CFS lecture in Perth -- objective evidence of digestive problems

Prof Kenny De Meirleir Speaking in Perth, WA.

Prof. Kenny De Meirleir & Dr. Henry Butt will be speaking to health
professionals and PWMEs in Perth Saturday 3rd November 2007 on ME/CFS.

A majority of patients with ME/CFS report gastrointestinal symptoms
and dysfunction, alongside other common symptoms such as cognitive
difficulties, muscle and joint pain, neurological disturbance and
abnormal persistent or fluctuating fatigue.

Prof. De Meirleir will discuss evidence indicating ME/CFS patients have a compromised lining of their gut similar to that found in HIV.
He will explore links to evidence suggesting the gut of patients is
infected with bacterial and/or viral pathogens and how this may
contribute to an altered immune state. Prof. De Meirleir will
describe treatments that have successfully restored the gut lining of
patients and led to a significant improvement in multiple symptoms.

Dr. Butt will discuss evidence indicating significant changes in the
normal bacterial population found in the gut of ME/CFS patients. He
will explore a close correlation between the severity of symptoms
reported by patients (cognitive dysfunction, gastrointestinal
symptoms, pain and fatigue), the degree of changes observed in the
population of gut bacteria, and the quantity of microbial bi-products
produced and released into the body. Prof. Kenny De Meirleir MD PhD
is Professor of Physiology, Pathophysiology, Internal Medicine and
Sports Medicine at Vrije Universiteit, Brussels, and Clinical
Professor, University of Nevada Medical School, USA. Dr. Henry Butt
MSc PhD is Director, Bioscreen Laboratory, and Senior Fellow (Hon) at
Bio21 Molecular Science & Biotechnology Institute, University of Melbourne.

Venue: Social Sciences Lecture Theatre, University of Western Australia.

Tags: CFS, ME/CFS, CFS/ME, Australia, gut, stomach, digestive, bacteria

Sleep

One reason for the perception that CFS=depression is the amount of time CFS patients spend in bed.

My first specialist explained it quite succinctly, that I might be spending 20 hours in bed with my eyes closed, but if I was never getting into the Stage 4 deep healing sleep, I was getting less out of those 20 hours than someone who spent 8 hours sleeping well. Numerous sleep studies have shown that CFS patients get little or no Stage 4 sleep, and many exist in a sort of twilight world, not quite asleep but not quite awake, either. It’s not "sleeping for escapism", but trying to get the same amount of rest and recuperation provided by 8 hours of good sleep. His recommendation (seconded by other CFS specialists) is that the first step in treatment must be fixing the sleep problem; if you don’t do that, then everything will continue getting worse because of lack of quality sleep.

In this relapse, I’ve had the added problem of pain from arthritis, bursitis, tendinitis and just plain overuse. Because no sleep study was ever ordered, my doctors didn’t have to deal with the objective proof that my spending 20 hours a day in bed might only produce 3 hours of actual sleep (and poor quality at that). They wanted to hear that I was depressed over the divorce, so there was, in their minds, no need for a sleep study. In fact, the sleep study would have proven that I was not, as they chose to understand, "sleeping" 15-20 hours a day, but spending 15-20 hours "in bed" simply trying to get enough sleep to not die from extreme sleep deprivation. There’s a big difference between "going to bed" and "going to sleep", as any mother of a toddler on his sixth potty trip can tell you.

Had a sleep study been done, the treatment might have been different. Instead of, as one doctor stated he understood, that the problem was "sleeping too much", they would have had to confront head-on my statements that both quality and quantity of sleep were affected by the pain that started the vicious cycle of insomnia (fibro-like symptoms can be induced in healthy volunteers just by depriving them of sleep, and that pain goes away when they are allowed to return to a normal sleep schedule). A sleep study would have verified the truth of my statement that every time I rolled over onto my painful left shoulder, I woke up, and remained awake. A left shoulder that was so affected by bursitis that I couldn’t raise my arm even all the way to shoulder level; but because the doctor was attributing all my problems to psychological reasons, it was almost two years after the shoulder problem started before anyone checked the range of motion in that shoulder, and saw I could not raise the arm over my head. I knew it was a problem – for weeks, I had been unable to access the top file drawer at work because I couldn’t get my left arm up high enough to assist my right in lifting the heavy older files stored there – but no one was listening to my full recitation of objective problems, because they had the erroneous depression diagnosis to explain away the pain. (In fact, CFS patients describe a much different type of pain than people with depression. When I was diagnosed, I complained that "even my hair hurts" ... a sure sign of neurological involvement!)

There was, in their minds, no reason to do a physical exam because if I had depression, there would be nothing to find on a physical exam. One doctor never asked me to undress at all; he saw no need to perform any sort of physical exam on a CFS patient, not even to check for the telltale swollen glands. In fact, if they’d done a physical exam, or taken a thorough injury history, they would have found legitimate reasons for my pain: post-traumatic arthritis from old sports injuries and three fractured vertebrae. But because I have CFS, there was "no need" for any further investigation of any symptom, they assumed it was all caused by the CFS, and therefore, there was "no need" for the pain medication that would be given to someone who had arthritis without CFS.

Add in the fibromyalgia, which is easiest explained as "The Princess and the Pea". When my fibro is in flare, a small wrinkle in my nightgown can feel like an iron rod under my hip. I spend a lot of time getting out of bed and smoothing wrinkles out of the mattress pad, the sheet, the sleepwear, and the next time I shift position trying to get comfortable, I have to do it again. Fibromyalgia has been demonstrated to be caused by abnormal levels of the pain-processing chemical Substance P; it’s not baseless hypochondria, but has a legitimate biochemical origin.

Informed specialists believe that the first step in treating CFS is to address the sleep problem. This does not mean that CFS=insomnia, but that if sleeping pills and pain pills can help the patient achieve Stage 4 sleep, the body can begin to heal itself. Once I had been sleeping well for a few months, my immune system re-activated and finally began attacking the virus; I ran a 101 fever non-stop for six months. Three years after first requesting a sleeping pill, I finally had the proof that what I asked for was the correct treatment for what truly ailed me. But that was three years of physical damage from the virus that didn’t need to occur, while I was being treated for "depression" which I didn’t have.

When you sleep better, everything else works better. That is such a basic tenet of medicine that it’s inexcusable for doctors to ignore patients’ requests for something to help them get adequate sleep. As one of the later specialists inquired "what would it have hurt?" for them to humor me with a trial run of sleeping pills. It would have hurt the doctor’s ego to have his diagnosis proven wrong, but it would have prevented further hurt to my body. His arrogance led him to act in ways that were detrimental to the patient’s health, and I will pay the price for his ego-centric approach to medicine every day for the rest of my life.

It’s simply counter-productive for a doctor to tell the patient what she "should" be feeling instead of listening to what she actually reports, and to insist that she must be confused if she thinks a prescription made her worse instead of better. Dr. Groopman’s book makes it clear that if the treatment doesn’t work, the problem is the diagnosis and other possibilities should be considered. Those other possibilities should not include verbally abusing the patient for "refusing" to get well; if the patient did not want to get well, she would not be spending money on doctors and prescriptions!

Anti-depressants work wonders on depression. They do absolutely nothing for post-viral CFS. Had my doctors known that, they would have recognized that the reason I kept saying the anti-depressants didn’t help was because they’re not supposed to help what I was previously diagnosed with, and therefore, I clearly did not have "post-divorce depression" as assumed.

One of my teachers used to say "a little learning is a dangerous thing". And it’s true. Knowing "a little" about CFS can be very dangerous if all you know is that it has something to do with fatigue, and depression also causes fatigue, so you’re going to treat it like depression. Doctors who know it has neurological components will understand why the patient complains of pain without obvious injury – neurological damage cannot be seen with the naked eye, and why the patient complains of cognitive/memory problems – brain lesions cannot be seen with the naked eye, and that these things cannot be fixed by treating the patient for depression, nor by jollying the patient "you can do it if you try harder". No polio patient has ever been made to walk by mere cajoling, and no true CFS patient will ever be cured by being coaxed to "do more". (A true CFS patient will relapse if she exceeds her known limits in following doctor’s orders to "do more and you’ll feel better".)

Tags: sleep, depression, CFS, fibromyalgia

Article & response

ARTICLE:

http://www.eastbourneherald.co.uk/features/ME-more-sufferers-more-support.3418542.jp

*ME: more sufferers, more support (Eastbourne Herald, 25 October 2007)*

Joanne Smith

How a local man used his own experience to bring chronic fatigue syndrome
patients together to talk

Oliver Rooke was 19 when he was struck down by glandular fever.

The Seaford resident was studying at Kent University when he first became
ill.

He said, "I went to the university doctor and did some tests and they came
through positive for glandular fever. She said to rest for about four - six
weeks and it would just pass."

But Oliver, now 31, was so ill that a couple of months later he had to leave
his course because he was suffering continuously from mental tiredness.

A year later he was diagnosed with Chronic Fatigue Syndrome (CFS).

Oliver said, "The unique thing about CFS is it's an umbrella term for lots
of things which may have different causes. Mine was triggered by glandular
fever and it can be triggered by stress or trauma."

The illness, which is also known as ME (Myalgic Encephalomyelitis) and can
affect anyone of any age, meant he was unable to return to university.

It is estimated that around 250,000 in Britain are affected by this illness
of unknown cause, which has many different names and symptoms.

Oliver said, "It's a case of managing the symptoms, managing day to day and
trying to live with the illness.

"They set up a clinic in Haywards Heath a couple of years ago that is seeing
patients who have been referred by GPs because they recognise the cases are
increasing."

Oliver's illness has affected him in that he sometimes has difficulty with
concentration, for example, reading a book, watching a TV programme or
playing a board game can be challenging for him. But other sufferers find
they are physically tired rather than affected mentally and may even
struggle to get out of bed.

Oliver says the best way forward is to keep positive and pace yourself when
doing various activities.

He is currently kept busy with running the Defenders of the Ouse Valley and
Estuary (DOVE) website and is a volunteer for Newhaven Community Employment
Partnership (NewCEP), which aims to assist local people to access work,
learning and volunteering opportunities.

Because of his illness Oliver decided to set up a local branch for fellow
sufferers two-and-a-half-years ago.

He said, "There were groups in existence in the area through the Sussex
ME/CFS Society (a registered charity). There were groups in Lewes and
Eastbourne and I went to a few of these and I thought I would try to start a
local group operating in Seaford to see what the reaction would be.

"In the early days it was quite small but as time has gone on it has
gradually grown and is now quite popular."

The group, which meets once a month at Nott's Coffee House in the town, chat
to each other about their symptoms and how they have been coping.

"It's general support, having someone to listen to and talk to.

"It's good for people because often others they speak to do not thoroughly
understand the illness and how it affects them."

Oliver, who is hoping to eventually work full-time in a job that is
computer-related, has been referred to the clinic in Haywards Heath where
various activities he does are being assessed.

The aim is to build up activities to a level he can manage without
stretching himself.

He added, "I think awareness is better now and this is particularly down to
the numbers of sufferers, more and more people are starting to suffer with
it and seeing their doctors and talking to their friends about it. There are
more people who know someone with ME or who have ME.

"I have to try and look at things, things could be worse and so I have got
to try and look at the positive and think of what I can do rather than what
I can't do.

"There are some people who can't get out of bed and are worse off than me."

Anyone who would like more information can call the information line on
01273 674828 or visit the website www.measussex.org.uk Or you can contact Oliver direct on 01323 896741 or e-mail him oliver@seaford.me.uk

RESPONSE:

It is illogical to consider M.E. (Myalgic Encephalomyelitis ) as, both,
synonymous with Chronic Fatigue Syndrome (CFS) and, at the same time, as an
illness subsumed under its umbrella; it can't be both. In fact, it is
neither. M.E. is a discrete neurological illness and trying to treat them
the same is doing nobody any good. It is because chronic fatigue patients
are being added to M.E. sufferers and them all being thought of as people
with M.E . that the number is, erroneously, thought to be increasing (ME:
more sufferers, more support, Eastbourne Herald, 25 October 2007).

It is widely known and agreed that M.E. is frequently preceded by a virus,
such as glandular fever, or, sometimes, by a vaccination, such as for TB or
Hepatitis or, perhaps, by chemical poisoning, though it is not certain
whether any of these is the "trigger" or cause. But, since there are no
figures for each of the suspected culprits, of which I am aware, it is
worrying that Oliver Rooke - and he is not alone in doing this - so confidently ascribes it to stress and trauma when, in 19 years, this Research Psychologist and M.E. sufferer has not known of a single one and believes that there is no evidence for any greater incidence of psychiatric history amongst M.E. patients than in the general population. This is a wild assertion that needs either backing with evidence or - as I believe - withdrawing as a myth that is very unhelpful for research and treatment of M.E.

* * *

Again, the flawed notion of stress and emotional illness is allowed to shout down the patients' own reports of "it started with a virus".  Evidence that there is no history of psychiatric problems in the majority of CFS/ME sufferers counts for nothing to the many "experts" who, in actuality, have no clue what they're talking about.

As my own experience demonstrates, if the doctor reads off a long enough list of potential stressors, he will eventually find something to blame your illness on.  Something as common as taking a vacation or changing jobs can be a source of stress; next time you get a cold, you should blame the vacation you took two months ago, and not a virus ... that's what these "experts" want CFS patients to do!

Yet, this Research Psychologist, who certainly knows more about psychological problems than the average MD, states confidently that he knows of NOT A SINGLE CASE of True ME/CFS that had a psychiatric origin.  There are psychiatricproblems which have fatigue as a symptom, but despite the prevailing notion that CFS and depression are identical, the fact is, there are many symptoms of CFS that are simply unheard of in depression, and a cortisol test can quickly prove which of the two a patient is suffering from.  If the patient does not improve when given anti-depressants, then it is quite clear which of the two the patient has ... anti-depressants have repeatedly been proven absolutely useless against CFS/ME.  They will work for someone who has depression who was given an erroneous CFS diagnosis, but not for someone who has that post-viral thing that used to be called Myalgic Encephalomyelitis and was renamed CFS.

If you're talking about the type of CFS that I have, the type of CFS that occurred in Incline Village which formed the basis of the original diagnostic criteria, then there is absolutely no proof whatsoever that stress is a "cause".  As with any illness, stress can make an existing health condition worse, but a stressor that occurs months later clearly is not a "cause" of the initial health problem.

And the big laugh is that while my doctors were telling me to "avoid stress", they were contributing to my stress by refusing to sign the application for disability benefits that would have reduced my financial stress substantially.  They couldn't bring themselves to practice what they were preaching.

Tags: CFS, CFS/ME, ME/CFS, myalgic encephalomyelitis, fever, virus, glandular, stress

Turning the Tide

Thanks to LKW for finding this one!

* * *

 

I wish I could determine precisely when this article was written, as it
would be helpful to know historically how long some, like the author Del
Kennedy, have realized exactly what is going on with the ME and CFS
'blending' these past 20 years (since the USA CDC made up 'CFS' (Fukada, et
al) in 1988.)

Certainly it's been clear to serious ME advocates like myself that others
before us and around the world have fought the good fight all along, against
the ever-increasing and skewed vested interest efforts. LKW

~~~

Turning the Tide

All over the UK, there are thousands of people debilitated and disabled by
this horrific disease, some bedbound, some in wheelchairs, many in constant
pain. But because their condition cannot yet be detected in a test-tube at
the local pathology lab, all of these desperately ill and suffering people
are labelled liars or loonies; all of the scientific evidence that there is
a real illness at work is dismissed out of hand; and those who highlight
this grotesque injustice are labelled paranoid and hysterical.

The history of the cover-up of ME by the Medical Establishment over the last
45 years is a nightmare story like no other. Quiet, painstaking scientific
research has been stonewalled by the Medical Establishment in favour of
contemptuous power-politics : denigration by design. If this were a
scientific debate, there would be no contest. ME Denial is a political
issue.

What makes the battle over the recognition of ME so significant is that we
seem to have a situation where the majority of the medical profession have
lost the humility to say "we don't know", and are prepared instead to defend
against any suggestion that there might be any ailment that they cannot yet
detect 'in a test tube' on a per-patient basis. Technology has not only come
to dominate intellectual endeavour in the field of medicine; it seems to
have displaced it. 'Somatoform disorder' (psycho-somatosis or now,
'functional somatic syndrome') is the dustbin diagnosis at the end of a
battery of tests. Any other diagnosis requires positive evidence; the
diagnosis of somatoform disorder requires none. This is not science, and
should never be allowed to masquerade as such.

It seems to me that the only way out of the present impasse is to ensure
that every study into the cause or treatment of ME is conducted exclusively
with the most severely disabled sufferers. We have to get back to basics :
back to the original definition of ME - Melvin Ramsay's. I am sure there are
many people whose lives have been devastated by this disease who would yet
fall outside Ramsay's narrow definition of ME. Many would fall within it in
the morning, and outside it in the afternoon, or vice-versa; my own
condition used to fluctuate between extremes.

But the more exclusive our definition, the more the psychiatrists' absurd,
nightmare bangwagon will be confronted with reality. Let's make them face
the truth. Let's put those in wheelchairs first.

Chronic Fatigue Syndrome is a term introduced in 1988 (32 years after the
discovery of ME) by the U.S. Centres for Disease Control (CDC). It was felt
at first by many British ME sufferers to be transparently contrived in order
to denigrate our illness and downgrade its priority below a level that might
warrant serious funding of research. Unfortunately, the two major British ME
charities were of another opinion.

NOTE: ME was 'discovered' earlier; it was 'formally recognized' later on
then. LKW

Everything that has happened since then has confirmed this first grassroots
impression. The new name was followed by new and ~broader~ diagnostic
criteria, until it became possible to conduct a study into CFS that might include not one single genuine ME sufferer.

Now there is a move to group a whole host of ludicrously unrelated
conditions (IBS, CFS, PMT, FMS, Temporomandipular Joint Pain, Tension
Headache, Atypical Chest Pain, MCS and Globus Hysterictis) together under an
even larger umbrella - "functional somatic syndromes". It's high time we
threw a spanner in the works of this drivel-factory; it's time we returned
to Ramsay.

Magna est veritas et praevalebit
(great is truth, and shall prevail).

Del Kennedy

Posted on: http://www.meactionuk.org.uk/tide.html

 

Tags: CFS, CFS/ME, ME/CFS, Ramsey, myalgic encephalomyelitis

On a Personal Note

David Paulison of FEMA says "Nobody does disasters better than California". Yeah, maybe you and Heckuva-Job-Brownie should come out here and take a few lessons from the masters.

The difference is, our annual disaster drill isn’t a dry run like other states – between the fires and the earthquakes, our annual practice is the real thing, all hands on deck, this one really counts. Our state Office of Emergency Services has matters well under control before FEMA even knows there’s a problem. We don’t just have theory on how to move a thousand trucks of bottled water to the far end of the state; we’ve done it for real and often enough to have experienced all the possible difficulties.

My family in SoCal evacuated sequentially over the past few days: one aunt went to another aunt’s house. From there, they were evacuated to one son’s house, and from there to the other son’s, who wisely lives far enough from the other family members that he’s safe when they’re threatened (and vice versa). All well-planned (the aunts have planned their evacuations for decades, and have used those plans more than once) and orderly. Another cousin loaded the valuables into the RV and is camped out on a beach, again, all according to plan.

When I lived in San Diego, we had a canyon fire come within a mile of our house. Our biggest worry was whether one side of the family would be offended if we refugeed to the other’s family instead. We had a list of what to take with us, and were calmly boxing it up and setting it on the couch, positive that our list contained everything we would need, because it was based on the list my aunt had used for decades of evacuations from her house.

More evidence it's a virus, not psychological

Source: Journal of Clinical Virology Vol. 37 Supplement #1, pp. S33-S38 Date: December 2006 URL: http://www.sciencedirect.com/science/journal/13866532

Use of valganciclovir in patients with elevated antibody titers against Human Herpesvirus-6 (HHV-6) and Epstein-Barr Virus (EBV) who were experiencing central nervous system dysfunction including long-standing fatigue

Andreas M. Kogelnik(a), Kristin Loomis(b), Mette Hoegh-Petersen(c), Fernando Rosso(a,c), Courtney Hischier(b), Jose G. Montoya(a,c,*) a Stanford University School of Medicine, Stanford, CA, USA b HHV-6 Foundation, Santa Barbara, CA, USA c Palo Alto Medical Foundation Research Institute, Palo Alto, CA, USA * Corresponding author. E-mail address: gilberto@stanford.edu (J.G. Montoya).

Abstract

Background Twelve patients with long-standing symptoms of central nervous system (CNS) dysfunction were found to have elevated antibody titres to human herpesvirus-6 (HHV-6) and Epstein-Barr virus (EBV). All patients had four or more of the following neurocognitive symptoms: impaired cognitive functioning, slowed processing speed, sleep disturbance, short-term memory deficit, fatigue and symptoms consistent with depression.

Objectives We sought to determine whether elevated antibodies to EBV and HHV-6 indicated chronic viral activation in patients with CNS dysfunction and if their symptoms could be improved by suppressing viral activity with oral valganciclovir.

Study design Patients with high IgG antibody titers against HHV-6 and EBV who were suffering from central nervous system dysfunction and debilitating fatigue for more than one year (median 3 years, range 1-8 years) were treated with 6 months of valganciclovir in an open label study.

Results Nine out of 12 (75%) patients experienced near resolution of their symptoms, allowing them all to return to the workforce or full time activites. In the nine patients with a symptomatic response to treatment, EBV VCA IgG titers dropped from 1:2560 to 1:640 (p=0.008) and HHV-6 IgG titers dropped from a median value of 1:1280 to 1:320 (p=0.271). Clinically significant hematological toxicity or serious adverse events were not observed among the 12 patients.

Conclusion These preliminary clinical and laboratory observations merit additional studies to establish whether this clinical response is mediated by an antiviral effect of the drug, indirectly via immunomodulation or by placebo effect.

1. Introduction

Chronic fatigue syndrome (CFS) is a clinically defined condition characterized by severe disabling fatigue and a constellation of symptoms that prominently feature self-reported impairment of concentration and short-term memory, sleep disturbances, and musculoskeletal pain. Patients suffering from CFS typically experience these symptoms for 6 months or longer. Suggested etiologies of CFS include, but are not limited to: viral or bacterial infections, endocrine-metabolic dysfunction, immunological imbalance, neurally mediated hypotension and depression (Afari and Buchwald, 2003; Fukuda et al., 1994). Most prior studies have found laboratory evidence that EBV and HHV-6 are reactivated more often in patients with CFS than in healthy control subjects or disease comparison groups, but causal inferences have not been made from such an association.

Epstein-Barr virus (EBV) and human herpesvirus type 6 (HHV-6) are enveloped double-stranded DNA viruses belonging to the herpesviridae family. Both viruses are lymphotropic and neurotropic, and both are capable of producing latent infections with immunomodulatory effects (Ambinder, 2003; Ambinder and Lin, 2005; Krueger and Ablashi, 2003). Furthermore, in vitro studies of co-infection with both viruses have revealed that a significant interplay may occur between them (Cuomo et al., 1998; Flamand et al., 1993). The clinical consequence of this interaction remains unknown. However, it has been suggested by various investigators that infection with EBV and/or HHV-6 may trigger or contribute to the pathogenesis of certain diseases including chronic fatigue syndrome (Bertram et al., 1991; Sairenji et al., 1995) and multiple sclerosis (Hollsberg et al., 2005).

The seroprevalence in the adult population for EBV and HHV-6B is about 90% and most people undergo asymptomatic seroconversion. The high seroprevalence in the general population complicates the interpretation of serological tests in diagnosing reactivation of either virus. Unlike many other viruses, the DNA for EBV and HHV-6 are difficult to detect in either the peripheral blood cells or serum except in cases of primary infection or acute reactivation. Most (Ablashi et al., 2000; Manian, 1994; Natelson et al., 1994; Patnaik et al., 1995) but not all (Buchwald et al., 1996) studies that have examined antibody titers to HHV-6 and EBV in CFS patients have found that there is a significant difference between patients and controls: Manian found 55% of CFS patients had EBV VCA antibodies of 1:320 or above compared to 15% of controls (Horwitz et al., 1985). Sairenji et al. found that CFS patients had elevated antibodies to EBV, HHV-6, human herpesvirus 7 (HHV-7) and ZEBRA (a protein of the immediate early EBV gene BZLF1) compared to healthy controls (Sairenji et al., 1995). Highly elevated early antigen (EA) antibodies are considered indicative of active infection for both EBV and HHV-6. Both Patnaik and Ablashi found elevated antibodies to the HHV-6 EA antibody in CFS patients compared to controls (Ablashi et al., 2000; Patnaik et al., 1995).

HHV-6 and EBV infections can cause immunosuppression and HHV-6 can impair immune response to fungal infections (Cermelli et al., 2006; Sauce et al., 2006; Smith et al., 2005). We suspected that their symptoms could be the result of an immune dysregulation triggered by EBV and HHV-6, especially when reactivated jointly. Alterations in the immune system such as aberrant cytokine profiles have been proposed as the central abnormality in patients with other viruses such as parvovirus B19 (Kerr et al., 2003). Latent EBV and HHV-6 virus can also alter cytokines and induce sickness behavior (Glaser et al., 2006; Yoshikawa et al., 2002).

Valganciclovir is the only known antiviral drug with efficacy against both EBV and HHV-6 that can be administered orally. It has the potential for toxicity, but our experience in using the drug to treat reactivation of viral infections in immunocompromised patients (Gao et al., 2003; Montoya et al., 2001; Montoya, 2004) with minimal adverse effects has made us comfortable with this treatment. If patients are supervised properly, the risk of significant side effects is greatly reduced and antiviral treatment is manageable. We hypothesized that a long course (i.e. 6 months) of valganciclovir could effectively decrease or stop ongoing viral replication of both HHV-6 and EBV and result in a sustained clinical improvement (decrease in antibodies or resolution of lymphadenopathy and fatigue).

2. Materials and methods

2.1. Patients

Twelve patients, ages 21-57 (75% female) were referred to the Infectious Diseases Clinic at Stanford University Medical Center between February 2004 and August 2005 because of their history of chronic fatigue syndrome suspicious for infectious etiology. Patients had been seen by at least five other physicians (range 5-20). Other causes of fatigue had been appropriately excluded. The following laboratory tests were within normal limits in each of the patients who were tried on valganciclovir: complete blood count (CBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), alanine aminotransferase (ALT), total protein, albumin, globulin, alkaline phosphatase, calcium, phosphorus, glucose, BUN, creatinine, electrolytes, and urinalysis. All patients met the CDC case definition for CFS (Fukuda et al., 1994) and all had neurocognitive complaints that included four or more of the following symptoms: impaired cognitive functioning, slowed processing speed, sleep disturbance, short-term memory deficit and symptoms consistent with depression. In addition, all had a history of a "flu-like" onset.

2.2. Drug regimen, toxicity monitoring, and fatigue evaluation Valganciclovir (VGCV) was prescribed as 900 mg twice per day for three weeks followed by 900 mg every day to complete a total of 6 months on the drug. Ganciclovir was approved in June 1989 by the United States Food and Drug Administration for the treatment and prophylaxis of diseases caused by cytomegalovirus (CMV). Ganciclovir has been used at Stanford Medical Center since 1987 for the treatment of several viral diseases observed in immunocompromised patients (Montoya, 2004). A second oral formulation (valganciclovir or L-valine esther of ganciclovir) was introduced in 1991 and achieves serum levels similar to those reached by the intravenous form.

CBC's were followed twice per week for three weeks, followed by once per week for three weeks, and once per month thereafter until VGCV was discontinued. None of the patients in our cohort was taking drugs with known adverse hematological or renal effects. While on VGCV, patients were instructed to report any new symptoms and on each medical visit they were explicitly asked whether they had experienced fever, chills, unusual bleeding or bruising, infection, unhealed sores or white plaques in mouth, headache, seizures or gastrointestinal symptoms. Pregnancy was not a consideration for any of our patients in the childbearing age; none of them was sexually active. At baseline, and again at each visit, patients were asked to report on their current activity level as a percentage of their pre-illness activity level.

2.3. Serological and molecular testing

In each of the 12 patients, the following serological tests were performed: EBV Viral Capsid Antigen (VCA) IgG and IgM antibodies, antibodies against EBV nuclear antigens (EBNA), antibodies against EBV early antigens (EA), HHV-6 IgG and IgM antibodies and CMV IgG and IgM antibodies (Focus Diagnostics, Inc., Cypress, CA, USA). HHV-6 and EBV testing was done by IFA and CMV tests were done by ELISA. The HHV-6 kits were purchased at Panbio (Columbia, MD) and the EBV kits are FDA approved kits sold by the Products division of Focus Diagnostics. At initial evaluation, each of the 12 patients had a polymerase chain reaction (PCR) test performed in serum for the following viruses: EBV, HHV-6, and CMV.

2.4. Statistical testing

To compare EBV and HHV-6 serologic titers before and after valganciclovir therapy among the 12 patients, paired non-parametric tests were performed (Sign test). To compare demographic and serologic variables between those who responded to valganciclovir and those who did not, the Mann ­Whitney test was used. Statistical analysis was performed using the Epi Info Version 3.3.2.

3. Results

As shown in Table 1, of the 12 patients, 9 "responders" had a dramatic improvement in their fatigue and central nervous system symptoms (p=0.007) and 3 "non-responders" failed to report any progress. Central nervous system symptoms such as "brain fog" and other cognitive abnormalities were among the first symptoms to improve. Most improvement of clinical symptoms occurred between weeks 6 and 12. In the first several months, significant improvement was observed in physical activity at home. Subsequently, each of the responders was able to return to work or full time activities. The new level of "near-normal" activity has been sustained for greater than 9 months (up to 31 months) after discontinuation of the drug at week 24 in each of the nine patients.

The mean age of the responders was 35.4 years (range: 14-57) and that of the non-responders 43 years (range: 28-52). Of the 9 responders, 9 (100%) experienced the onset of their chronic fatigue syndrome as a "flu-like" illness and 4 (45%) developed lymphadenopathy. Whereas of the 3 non-responders, only 1 (33%) had a "flu-like" illness at the onset of the disease and 1 (33%) developed lymphadenopathy. The activity level of both responders and non-responders was severely compromised, compared to pre-illness activity level, at baseline (10% in responders, 15% in non-responders).

All of the nine responders experienced an initial worsening of their already severe symptoms. This worsening occurred between weeks 2 and 4, and wassevere enough to make several patients stay in bed for several weeks. In one patient where the WBC differential data was collected, this worsening period coincided with a 25% drop in WBC count and an 80% drop in monocytes. The three non-responders did not experience this worsening in their symptoms.

None of the 12 patients experienced any side effects to VGCV that required its discontinuation or experienced abnormalities in their laboratory tests including clinically significant hematological toxicities.

IgG antibody titers against HHV-6 and EBV antigens at baseline and after valganciclovir therapy for the responders and non-responders are shown in Table 2. In responders, the median HHV-6 antibody titer dropped from 1:1280 to 1:320 (p=0.271) and the median EBV VCA titer dropped from 1:2560 to 1:640 (p=0.008). Two of the 3 non-responders had no significant change in their titers against EBV antigens after VGCV therapy and values were not obtained for the third. Two of the non-responders did not have elevated antibody levels that meet our current threshold for treatment, but had other evidence of a viral syndrome.

Of the 12 patients in our cohort, only one patient had a positive IgM for HHV-6 (patient #8). The 12 patients were negative for EBV VCA IgM antibody. Neither EBV, HHV-6 nor CMV DNA was detected by PCR in the serum; assessment of viral DNA on whole blood was not performed. Seven of the patients had high HHV-6 antibody titers (patients #2-6, 8, 9), five had elevated antibody titers to EBV (#1, 2, 6-8), and three had elevated antibodies to both viruses (#2, 6, 8).

Reduction in IgG antibody titers, duration of fatigue and level of activity change in 9 patients whose clinical improvement was associated with the use of valganciclovir are shown in Table 1. In three of the nine responders the EBV EA antibody dropped by four-fold or more. EBNA antibodies dropped in six of the nine responders. Of the 9 responders, 4 (45%) were positive for CMV IgG and 1 was positive for CMV IgM. Of the 3 non-responders, 2 were CMV IgG positive. Only one patient was positive for CMV IgM antibodies (patient #8).

Tags: CFS, virus, treatment, Stanford

Footnotes to Montoya Research

4. Discussion

This was an open-label study of valganciclovir (VGCV) in 12 patients with CFS and elevated antibody titers to both HHV-6 and EBV. VGCV treatment was associated with reduction in antibody titers in most patients. A majority of the treated patients also had dramatic improvement in activity level, although three did not. Obviously, a placebo effect is always possible in open-label studies. Many previous treatments had been tried in these 12 patients, without any benefit, suggesting that they were not placebo responders. Moreover, patients with CFS appear to be less likely than patients with other diseases to experience a placebo effect (Cho et al., 2005). Nevertheless, large randomized trials are essential before VGCV therapy is given routinely in patients with CFS and elevated antibody titers to HHV-6 or EBV. Based on our experience, such studies should probably be restricted to CFS patients whose illness began with an acute flu-like illness, which may be a minority of patients with CFS in the community at large (Solomon and Reeves, 2004).

Since HHV-6 is typically acquired by the age of two and EBV is generally acquired in early childhood or as a young adult, we interpreted the elevated titers as a sign of reactivated rather than primary infection. The antibody titers of the patients were considerably higher than those in 12 healthy controls, tested in the same laboratory. However, reference values for antibody titers against HHV-6 and EBV do vary by laboratory and variations of 1-2 dilutions in results on tests run on the same sample are considered common in most commercial laboratories. Focus Diagnostics, the laboratory used by Stanford for the EBV, HHV-6 and CMV serological tests, has a reference range that is higher than what has been reported in the literature (Savoldo et al., 2002; Straus et al., 1985; Tobi et al., 1982). At our request, Focus Diagnostics tested 12 healthy controls and the median titers were 1:80 for HHV-6 IgG and 1:320 for EBV VCA IgG. When fifty laboratory workers were tested at Focus, median values were slightly higher: 1:160 for HHV-6, and 1:640 for EBV VCA.

Although EBV EA antibodies dropped in three responders, it did not drop in the others, which was contrary to our expectations. Since antibody levels fall slowly over time, these results may understate the full extent of the drop. Antibody measures cannot determine whether a patient has an active viral reactivation. However, the fact that we observed falling EBV and HHV-6 titers concurrent with clinical recovery is significant. Larger studies and standardized assays are necessary to determine how useful these serological assays can be in identifying prospects for treatment. Molecular assays available in clinical laboratories were not informative. None of the responding patients was positive for HHV-6 or EBV DNA using an assay capable of detecting as few as 200 copies/ml. DNA of these viruses is typically detected only during a primary or acute infection. Better biomarkers are needed to identify reactivation of chronic disease and assess response to treatment.

Both HHV-6 and EBV can reactivate in a healthy person in response to an acute illness and normal controls can be found with elevated antibody titers to HHV-6 and EBV, especially in those under the age of thirty who are more likely to have had a recent primary infecton. This makes the assessment more complex and underscores the necessity of a careful evaluation by an experienced clinician, in order to differentiate between transient reactivation due to other illness, asymptomatic elevation of viral titers, and a chronic reactivated viral infection which would deserve treatment.

Clinical evaluation and a history suggestive of a viral etiology must remain the primary determinant for treatment. Treatment cannot be based solely on antibody levels or detection of viral DNA. In cases where humoral immune response is impaired, antibody levels may not be elevated at all or only slightly elevated above the mean. Also, there may be persistent viral infection in the CNS tissue with no trace in the peripheral blood. A prospective placebo controlled trial of valganciclovir is necessary to determine whether a subset of CFS patients would benefit from treatment. The fact that antibody titers to either HHV-6 or EBV dropped four-fold or more in several of these patients suggests (a) some if not all of these patients had active infections and (b) elevated antibody levels can be useful to confirm a suspicion of a chronic infecion that has reactivated.

In this study, treatment with oral VGCV did not produce any serious adverse effects, but it was not without some difficulties. As noted above, all of the responding patients reported some degree of worsening of their condition during their inital month of treatment. This worsening resembled a Jarisch ­Herxheimer-like reaction and included several days of myalgias, chills, headache, worsening of the "brain fog" and fatigue, and skin rash in some patients. The pathology of this response is unclear, but may be mediated by an immune response to transiently increased circulating viral antigen(s).

Adverse events for patients using VGCV is far higher for immunocompromised patients including those with AIDS-associated CMV retinitis and solid organ transplants with CMV disease. Neutropenia was reported to be 27% for retinitis patients (Roche Valcyte product information: (http://www.rocheusa.com/products/valcyte/) and 8% in solid organ transplants (Paya et al., 2004). In this small study, none of our patients experienced any hematological adverse effects or untoward reactions requiring the discontinuation of the VGCV.

Several other limitations of this study need to be acknowledged. We did not test for HHV-7 or distinguish between the HHV-6 A and B subtypes. Also, despite the fact that the improvements in physical activity and cognitive functions were dramatic and impressive, they were self-reported and not objective measurements. We are planning a double-blind placebo controlled trial with more comprehensive evaluation of the functional status of subjects, using established and validated instruments as well as better documentation of viral activity.

In summary, the results of this preliminary study suggest that a subset of patients with CFS and elevated antibody levels to HHV-6 and EBV may have an illness that is caused by reactivation of these viruses, and that is responsive to VGCV antiviral therapy. Further definition of this subset of patients with better and more standardized viral assays is required, as are large randomized controlled trials with long-term follow-up to confirm the possible value of antiviral therapy in patients with CNS dysfunction and symptoms of sustained fatigue. In addition, we propose a new medical term for the syndrome that may best describe our patient cohort: Virus Induced CNS Dysfunction. It may be applied to the subset of CFS patients who have elevated HHV-6 and EBV titers and clinical symptoms of a viral syndrome with neurocognitive complaints and sustained fatigue. Other viruses may also play a role in defining additional CFS patient sets.

References

Ablashi DV, Eastman HB, Owen CB, Roman MM, Friedman J, Zabriskie JB, et al. Frequent HHV-6 reactivation in multiple sclerosis (MS) and chronic fatigue syndrome (CFS) patients. J Clin Virol 2000;16:179-91.

Afari N, Buchwald D. Chronic fatigue syndrome: a review. Am J Psychiatry 2003;160:221-36.

Ambinder RF. Epstein-Barr virus-associated lymphoproliferative disor- ders. Rev Clin Exp Hematol 2003;7:362-74.

Ambinder RF, Lin L. Mononucleosis in the laboratory. J Infect Dis 2005; 192:1503-4.

Bertram G, Dreiner N, Krueger GR, Ramon A, Ablashi DV, Salahuddin SZ, et al. Frequent double infection with Epstein-Barr virus and human herpesvirus-6 in patients with acute infectious mononucleosis. In Vivo 1991;5:271-9.

Buchwald D, Ashley RL, Pearlman T, Kith P, Komaroff AL. Viral serologies in patients with chronic fatigue and chronic fatigue syndrome. J Med Virol 1996;50:25-30.

Cermelli C, Cenacchi V, Beretti F, Pezzini F, Luca DD, Blasi E. Human herpesvirus-6 dysregulates monocyte-mediated anticryptococcal defences. J Med Microbiol 2006;55:695-702.

Cho HJ, Hotopf M, Wessely S. The placebo response in the treatment of chronic fatigue syndrome: a systematic review and meta-analysis. Psychosom Med 2005;67:301-13.

Cuomo L, Trivedi P, De Grazia U, Calogero A, D'Onofrio M, Yang W, et al. Upregulation of Epstein-Barr virus-encoded latent membrane protein by human herpesvirus 6 superinfection of EBV-carrying Burkitt lymphoma cells. J Med Virol 1998;55:219-26.

Flamand L, Stefanescu I, Ablashi DV, Menezes J. Activation of the Epstein-Barr virus replicative cycle by human herpesvirus 6. J Virol 1993;67:6768-77.

Fukuda K, Straus SE, Hickie I, Sharpe MC, Dobbins JG, Komaroff A. The chronic fatigue syndrome: a comprehensive approach to its definition and study. International Chronic Fatigue Syndrome Study Group. Ann Intern Med 1994;121:953-9.

Gao SZ, Chaparro SV, Perlroth M, Montoya JG, Miller JL, DiMiceli S, et al. Post-transplantation lymphoproliferative disease in heart and heart-lung transplant recipients: 30-year experience at Stanford University. J Heart Lung Transplant 2003;22:505-14.

Glaser R, Litsky ML, Padgett DA, Baiocchi RA, Yang EV, Chen M, et al. EBV- encoded dUTPase induces immune dysregulation: Implications for the pathophysiology of EBV-associated disease. Virology 2006;346: 205-18.

Hollsberg P, Kusk M, Bech E, Hansen HJ, Jakobsen J, Haahr S. Presence of Epstein-Barr virus and human herpesvirus 6B DNA in multiple sclerosis patients: associations with disease activity. Acta Neurol Scand 2005;112:395-402.

Horwitz CA, Henle W, Henle G, Rudnick H, Latts E. Long-term serological follow-up of patients for Epstein-Barr virus after recovery from infectious mononucleosis. J Infect Dis 1985;151:1150-3.

Kerr JR, Cunniffe VS, Kelleher P, Bernstein RM, Bruce IN. Successful intravenous immunoglobulin therapy in 3 cases of parvovirus B19- associated chronic fatigue syndrome. Clin Infect Dis 2003;36:e100-6.

Krueger GR, Ablashi DV. Human herpesvirus-6: a short review of its biological behavior. Intervirology 2003;46:257-69.

Manian FA. Simultaneous measurement of antibodies to Epstein-Barr virus, human herpesvirus 6, herpes simplex virus types 1 and 2, and 14 enteroviruses in chronic fatigue syndrome: is there evidence of activation of a nonspecific polyclonal immune response? Clin Infect Dis 1994;19:448-53.

Montoya JG. Successes and limitations of antimicrobial interventions in the setting of organ transplantation. Curr Opin Infect Dis 2004;17:341-5.

Montoya JG, Giraldo LF, Efron B, Stinson EB, Gamberg P, Hunt S, et al. Infectious complications among 620 consecutive heart transplant patients at Stanford University Medical Center. Clin Infect Dis 2001;33:629-40.

Natelson BH, Ye N, Moul DE, Jenkins FJ, Oren DA, Tapp WN, et al. High titers of anti-Epstein-Barr virus DNA polymerase are found in patients with severe fatiguing illness. J Med Virol 1994;42:42-6.

Patnaik M, Komaroff AL, Conley E, Ojo-Amaize EA, Peter JB. Prevalence of IgM antibodies to human herpesvirus 6 early antigen (p41/38) in patients with chronic fatigue syndrome. J Infect Dis 1995;172:1364-7.

Paya C, Humar A, Dominguez E, Washburn K, Blumberg E, Alexander B, et al. Efficacy and safety of valganciclovir vs. oral ganciclovir for prevention of cytomegalovirus disease in solid organ transplant recipients. Am J Transplant 2004;4:611-20.

Sairenji T, Yamanishi K, Tachibana Y, Bertoni G, Kurata T. Antibody responses to Epstein-Barr virus, human herpesvirus 6 and human herpesvirus 7 in patients with chronic fatigue syndrome. Intervirology 1995;38:269-73.

Sauce D, Larsen M, Curnow SJ, Leese AM, Moss PA, Hislop AD, et al. EBV-associated mononucleosis leads to long-term global deficit in T-cell responsiveness to IL-15. Blood 2006;108:11-8.

Savoldo B, Huls MH, Liu Z, Okamura T, Volk HD, Reinke P, et al. Autologous Epstein-Barr virus (EBV)-specific cytotoxic T cells for the treatment of persistent active EBV infection. Blood 2002;100:4059-66.

Smith AP, Paolucci C, Di Lullo G, Burastero SE, Santoro F, Lusso P. Viral replication-independent blockade of dendritic cell maturation and interleukin-12 production by human herpesvirus 6. J Virol 2005;79: 2807-13.

Solomon L, Reeves WC. Factors influencing the diagnosis of chronic fatigue syndrome. Arch Intern Med 2004;164:2241-5.

Straus SE, Tosato G, Armstrong G, Lawley T, Preble OT, Henle W, et al. Persisting illness and fatigue in adults with evidence of Epstein-Barr virus infection. Ann Intern Med 1985;102:7-16.

Tobi M, Morag A, Ravid Z, Chowers I, Feldman-Weiss V, Michaeli Y, et al. Prolonged atypical illness associated with serological evidence of persistent Epstein-Barr virus infection. Lancet 1982;1:61-4.

Yoshikawa T, Asano Y, Akimoto S, Ozaki T, Iwasaki T, Kurata T, et al. Latent infection of human herpesvirus 6 in astrocytoma cell line and alteration of cytokine synthesis. J Med Virol 2002;66:497-505.

Tags: CFS, Stanford, treatment, virus, Montoya

Worldwide Epidemic Alert (cover up and striking medical info)

http://www.geocities.com/tcjrme/CurrentTopics4.html

Atypical Polio was first identified in 1934 by a US Public Health Service investigation of the California outbreak. The Surgeon General took interest because of the very high number of medical personnel that were affected at the Los Angeles county hospital. The hospital was dealing with a large number of Polio cases that summer. This pattern of conditions was similar to many of the outbreaks of this rare disease that occurred over many years worldwide. The increased frequency of these outbreaks during the 1950’s brought greater interest to our disease. Dr Melvin Ramsay and others further defined the illness, and Myalgic Encephalomyelitis became the recognized term for this neurologic infectious disease.

A number of distinguished doctors continued to study and report on ME outbreaks, including Wallis, Acheson, Richardson, Parish, Henderson, Shelokov, Dowsett, Ryll, Behan, and Hyde. Their writings have brought us a wealth of information about Myalgic Encephalomyelitis, and a continuous historical record of our disease over many decades. Perhaps most impressive among them, Dr Richardson could attest that the cases he saw in the year 2000 have the same disease as patients that he and Dr Ramsay encountered in the 1950's: the neurological disease defined as Myalgic Encephalomyelitis.

In 1984 the Outbreak at Lake Tahoe heralded the emergence of the massive modern explosion of epidemic Myalgic Encephalomyelitis (ME). The response from the American Centers for Disease Control (CDC) was to initiate a tragic and devastating pattern of denial, misinformation and confusion about this disease. The capstone of this deception came in 1988, with the use of a vague definition, the fabrication of a "new" illness, CFS, along with a disorienting barrage of propaganda; instead of taking advantage of the advice of the medical experts and pursuing an immediate investigation of the devastating and growing ME epidemic. This effort included encouraging journals to never again publish articles about Myalgic Encephalomyelitis.

The immediate effect of these actions was to render the medical community ignorant of the true nature of this disease, and unaware of the established record of previous outbreaks and reports. With this new CFS label, no one would realize that it referred to a disease similar to multiple sclerosis, chronic polio encephalitis or today's Post Polio. Clearly, in effect a program of deception.

The invention of the vague "CFS" construct was immediately followed by the enlistment of psychiatrists, and a frenzy of redefinitions and expansion of the disease criteria. These redefinitions created an opportunity to identify as patients people with vague symptoms and psychiatric disorders if that was opportune for the researcher and sponsors. The effect was to pollute the subject pool and thus mystify the research data with conflicting results. This inclusion of the psychiatric brigade, that postulated theories, promoted confusion and distracted the focus away from the origins and infections, was to the delight and benefit of the Defense department and an Insurance industry driven to limit their liabilities.

These major moves to confound and confuse, and to use the cover of the psychological theories, can be seen as part of a deliberate protracted plan. The expansion of the criteria would help provide ammunition to distort or waterdown the growing scientific data. Data, that demonstrate the neurological, immunological and circulatory abnormalities that confirm the Ramsay clinical criteria of Myalgic Encephalomyelitis. For the insurance industry, the promotion of the psychological theories would provide them with opportunities to limit disability coverage and avoid liability payouts, and thus enhance the Bottom Line.

By 1994, these tactics of deception progressed further with the overhaul of the "CFS" criteria to increase the focus on fatigue and stress. All the key features that defined the neurological disease, ME, became optional. Meanwhile the number of ME victims succumbing to lymphoma, cancer and organ failure continued to mount.

In a stepwise progression, the CDC program to obscure the ME epidemic and the identity of the disease became broader and more determined. As doctors and studies revealed more and more of the features (brain scans of damage to the brain stem similar to polio) and considerable organic abnormalities of ME, so too, the designs and policies from the CDC to confuse became more elaborate. By 2000, the proposal included the creation of a wide umbrella of "unexplained" illnesses. Thereby, a method to truly bury the scientific and programmatic focus on the epidemic of ME amid a vast multitude of non-infectious, non-neurologic and many psychological conditions. A category of illnesses was created where confusion would reign and for which there would be little public interest or concern, once shrouded in the cloak of psychological theories.

A cover-up of grand scale is being institutionalized, with all the trappings of official interest, appeasement, advisory boards and workgroups, with zero funding for the infectious causes. All of these developments would be consistent with a plan to not discover the cause.

A government investigation (GAO) found that many millions of dollars authorized by Congress for CFS was diverted and not used for CFS research. In effect, years of effort and opportunity and hope were lost. Many patients died during this time.

The patient community is aware of the CDC's long-standing culture of bias regarding our disease: the refusal to investigate the outbreaks, the diversion of funding, the deceitful design of laboratory studies, to the offensive and derogatory attitudes toward patients. This attitude includes Reeves having fun by ridiculing patients at public meetings. The CDC history and their record with the ME epidemic, and experiences of ME patients, strongly suggests that in order to help save lives the CDC must be prohibited from any further involvement with any decisions about our disease.

It is clear to us that there is a fundamental conflict between the interests of the large and growing patient community disabled by ME with their desire for progress, and the program of the CDC, which has been to delay and derail the search for the cause and cure. The trademark of the CDC strategy to cause confusion and to conceal the identity of this ME epidemic was the change of name to Chronic Fatigue Syndrome.

The myriad series of events, delays, mistakes and supposed bungling is so extensive that it fills an entire book, Hillary Johnson's Osler's Web, published in 1996. This work is essential reading for understanding of the medical, social, and political history of ME, as well as providing a context for the current events.

The Disaster of Policy

Without regard to the origins of the ME epidemic or why the health authorities have worked to conceal the epidemic from the public, the effects these policies on patients is devastating. As patients we know the brutality of both the medical and social disasters imposed by the CDC policies. They advise doctors not to do any of the numerous tests that demonstrate the immune, infectious, central nervous system and metabolic abnormalities that can support the diagnosis. Where does this leave the doctor? If there are no specific tests recommended, then this advice can encourage the doctor to be skeptical that the condition exists, certainly could not be serious. Where does this leave the patient? Without complete medical investigation and tests, the doctor is unable to proceed with treatments.

Untrained and unsure of the disease, induced by CDC policy the patient is not treated, leading to further deterioration. Severely disabled and without the validation of medical testing, the patient is confronted with an impossible task to obtain disability assistance. Many become homeless and fatalities increase.

These policies have fostered a pervasive negative attitude toward ME Patients, of which we are well aware. There exists the common experience at hospitals: the snickering by staff when they learn you have "CFS". Or worse, the woman who went to hospital with severe respiratory symptoms, she was not properly treated, given a bottle of syrup and sent home. She died a few hours later. She was not properly treated because she was known at the hospital to have CFS.

Advance Your Understanding

At the present time the medical community is attempting to understand the symptoms of ME, attempting to gain entry with their tools and methods and physiologic models, in order to explain the disease to their colleagues. This means that at the present time it is the patient community that has a far greater understanding of the realities of ME than the medical community. To us, ME is no mystery, it is a lived experience. This is a fundamental aspect of the current situation that must be accepted in order to gain a better understanding of this disease. Doctors will learn much about this disease by listening to patients. Progress in ME treatment and research begs for the guidance of clinical science. The patients' experiences are a valuable source of valid data. Government officials will also learn much about this disease by listening to patient representatives directly affected by this disease and by the actions of this committee.

Advance your understanding. Recognize the epidemic of Myalgic Encephalomyelitis. Protect the Public.

Why We Are Here

We are here today, because a widespread epidemic of Myalgic Encephalomyelitis has descended upon this country. In less than twenty years time there are now over 1 million victims in the US alone and millions more worldwide. We are here because the national health agencies have not addressed this danger to the public health nor sought to find the cause or remedies for the suffering. We are here to inform the public that the national health agency policies are subjecting patients to a systematic denial of medical services and are maintaining doctors all across this country ignorant about this disease. These health agency policies have ensured that the cause of this disease is not discovered. These policies impact the health of thousands already disabled by ME and continue to place everyone at risk.

A principal issue must not be overlooked: Why has ME, which has an historical relationship to Polio, exploded into a worldwide epidemic, and what is the inordinate fear of the DHHS to recognize this and discover its cause?

For the health and welfare of our families, neighbors and fellow citizens everywhere, we insist that these matters be taken up now. We will not wait any longer for improvements, they must proceed now. Action to control this Epidemic must begin Now. It is time for truth and honesty. We are here for progress. Now!

http://www.geocities.com/tcjrme

TCJRME The Committee for Justice and Recognition of Myalgic Encephalomyelitis

CBT/GET "rehabilitation" -- success or failure?

A good analysis by Tom Kindlon

As has been previously been pointed out, last year a major report was
published on the Belgian CBT/GET Rehabilitation clinics for CFS.

It can be read, in French, at:
"Rapport d’évaluation concernant les centres de référence pour le syndrome
de fatigue chronique (SFC)"
http://www.inami.fgov.be/care/fr/revalidatie/studies/study-sfc-cvs/index.htm

