "fatigue", a symptom so universal that any insurance claim based on "tiredness" could be expediently denied. The new case definition bore little relation to M.E.: objections were raised by experienced international clinicians and medical scientists, but all objections were ignored. To the serious disadvantage of patients, these psychiatrists have propagated untruths and falsehoods about the disorder to the medical, legal, insurance and media communities, as well as to government, resulting in the withdrawal and erosion of both social and financial support (2003a, [Online]) (2001, [Online]).'
This is the reason why the charade that M.E. could be a psychiatric or behavioural disorder or even a 'aberrant belief system' involving mere 'fatigue' exists; not because there is good scientific evidence - or any evidence - for the theory, or because the evidence proving organic causes and effects is lacking; but purely because such a view is so financially and politically convenient and profitable on such a large scale to a number of extremely powerful corporations and government departments (Hooper et al 2001, [Online]).
The CFS definitions were written in such a manner that CFS becomes like a desert mirage: The closer you approach, the faster it disappears and the more problematic it becomes.
Chronic Fatigue Syndrome is a man-made construct created in the US in 1988.
The only way forward, for the benefit of society and every patient group involved, is that:
1. The fictional disease category of 'CFS' must be abandoned. Patients with fatigue (and other symptoms) caused by a variety of different illnesses need to be diagnosed correctly with these illnesses if they are to have any chance of recovery; not given a meaningless Oxford or Fukuda 'CFS' misdiagnosis. (Some of the conditions commonly misdiagnosed as 'CFS' are very well defined and well-known illnesses and very treatable - but ONLY once they have been correctly diagnosed). Patients with M.E. need to be given this same opportunity.
Patients with depression need to be diagnosed with depression and then treated for depression. Patients with cancer should be diagnosed with cancer and then treated as is appropriate for the kind of cancer they have, and so on. Each of the patient groups involved must be correctly diagnosed and then treated as appropriate based on legitimate and unbiased science involving theSAME patient group.
Physicians who diagnose 'CFS' in any patient experiencing new onset fatigue without looking and testing for the true cause of the symptoms do their patients - and themselves - a great disservice. Some of the conditions commonly misdiagnosed as CFS are very well defined and well-known illnesses and very treatable - but only once they have been correctly diagnosed. Some conditions are also very serious or can even be fatal if not correctly diagnosed and managed, including Myalgic Encephalomyelitis. (It is not uncommon for people with cancer - which causes significant fatigue - to be misdiagnosed with CFS and to die needlessly due to a lack of appropriate treatment, for example.)
Every patient deserves the best possible opportunity for appropriate treatment for their illness, and for recovery. This process must begin with a correct diagnosis if at all possible. A correct diagnosis is half the battle won. A diagnosis of CFS - based on any of the definitions of CFS - can only ever be a misdiagnosis. Doctors must return to the age-old medical principals of correct diagnosis (a) careful history, (b) detailed physical examination and (c) appropriate investigation (Hyde 2006, [Online])
2. The name Myalgic Encephalomyelitis must be fully restored (to the exclusion of all others) and the World Health Organization (WHO) classification of M.E. as an organic neurological illness must be accepted and adhered to in all official documentations and government policy. There were sound medical reasons for the creation of the name in 1956, and for the classification of the illness by the WHO in 1969; neither of which has changed in the interim. Professor Malcolm Hooper explains:
The term myalgic encephalomyelitis (means muscle pain, my-algic, with inflammation of the brain and spinal cord, encephalo-myel-itis, brain spinal cord inflammation) was first coined by Ramsay and Richardson and has been included by the World Health Organisation (WHO) in their International Classification of Diseases (ICD), since 1969. The currently version ICD-10 lists M.E. under G.93.3 - neurological conditions. It cannot be emphasised too strongly that this recognition emerged from meticulous clinical observation and examination. (2006, [online])
Despite misleading claims made to the contrary by vested interest groups, there is well-documented evidence of inflammation of the brain and spinal cord in M.E. spanning over 50 years, but it is true that there is no evidence of inflammation of the brain or spinal cord in states of 'chronic fatigue' or 'tiredness' and other non-M.E. illnesses which may be commonly misdiagnosed as 'CFS' (Hooper n.d., [Online]) (Hyde 2006, [Online]).