or http://tinyurl.com/2t8em6

or, in Dutch, at:
Evaluatierapport over de referentiecentra voor het Chronisch
vermoeidheidssyndroom (CVS)
http://www.riziv.fgov.be/care/nl/revalidatie/studies/study-sfc-cvs/index.htm
or http://tinyurl.com/35btan


Dr. Bart Stouten and I have sent three previous messages to Co-Cure on the
report on the Belgian Clinics with information in English:
http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0701D&L=CO-CURE&P=R3379&I=-3&
m=16601 or http://tinyurl.com/2uqoqs

http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0701E&L=CO-CURE&P=R427&I=-3&m
=16601 or http://tinyurl.com/366v5l .

And
http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0702C&L=CO-CURE&P=R4161&I=-3
or http://tinyurl.com/225qje

Dr Eleanor Stein also discussed them at the New Horizons: International
Conference on ME/CFS Biomedical Research
http://www.meresearch.org.uk/archive/newhorizons.html

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

Over the weekend I noticed something that I thought some people might find
of interest:

Background Statistics:
- They found that 6% worked more after the rehabilitation and 10% worked
less.
- They found that 5% who were not working at the start of the rehabilitation
were working at the end of it.
- They found that overall 27% of the people who did the programme were
working at the start of the programme and 25% of the same group of people
were working at the end.


This leads to the following observation:

The only people who could work less were people who were already working (as
the people who were doing 0 hours couldn't do less).

That means that we are only looking at 27% were working at the start:
So 10/27 = 37% of the people who were working at the start, were working
less!
That's a large percentage.

Given that we know that 5% of the people who weren't working at the
start were working at the end, then they make up .05*.73=3.65% of
the 6% who were working more. So the existing workers only make up
2.35% of this (approx.). That means that, if one lets x=% working
more (of the people already working): x*(27/100)=2.35, x=8.70 so only 8.7%
of the people who were
already working, worked more compared to 37% working less!

[Full equation: (5*(73/100)) + (x*(27/100)) = 6]

Also given that 27% were working were working at the start and we
know 3.65% of the total are now working (the 5% of the 73% who
weren't working at the start), that would mean the total number working
would go up to 30.65% if nobody gave up work. But we know that only 25% of
the whole group are working at the end, so the drop
of 5.65% must come from the group who were working at the start.
This means that 5.65/27 = 20.93% of the people who were working at
the start had given up work completely by the end of the rehabilitation program.


To summarise - the new "data" in this message (not explicitly given in the
report):
Effect on work status of the CBT/GET rehabilitation program
Of the people who were working at the start of the rehabilitation program,
after the 6-month program, 8.7% were working more and 37% were working less.

21% had stopped working totally.


Another interesting statistic is regarding the amount of people who
undertook full-time working (Table 70) who were not working at the start:
It shows that 8% of the people were working 12 months after they had
finished the program.  It says that 82% of the 22 who were working were
working part-time so only 18% were working full-time.  That means that of
the 266 who started the program, 266*.18 = 3.96  i.e. 4 people (as some
rounding) out of the 266 were working full time or 4/266 = 1.5%.

[Table 70 shows that the sort of people who weren't working at the start
were out of work for a variety of periods - they weren't all out of work a
long time so it can't be claimed from this that the treatment would be
effective (say) for people who had been out of work for 6-12 months:  Of the
44 people in this group, 0 people were working at the end of the program, 1
person (2%) was working (part-time or full-time) 6 months later and 1 person
(2%) was working (part-time or full-time) 12 months after the program.
We're not told which group of people were working full-time but as was
previously pointed out, only 18% of the people back working, were working
full-time]


Remember that, as the report itself says:
"l’amélioration significative du fonctionnement socioprofessionnel des
patients est l’un des objectifs de la rééducation."
(rough translation) "significant improvement in the socioprofessional
functioning of the patients is one of the aims of the rehabilitation
(program)".


Proviso: None of these figures are likely to be exactly correct as
we're dealing with round figures (6%, 10%, 25%, 27%) but useful to
show/quote in discussions/debates (esp. given all the hype about CBT and GET
for CFS).


Tom Kindlon

PS. Let me know if I've made a mistake anywhere.  French is not my first
language.

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

Background information:

The numbers I've used are:
Table 69:
Top third of table
Activités professionnelles salariées

M1: at the start of the programme.
M2: immediatedly at the end.

Hours worked (% of 38 hour week): at start 18.3%; at end 14.9%.
Move across:
% who increased during the period (%+): 6%
% who did the same amount (%=): 84%
% who decreased during the period (%-): 10%

Table 70:
"Reprise de travail après la rééducation en fonction de la durée depuis que
les patients n’ont plus travaillé avant le début du programme de rééducation
de bilan"

Rough translation/meaning:
"The re-taking of work after the rehabilitation broken down by the length of
the time the patients had not worked before the start of the rehabilitation
programme/similar."

"Pourcentage de patients n’effectuant aucune activité professionnelle
salariée au moment du programme de rééducation de bilan mais bien …"

Percentage of the patient who were not doing any paid/professional activity
at the start of the rehabilitation programme but

"… à la fin de la rééducation:"
at the end of the programme:

5%
(6 months after: 8%; 12 months after 8%).

"82% des 22 patients reprenant le travail le font à temps partiel"
82% of the 22 patients retook part-time work.

Table 71:
"Evolution en ce qui concerne les sources de revenus des patients qui ont
suivi la rééducation. Comparaison des sources de
revenus des (mêmes) patients au moment du programme de rééducation de bilan
(= M1) et à la fin de la rééducation (= M2)."

Evolution with regard to the sources of income for patients who followed the
rehabilitation.  A comparison between the sources of income of the (same)
patients at the inception of the rehabilitation (denoted by M1) and at the
end of the rehabilitation programm (denoted by M2).

"Profession propre" = their own job.
M1: 27%
M2: 25%

* * *

The fact that people who WERE working before the therapy had to STOP working as a result of the therapy proves that CBT/GET is completely useless for CFS, and, in fact, makes things worse.

Most CFS/FMS patients I talk to say that they stopped working at their employer's behest: they were either fired or "requested to resign" (i.e., submit your resignation so the firm doesn't see its Unemployment Insurance premiums go up as a result of the firing).  So, the notion that we could work if we made the effort, or that we're "too lazy to work" is inaccurate; the simple fact is, we cannot do the work well enough to satisfy an employer.

Exercise has repeatedly been shown to objectively make CFS symptoms worse; there are testable chemical changes.  Yet, the CBT/GET lobby ignores those objective results and continues to tout the notion that coaxing and cajoling the patient to return to full activity is all that is necessary for a "cure".

This study of such rehabilitation proves that it's actually DIS-habilitation, resulting in patients being even less able to work after therapy.

I can tell you, after 7+ years of experimentation, there is a certain number of hours per week that I can work, and anything after that causes relapse.  There's no reason that someone with no supporting spouse and no SSDI benefits should choose to work less -- you need the money to pay your bills -- yet every time I made the effort to work enough hours to pay the bills, I wound up in bed for days. 

I don't need a doctor to encourage me to work ... if you have no one supporting you, the need to eat is quite enough encouragement to work.  What I need is a doctor to fix the problems that prevent me from working full-time, so that I can earn enough to pay the bills.  But when they're so focused on the idea that you simply "don't want to work", they're not addressing the viral cause for the symptoms, and if they don't fix the root of the problem, no amount of brainwashing is going to cure the patient enough to work.

Tags: CBT, GET, therapy, CFS, employment, work, rehabilitation

A Most Personal Statement from Jane Bryant

           Jane Bryant - A Most Personal Statement<?XML:NAMESPACE PREFIX = O />

One Click Group Director Jane Bryant appeals to all the readers and contributors of One Click around the world and writes:

Dear All

For disenfranchised patients in conflict from many fields and the doctors,  scientists, politicians and disparate advocacy groups et al who support them, this short paper is perhaps one of the most important that you may ever read in your lifetime. 

This paper is about David against Goliath, harnessing the power of the internet and every other means possible to raise funds to prosecute the case for patients in conflict through the courts.  It is about previously powerless patients taking the reins. Never has this been done in this way before. The eyes of the world are upon us.  This initiative may well change the face of fundraising as we know it to be today.  We are making legal history.

I would like to start by thanking everybody who has lent of their help and support in so many ways for all this time in getting this challenge of the CFS/ME NICE Guidelines by Judicial Review ready for publication, action and off the ground. Hugs, slapped backs, victory signs, the lot!   Thank you!

I would particularly like to thank James Saunders, Senior Partner of Saunders Solicitors LLP, the firm conducting this case.  The firm's sincere belief in the justice that is well overdue to all those wronged patients in conflict has kept us all going on One Click in the darkest of days, to culminate in the legal action put before you today. 

Although this case is specifically about legally challenging the appalling National Institute for Health and Clinical Excellence (NICE) CFS/ME Guidelines, the implications and importance of it are in fact much wider than this.

Whether you fully understand the extensive history of the disgraceful saga of what has been done to ME/CFS labelled patients in the <?XML:NAMESPACE PREFIX = ST1 />UK and all over the world for so many years or not is almost irrelevant in this case.

This issue is about the rights of previously powerless patients to take their case to court and to let the judiciary decide.  Not the government and not the psychiatrists, but the law.  As such, this case has worldwide appeal to millions.

The Worldwide Appeal

Other groups from different countries - all of whom read and/or distribute One Click material - may well ask: what has this Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) UK legal battle got to do with us?  The answer is simple.  Everything. 

From Australia, New Zealand, the United States, France, Germany, Italy, Switzerland to name but a few countries and everywhere else, this case of the maltreatment of patients in conflict specifically concerns YOU.

ME/CFS misdiagnosis is being carried out on a massive scale around the world because it is an easy box to tick and a simple label to append. It is the ultimate wastepaper basket diagnosis.  From cancer to variantCreutzfeldt Jakob Disease (vCJD/Mad Cow), Multiple Sclerosis, Lupus, Parvovirus Infection, Guillam-Barre, Lyme Borreliosis, Stroke and so on as but a VERY few examples, many patients have died whilst under the exclusive care of the psychiatrists who go to extraordinary lengths to bury their mistakes. 

From vaccine damage to those sick children forcibly ripped from the arms of their parents by the State through the devastating secrecy of the Family Courts with the much discredited catch-all label of Munchausen Syndrome by Proxy/FII, this legal challenge mounted by One Click concerns YOU ALL.

I fully recognise that many others have their own projects that equally deserve meritorious financial attention.  But I would say this.  One Click has helped many disparate advocacy groups and people down these years by publishing their material to maximum worldwide effect and distribution.  We have provided this service completely for free and have never asked for a penny. Not one. Now we are asking, please, in the nicest possible small way.  

We fully appreciate the financial constraints under which many labour.  But surely, even if you are on the terribly limited government benefits provided for by the State with which you are forced to eke out the most painful existence due to your ill health inability to work, you too can surely afford the equivalent of the cost of a cup of coffee and a sandwich that will help One Click and their excellent solicitors put the legal case for these patients from so many ill health walks of life? 

Of course it would be great if people could/would pledge large sums for this most deserving legal case, but we need to be realists and pragmatists.  If every person who reads One Click (between 4,000 to 8,000 hits per day on the website, every day of the week from 120 countries around the world) would pledge just £10 (or whatever currency denomination equivalent) to this Legal Appeal, our legal costs would be covered in an instant.

Please do not think for one single moment that what is being done by the psychiatric lobby to patients in Britain is none of your business.  It most certainly is - morally, ethically and legally.  If the psychiatric lobby is allowed to proceed full steam ahead without legal check with these CFS/ME NICE Guidelines successfully clinicised in Britain that are granting this lobby in excess £300 million, you may absolutely rest assured that what is being done to patients in Britain will be coming down your way very soon.  An equivalent of this is already happening in some other countries.

We are asking for pledges, please, from all of you around the world - Australia, New Zealand, the United States, everywhere.  In dollars, francs, euros, pesos, pounds, rupees, shekels, rials, rubles, bahts, dinars and yuans et al, the currency denomination is of no import.  What counts is that you make your pledge to help us all and our children.  

I will personally be contacting many of you directly, shortly. I predicate that there will not be another opportunity like this so perfectly crafted to call the psychiatric lobby to account in my lifetime and as such, I will leave no stone unturned to help patients.

History

I would now like to turn, please, to give you a very short potted history of why this legal challenge is so important.  It is impossible to encapsulate the psychiatric lobby history of some fifty years malfeasance in this short paper and so I won't even try.  Instead, I will do my poor best to provide you with the most sincere rationale of why the issue put before you today matters so much to so many and is why it is so very important.

ME/CFS labelled patients have been appalling badly treated for many years. This goes straight to the heart of Patients' Human Rights.

We illustrate, for example, the overwhelming case of very ill children forced to exercise by the psychiatrists and told that their illness is all in their heads with feeding tubes shoved into their stomachs, lying in darkened rooms or locked away from their families in psychiatric wards.  This has been done to them simply because they have had the terrible, terrible misfortune to be labelled with ME/CFS, recognised by the World Health Organisation as a neurological illness, but denied by the psychiatrists.

Numerous families have been utterly destroyed with what has gone down, with many children forcibly removed from their homes by the State under spurious grounds to force treatment. 

We give you as but one example, the case of what was done to young Ean Procter  as recounted by his Mum that is a matter of public record on the Isle of Man and everywhere else.  

This semi-paralysed eleven year old ME/CFS labelled child was deliberately thrown into a swimming pool by the psychiatrists with no floating aids to see if he would sink or swim, to ascertain whether his paralysis was genuine or not.  This is what these psychiatrists do to children in their atrocious financial championing of 'somatoform disorders'.  Ean sank and had to be rescued from the bottom of the pool.  These people nearly killed this child in an attempt to try to prove their risible 'somatoform disorders' point. This is what the psychiatrists do to ME/CFS labelled children in Britain, whether their parents approve or not.   The cases are legion and still occurring today in one f orm or another right around the world as I write this to you now.

In 1999 the BBC took up the case for patients and broadcast a chilling and devastating exposé of the plight of ME/CFS labelled patients in the Panorama programme, Sick and Tired.  Despite much public hand wringing and angst subsequent to the programme’s broadcast, once the waves of public outrage had subsided, matters moved on much the same as before.

The damaging power of the psychiatrists that has no basis in any credible science has grown exponentially down these years to become a global epidemic.  Psychiatry is the one branch of medicine that never has to prove its case and yet is permitted to wreak havoc on the lives of those that it most unjustifiably targets.

Today

So what has changed since the BBC broadcast the Panorama programme in 1999?  

Today in the year 2007, the National Institute for Health and Clinical Excellence (NICE) through a documented process of utterly corrupt medical and political manipulation of formal due process in the production of the CFS/ME Guidelines is proposing to squander £300 million of British taxpayer's money on these very same psychiatrists. 

If the CFS/ME NICE Guidelines are successfully clinicised, £300m of your money and mine will be used to completely and utterly legitimise psychiatric abuse of patients.

Benefits and insurance payments will continue to be refused and inappropriate and harmful treatments administered. New patients naive to the politics will be duped into believing that it is all being taken seriously and that the Guidelines mean that doctors have accepted that 'CFS/ME' is real. As with many of us, they may not find out until it is too late for them that the psychosocial treatments of Graded Exercise Therapy/Cognitive Behavioural Therapy (GET/CBT) and antidepressants were a one-way ticket to permanent disability.

Conclusion

If I have not managed to convince you of the crying, nay SCREAMING NEED to get behind this legal action in some small way through the use of my poor words and hard work, then I am so sorry.  I will have miserably failed patients and therefore failed you all. I will have specifically failed my child whose childhood and entire life have been absolutely ruined by the psychiatric lobby dicta that has damaged millions.

We have the opportunity to challenge the psychiatric lobby through the courts by Judicial Review. Not from a tin pot firm of back street solicitors, but from  Saunders Solicitors LLP, one of the finest in the land, so familiar with the biomedical case.

We need to bury all of our past differences.  We need the ME/CFS charities who have declared the CFS/ME NICE Guidelines as 'Unfit for Purpose' to contribute some of the money that patients have given them to support this case.  To do otherwise is completely unconscionable.

I am happy to report that since the launch of this appeal on Saturday, pledges - including those from academics and doctors - have been coming in thick and fast.  We need more. Much more. This matter is urgent. We need to obtain pledges of £20,000 in total by 5 November 2007 to bring the psychiatric lobby to account through the courts.

Because of the sensitive (and wonderful!) identities of some of the people making these pledges that are now coming in, One Click will specifically not be publishing any names. It is far more important to get the pledges in to fight this good fight than to give publicity to those good people who are making it happen. 

Here are the documents that you will need to inform your decision.

• Legal Appeal Instructions      
• NICE Guidelines - Judicial Review Legal Briefing
• Judicial Review - Legal Appeal

I personally will not rest until justice has been done.  Please join me and the One Click organisation in helping to make this happen.  Please place your pledge.

This is history being made. Please try and be part of it.

Thank you for listening.

Jane Bryant
Director
The One Click Group

 

***************************************
CFS/ME NICE GUIDELINES JUDICIAL REVIEW

*The CFS/ME NICE Guidelines have been produced by a process of documented unethical political and medical manipulation of due process.
* Please help us to challenge the atrocious actions of the National Institute for Health and Clinical Excellence (NICE) and the psychiatric lobby through the courts

What It Is: Judicial Review - CFS/ME NICE Guidelines
Who Will Conduct It: Saunders Solicitors LLP
What It Will Cost: Approximately £20,000
Pledges Due In: 5 November 2007
Court Application File Date: 22 November 2007

* See NICE Guidelines - Judicial Review Legal Briefing.
* See Judicial Review - Legal Appeal
* See Legal Appeal Instructions

Email your financial pledge to One Click and Saunders Solicitors LLP.
Our legal fundraising target is eminently reasonable and entirely possible when addressed by the collective. It is that simple.

We look forward to receiving your tangible support for this legal campaign.

FORCE NICE TO DO ITS DUTY TO ME/CFS LABELLED PATIENTS THROUGH THE COURTS NOW!
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