M.E. is a distinct recognisable entity, with several unique features, which can be diagnosed relatively early in the course of the disease providing the physician has some experience with the illness. M.E. can easily be distinguished from various chronic fatigue states, and other unrelated 'fatiguing' illnesses. People with M.E. must be diagnosed with M.E. and treated for M.E., based on research which also involves M.E. patients again, finally. The M.E. community does not need to wait for official 'permission' to renew the name and scientifically and historically correct definition of M.E., these rights exist today (as they have since 1969) under the WHO ICD.
3. People with M.E. must also immediately stop being treated as if they are mentally ill, or suffer with a behavioural illness, or as if their physical symptoms do not exist or can be improved with 'positive thinking' or exercise - or mixed in with various non-M.E. 'fatigue' sufferers in any way.
People with M.E. must also be given access to basic medical care, financial support and other appropriate services (including funding for legitimate M.E. research) on an equal level to what is available for those with comparable illnesses (eg. multiple sclerosis or Lupus). The facts about M.E. must again be taught to medical students, and included in mainstream medical journals and already practicing physicians must be brought up to speed about M.E. It must be as unacceptable for physicians to be ignorant about M.E. as multiple sclerosis, diabetes or any other common and serious disease. M.E. expert Dr Elizabeth Dowsett explains that:
M.E. Research workers must be encouraged and appropriately funded to work in this field. However they should first be directed to papers published before 1988, the time at which all specialised experience about poliomyelitis and associated infections seem to have vanished mysteriously! (2001a, [Online])
Myalgic Encephalomyelitis is a distinct infectious neurological disease - not a problem of medically unexplained 'fatigue.' Patients with M.E. must be treated based on the scientific facts, rather than misinformation and falsehoods based on political and financial considerations.
For the benefit of all of the patients groups involved, the medical community and society at large, the bogus disease category of CFS must be abandoned. There is no other logical or ethical solution
Permission to Repost
The UK Medical Research Council has a secret file on Myalgic
Encephalomyelitis (ME) that contains records and correspondence since at
least 1988; the file is held in the UK Government Archive at Kew and cannot
be opened until 2023. This present document is an overview of the
misinformation and contradictions about Myalgic Encephalomyelitis/Chronic
Fatigue Syndrome (ME/CFS) that have pervaded some UK Departments of State
and other agencies since 1988. It also considers the involvement of certain
UK psychiatrists who have proven vested interests in the propagation of this
misinformation that is contrary to world-wide scientific evidence and that
for two decades has resulted in the medical abuse of UK patients with
Professor Malcolm Hooper Eileen Marshall Margaret Williams
Contact address: [email protected]
Current Government Policy (based on the Wessely School beliefs)......... 4
The reality and nature of ME/CFS................................ 5
Two major but under-reported changes in relation to patients with ME/CFS....
The Wessely School control of ME/CFS issues....................... 10
The Wessely School and ME/CFS patients' charities..................... 11
Promulgators and purveyors of misinformation....................... 16
Consequences of opposing the psychiatric ideology................... 17
The UK National Health Service - Similarities with Russian State
The role of State Authorities in disseminating misinformation about ME/CFS
and their role in State-sponsored abuse of patients................... 18
The Centre for Reviews and Dissemination.......................... 19
The NHS Information Authority (now the Information Centre)............ 19
The National Institute for Health and Clinical Excellence (NICE), including
the Trent Institute Report......................................... 23
The Department of Health (including NHS Plus Policy Guidance and
the National Service Framework).................................. 39
The Department for Work and Pensions........................... 43
The Medical Royal Colleges and The Royal Society of Medicine........... 47
The Science Media Centre....................................... 51
NHS Direct................................................. 52
The Medical Research Council (including the House of Commons Inquiry
into the influence of the pharmaceutical industry "Big Pharma")............
The UK Medical Journals including the Medical Trade Journals............ 83
Tactics of Denial.............................................. 89
This important document from Professor Hooper has been compiled for use in a
Judicial Review (which has no connection with any other Judicial Review) and
has been written to assist lawyers who may not be familiar with the facts
that are so well-known to the ME/CFS community (who may recognise parts of
it from previous documents).
It contains previously undisclosed and astonishing information about the MRC
PACE trials (pages 64 -70) and evidence of what Simon Wessely really thinks
about those with severe ME/CFS i.e. that they are "outrageous, crazy,
engaged in fantasies, lies and distortions" (page 96-99).
It also submits evidence showing that in relation to ME/CFS, the claim about
"evidence-based medicine" is meaningless.
Read the Full document at the following address: