Malcolm Hooper 30th July 2011
with acknowledgement to members of the ME community
Tom Feilden’s notably excited introduction to his interview with Professor Simon Wessely about the disorder ME on the BBC’s Today programme on 29th July 2011 exemplified a failure to exercise the requisite journalistic neutrality when reporting a “story” (http://news.bbc.co.uk/today/hi/today/newsid_9550000/9550947.stm).
Feilden seemed excessively eager to inform the nation about Wessely’s claims of how he, a genuine scientist, is harassed and threatened by patients with ME to the extent that his mail has to be routinely scanned before he is allowed to access it and how he needs police protection as he has received death threats.
A dramatic and disturbing story by Wessely, but is it true or is it, as some people believe, an attempt to denigrate sick people and direct attention away from the ever-growing body of biomedical evidence which invalidates his own now-disproven beliefs about the disorder?
When challenged in the past to provide actual evidence – corroborated by the police -- of such threats to his life, did Wessely produce any evidence? The police take death threats seriously so each would be allocated a crime incident number. Have any of these alleged death threats been substantiated? Have there ever been any prosecutions and have they ever been reported in the press?
What must Wessely’s “protection” cost the nation in the currently straightened economic climate, and do a few immoderate emails and postings on the internet by desperate patients pushed to the brink by Wessely’s consistent denial of the very existence of the disease from which they suffer warrant such costly “protection”?
As for the “threats” allegedly suffered by Professor Myra McClure and Dr Esther Crawley, it seems they may be a matter of interpretation. Quite certainly, it is known that Professor McClure has dealt with a correspondent’s valid concerns about her work by sending a receipt six weeks later which said “Your message was deleted without being read” (http://tinyurl.com/3pftbtl) and Dr Crawley has admitted that she has not received explicit death threats but has interpreted one email in particular to constitute a death threat (http://www.bbc.co.uk/iplayer/console/b012nlcv).
Feilden seemed unaware that claiming vilification and abuse by ME patients is a regular pattern of behaviour exhibited by Wessely over the years, usually when yet more published evidence further disproves his belief that ME is perpetuated by patients wrongly attributing their symptoms to a physical disease. At such times, Wessely often appears to deflect media attention away from the emerging biomedical science by portraying himself as the victim of endless harassment from vicious and intimidating ME patients.
Is such behaviour not one of the tactics of denial used by “deniers” and “revisionists” of whatever discipline? It is common practice for “deniers” to claim that “pressure groups” are active against them and are attacking both them and the truth and to claim that there are “orchestrated campaigns” against them (“The Mental Health Movement: Persecution of Patients? Background Briefing for the House of Commons Select Health Committee”. Professor M. Hooper; December 2003: http://www.meactionuk.org.uk/Select_CTTEE_FINAL_VERSION.htm).
Can it be co-incidence that this latest well-orchestrated campaign of media coverage of the alleged threats to Wessely and his colleagues who share his views about ME has been mounted hard on the heels of the publication by Carruthers et al of the International Consensus Criteria for diagnosing ME compiled by 26 researchers and clinicians from 13 countries (Journal of Internal Medicine; Accepted Article: doi:10.1111/j.1365-2796.2011.02428.x)?
The sound biomedical evidence upon which those criteria are based completely vitiates the belief of Wessely and colleagues about the psychiatric nature of ME, so what does he do?
He once again claims he is being vilified and threatened by patients with ME and he publicly denigrates and “attacks” them by asserting that they would rather have a disease caused by a retrovirus than admit they suffer from a mental disorder.
There are many who hold that it is Wessely et al who are orchestrating a media campaign against patients with ME, not the other way round.
The campaign to “eradicate” ME by Wessely et al cannot be denied and the documented referenced evidence can be accessed at http://www.meactionuk.org.uk
In 1990 Wessely asserted that ME exists “only because well-meaning doctors have not learnt to deal effectively with suggestible patients” (Psychological Medicine 1990:20:35-53).
In 1991, he cited medical comments made between 1880 and 1908 on patients with neurasthenia, with the very clear implication that such descriptions apply equally well to today’s ME patients: “always ailing, seldom ill; a useless, noxious element of society; purely mental cases; laziness, weakness of mind and supersensitiveness characterises them all; the terror of the busy physician” (BMB 1991:47:4:919-941).
His dismissal and rejection of the biomedical evidence on ME has continued unabated.
On 6th October 2003 in her regular column “Doctor’s Notes”, Dr Margaret Cook, former wife of the late Robin Cook MP, wrote an article about Simon Wessely in The Scotsman entitled “ME sufferers have found an enemy in Wessely – so they need friends”, commenting: “It seems that he has been central to the psychiatric perspective that ME does not exist at all, and that the related “Chronic Fatigue Syndrome” is a mental condition best managed by a psychiatric therapeutic approach….He has downplayed the need for research into diagnostic markers…and such is his influence that no state funding is forthcoming to support any other research than his own….You can tell…that he is used to dictating principles and having everyone in his orbit humbly accept his gospel…When you have enemies like him, you need a powerful lot of friends”.
Wessely was both hurt and angry by that article and he demanded its retraction and an apology from The Scotsman, which meekly complied and as a result of his threats of litigation duly dispensed with the services of Dr Cook as a columnist.
Of note in relation to Feilden’s broadcast is that in Wessely’s reply to Dr Cook published in The Scotsman, he stated he had spent 15 years of his life looking after sufferers from ME.
That does not chime with the fact that for the most part he has denied the very existence of ME – how many other “caring” doctors have amused themselves by orchestrating a campaign in the BMJ about “non-diseases” and proposed that ME be one of those “non-diseases”, along with freckles and big ears, as happened in 2002?
Patients with ME know what Wessely really thinks about them, as his published views leave no room for doubt or conjecture (for illustrations of his descriptions of ME/CFS patients, see “Quotable Quotes about ME/CFS”: http://www.meactionuk.org.uk/Quotable_Quotes_Updated.pdf).
Later in October 2003, Wessely asserted that those who disagree with him and believe that ME is an organic disorder -- to whom he referred as “the radicals” -- are (quote) “crazy” and that they are “engaged in fantasies, lies and gross distortions”, that the “radicals” are left “fighting yesterday’s battles” (seemingly because he believes he has established that ME does not exist except as a false belief), that they need a “reality check” and “their behaviour is outrageous” (private communication).
Those words hardly concur with his claims to be a caring clinician who has looked after people with ME all his professional life.
Responding to Wessely’s claims of vilification and denigration by patients with ME that he made seven years ago, in his letter of 7th January 2004 to The Scotsman, Dr John Greensmith pointed out: “It is deplorable if he has been so treated, no matter how controversial his views. It is instructive, however, to examine how Professor Wessely has raised passions to this level of fervour by, perhaps, more than any other single individual, being responsible for making the area as controversial as it is”.
Referring to Wessely’s use of the term “battleground”, in a letter of 9th January 2004 to The Scotsman, DM Jones pointed out: “It is astonishing that he seemingly is blind to the fact that that this situation has arisen almost entirely due to his own prolific output and that of his like-minded collaborators, denying the existence of ME on the one hand and reclassifying (his) preferred term ‘CFS’ as a mental and behavioural disorder in the ‘WHO Guide to Mental Health in Primary Care’ on the other….Professor Wessely should be held accountable for his own role in this controversy over CFS/ME, which provides the basis for this ‘battleground’ and which has had such disastrous consequences for so many patients”.
Importantly, as Erik Johnson noted, Wessely has stated: “Right from the start, ME has been identified with a refusal to accept the doctor’s verdict” (Co-Cure EDU: 9th January 2004). Johnson drew attention to the dictum of Sir William Osler: “Listen to the patient. He is telling you his diagnosis”, commenting that Wessely’s name “threatens to stand as the epitome of physicians who refuse to listen to their patients”.
In another letter of 9th January 2004 to The Scotsman, Dr Joseph Lenz, a clinical psychologist, hit the nail on the head: “Science has no greater enemies that those who seek to confuse an issue, and those who create the most confusion are invariably those who believe that they already know the truth” (Co-Cure EDU: 10th January 2004).
This being so, can – or should -- one take at face value what Wessely says?
One moment Wessely states, as he did on 12th May 1994 in his 9th Eliot Slater Memorial Lecture: “I will argue that ME is simply a belief, the belief that one has an illness called ME” but ten years later he states, as he did in his article in the Scotsman on 5th January 2004: “I have been saying for 15 years that this is a real illness”.
Clearly both statements cannot be true.
Presently, Wessely has seized the opportunity to weave the theme of his alleged personal harassment into his responses in the current issue of Nature Reviews Neuroscience published online on 27th July 2011 (Viewpoint: Chronic fatigue syndrome: understanding a complex illness: doi:10.1038/nrn3087): in answer to the question “What is the best way for the field to make progress?”, his answer was: “So long as decent clinical and basic scientists continue to engage with the field it will make progress, although sadly that no longer includes myself….The ongoing antagonism that has been directed towards so many of the scientists who failed to replicate the original (XMRV) finding and who thus came up with what the extremists see as the ‘wrong answer’ has alienated yet another group of scientists from getting involved in this area”.
What Wessely and the media fail to acknowledge is that it was the utterly triumphant and contemptuous comments of certain of those scientists whose studies failed to replicate the original XMRV study published in Science (2009:326:585-589) that so incensed some people with ME, many of whom have daily to run the gamut of undisguised disdain amounting to abuse meted out by those who are supposed to be supporting and helping them cope with a devastating disease.
In the interests of common justice, Tom Feilden would do well to investigate the reasons why people with ME are so angry by checking the easily verifiable facts and then to redress the balance by reporting with equal enthusiasm the other side of the “battleground” because, compared with Wessely’s 25-year campaign of dismissal and denigration of extremely sick people that has resulted in no appropriate healthcare provision and in the relentless harassment by the DWP of people with ME, there may be those who consider that, whilst abusive emails and death threats are never in any circumstances to be condoned, complaints to the GMC are entirely understandable and legitimate.
July 29, 2011
via BBC, Tom Feilden
An estimated 250,000 people in the UK suffer from Chronic Fatigue Syndrome.
Scientists working on Chronic Fatigue Syndrome (CFS), or ME, say they are being subjected to a campaign of vicious abuse and intimidation that is hampering research into the causes of the condition.
The harassment has included death threats, vilification on internet websites, and a series of official complaints alleging both personal and professional misconduct to universities, ethical oversight committees and the General Medical Council (GMC).
"It's direct intimidation in the sense of letters, emails, occasional phone calls and threats," says Professor Simon Wessely, of King's College London, who has received a series of death threats and threatening phone calls, and now has his mail routinely scanned for suspect devices.
"But more often indirect intimidation through my employer or the GMC. All of it intended to denigrate and try and make you into a leper."
Behind the vitriolic nature of the attacks, the core objection, by some activists, is the association of Chronic Fatigue Syndrome with mental illness.
They claim the real cause is biological and want research to focus exclusively on identifying the - as yet undiscovered - virus responsible.
"Sadly some of the motivation seems to come from people who believe that any connection with psychiatry is tantamount to saying there is nothing wrong with you, go away, you're not really ill," says Dr Wessely.
"That's profoundly misguided. They fall victim to the label, and believe that the mere involvement of psychiatry denigrates them and denigrates the condition."
Chronic Fatigue Syndrome is a debilitating condition involving severe fatigue, painful muscles and joints, gastric complaints and poor memory and concentration. It is estimated there may be as many as a quarter of a million sufferers across the UK, but exactly what causes it is still a mystery.
That has been incredibly frustrating for patients who have often received short-shrift from doctors, and been branded as malingerers - the victims of "yuppy flu" - in the media. Even the existence of the condition has only recently received widespread acknowledgement by the medical establishment.
Speaking on the programme on Friday, ME Association's Dr Charles Shepherd condemned the abuse of researchers, but said sufferers had a justifiable complaint that almost no government-funded research was looking at the bio-medical aspects of the illness.
"The anger, the frustration, is the fact that all this effort, all this government-funding, has just been going to the psychological side," he said.
Hostility towards a psychiatric explanation for Chronic Fatigue Syndrome reached a peak in 2009 when research published in the journal Science appeared to show a link to the XMRV retrovirus.
But a series of follow-up studies failed to replicate the finding, unleashing another torrent of abuse - this time aimed at virologists, including Professor Myra McClure, of Imperial College, London.
"It really was quite staggeringly shocking, and this was all from patients who seemed to think that I had some vested interest in not finding this virus," she said. "I couldn't understand, and still can't to this day, what the logic of that was. Any virologist wants to find a new virus."
Professor McClure says she will not be doing any further research in this area, and that may be the single most important consequence of this campaign of abuse and intimidation.
According to the Wellcome Trust's Dr Mark Walport it would be a tragedy if serious researchers are put off working on Chronic Fatigue Syndrome.
"We clearly don't yet understand exactly what's going on, and if we're going to find out it needs good scientists to work on it," he says.
"But why would any scientist work on it if they know that all they're going to receive is a torrent of abuse?"
by Richard A. Van Konynenburg, Ph.D. (richvank@aol.com), February 21, 2006
For the past ten years I have been studying chronic fatigue syndrome as an independent researcher. Over the course of several years I developed a hypothesis for the pathogenesis of this disorder that prominently featured the depletion of glutathione. I presented a poster paper on this hypothesis at the AACFS (now the International Association for Chronic Fatigue Syndrome) meeting in October, 2004, in Madison, Wisconsin.
Anecdotal experience of people with CFS who acted upon my hypothesis suggested that while some were able to raise their glutathione levels by various means and experienced benefit from doing so, others were not able to do so. At the time I wrote my poster paper, I was aware of this, and I acknowledged in the conclusions of the paper that there appeared to be factors that were blocking the raising of glutathione in CFS. At that time, I was not sure specifically what they were. I also knew that there was evidence for a genetic predisposition in CFS, but I did not know the details of the genetic variations involved.
Shortly after that, I became aware of the work of S. Jill James et al. in autism (American Journal of Clinical Nutrition 2004 Dec; 80 (6):1611-7). They found that glutathione was also depleted in autistic children, that this was associated with a partial block in the methylation cycle (also called the methionine cycle), that this partial block was associated with genetic variations in the genes for certain enzymes and other proteins associated with the sulfur metabolism, and that it interfered with the synthesis of glutathione. They also found that by using certain supplements (methylcobalamin, folinic acid and trimethylglycine) they could lift the block in the methylation cycle and restore the glutathione level.
Upon learning of this work, I became very interested in possible parallels between chronic fatigue syndrome and autism. I attended the conference of the Defeat Autism Now! (DAN!) project in Long Beach, California in October, 2005, sponsored by the Autism Research Institute, headed by Dr. Bernard Rimland. As a result I became convinced that the genetic predisposition found in autism must be the same or similar to that in a major subset of chronic fatigue syndrome, and that the resulting biochemical abnormalities were also the same or similar. As far as I know, the genetic variations in people with chronic fatigue syndrome have not yet been studied in detail or published, but I am optimistic that this will occur soon, because of the rapid advances in the technology for doing so, and because of the current active interest of at least three groups in the U.S. and the U.K. in genomic aspects of CFS.
There are obviously major differences between chronic fatigue syndrome and autism. I believe that these result primarily from the different ages of onset. Autistic children experience onset early in life, before their brains are fully developed. I believe that this gives rise to the very different brain-related symptoms seen in autistic children from those seen in adults with CFS. However, there are many similarities in the biochemistry and symptoms of these two disorders as well, including oxidative stress, buildup of toxins, immune response shift to Th2, and gut problems, for examples.
The triggering factors for autism and chronic fatigue syndrome are also largely different. Although this subject remains controversial, there appears to be substantial evidence that vaccinations (containing either a mercury-based preservative or live viruses, many given within a short period of time) were responsible for triggering many of the cases of autism in genetically susceptible children (D. Geier and M.R. Geier, International Journal of Toxicology 2004 Nov-Dec; 23(6):369-76; and A.J. Wakefield, several publications beginning in 1997). In CFS, a variety of triggering factors (physical, chemical, biological, or psychological/emotional) have been found to be involved in various cases, as reviewed in my poster paper, cited above. All these factors have in common that they place a demand on glutathione.
It appears that genetically susceptible persons are unable to maintain normal glutathione levels when the total demand for it is high, and that once glutathione drops sufficiently in a genetically susceptible person, the sulfur metabolism becomes disrupted. In many cases the methylation cycle (part of the sulfur metabolism) becomes partially blocked, and the result can be a depletion of some or all of several important sulfur-containing metabolites, including S-adenosylmethionine (SAMe), cysteine, glutathione, taurine and sulfate. A vicious circle is thus formed, and the depletion in these metabolites causes an avalanche of pathogenesis, since they all have very important functions in the body. I think that much of this pathogenesis is common between autism and CFS. In autism, the loss of methylation capacity because of the drop in SAMe appears to be responsible for much of the interference with normal brain development.
There is also a major difference in the sex ratio between autism and CFS. In the book mentioned below, Dr. Jon Pangborn discusses possible reasons why autism is more prevalent in boys. In my poster paper, cited above, I suggested a hypothesis to explain the female dominance in the prevalence of CFS in adults.
I think that the reason why the people who have developed CFS as adults did not develop autism as children (even though I suspect that they have the same or a similar genetic predisposition) is that when they were children, not as many vaccinations were required. The schedule of vaccinations required for children in the U.S. has grown substantially over the past two or three decades, as has the incidence of autism. This is also true in the U.K.
Shortly after attending the DAN! conference, I also learned of the work of Dr. Amy Yasko, primarily in autism, but extending to a number of other disorders as well. Working independently of the DAN! project, Dr. Yasko develops her treatment recommendations by analyzing the specific gene variations in each patient. In addition to studying effects on the methylation cycle, Dr. Yasko has gone on to consider the effects on associated biochemistry, including folate metabolism, biopterin, the urea cycle and the synthesis of neurotransmitters.
My main message is that a great deal has already been worked out in autism by the researchers and clinicians associated with the Defeat Autism Now! project, and also by Dr. Yasko, and that I believe that the CFS community would benefit greatly by looking carefully at what they have already done. The doctors associated with the DAN! project treat autism by the use of nutritional supplements that compensate for genetic mutations in the sulfur metabolism. These include such supplements as magnesium sulfate, taurine, molybdenum, vitamin B6 and its active form P5P, magnesium, methylcobalamin, folinic acid, trimethylglycine, and dimethylglycine. They also use certain diets, and they perform chelation treatments to remove heavy metals. The results in many autistic children have been astounding, as can be seen in the webcast cited below, where several are interviewed.
Dr. Yasko, in cooperation with Dr. Garry Gordon, uses many of the same supplements as are used by the DAN! project doctors as well as some additional ones, including RNA supplements, and she is also reporting great success.
So I want to encourage everyone who has an interest in CFS to look at the results of the DAN! project and of Dr. Amy Yasko in autism.
To view videos of the talks given at the latest two DAN! conferences on the internet at no cost (unless you are paying for the internet time!), go to this site.
You can choose the more recent Long Beach conference or the earlier Boston conference. They cover much of the same material, but both are worthwhile to watch. If you want to see and hear a good explanation of the methylation cycle research, go to the Boston meeting first, so you will be able to view the talk by Jill James, who did not attend the Long Beach meeting.
After selecting one of the conferences, go to the lower left and register. This is free. They will email a password to you right away, and then you can choose a talk to watch.
Beyond this, I also want to recommend a book entitled Autism: Effective Biomedical Treatments. This is a new book (Sept. 2005). It is by Jon Pangborn, Ph.D. and Sydney Baker, M.D., a biochemist and an autism clinician, respectively. The cost for the book is $30 U.S.
This is an excellent book. It is a reference book, full of good information and good science, explained clearly. This book deals very practically with developing a treatment program for an individual child. I think that most of it will turn out to apply directly to adults with CFS as well.
In addition, I want to recommend the book by Amy Yasko entitled Genetic ByPass as part of the "Nutrigenomics Educational Starter Packet." The price is $49.95 US [note: Benetic ByPass is no longer available, though Autism: Pathways to Recovery is an excellent book by the same author a applicable to all illnesses]. It discusses treatments specifically tailored to the particular combinations of genetic variations found in different patients.
I think these two books complement each other. I would recommend reading the Pangborn and Baker book first, as it provides a good basis for understanding the technical aspects of the genetics found in the Yasko book.
Although I have been suggesting consideration of the DAN! treatments and the Yasko testing to people with CFS for only a short time, and it is too soon to draw conclusions, early feedback is very encouraging. While I am going out on a limb to some extent in announcing this now, I don't want to wait any longer, because I think this could help a lot of people. Of course, we should all keep in mind that with the current case definition of CFS we have a very heterogeneous population, and the autism treatments will very likely not help everyone who has CFS, but I am convinced that they will help a substantial subset. So I want to encourage those who have CFS and those who treat it to look into this in the strongest way I can. It could be the answer for many of you.
[Disclaimer: I have no financial interest in anything recommended in this article.]
Rich
NASA, along with the Associated Landscape Contractors of America (ALCA), conducted a classic study on the benefits of plants on indoor air.
NASA reported that houseplants were able to reduce up to 87 percent of air toxins in 24 hours. They recommended using 15 to 18 'good-sized' houseplants in 6 to 8-inch diameter containers for an 1800 square-foot house.
And not just any house plants will do. Here's a list of the top 10 anti-pollutant plants rated best by The New Ecologist.com…
- The Feston Rose plant
- Devil's Ivy
- Phalaenopsis
- English Ivy
- Parlor Ivy
- African Violets
- Christmas Cactus
- Yellow Goddess
- Garlic Vine
- Peace Lily
NASA, at the Stennis Space Center, also constructed what they called a BioHome, which incorporated bioregenerative technology with the ultimate goal of providing a life support system for permanent human habitation in space. Inside the BioHome structure are common houseplants, which NASA says act as living air purifiers to absorb as much chemical pollutants as possible from synthetic materials in the living area.
If houseplants are capable of cleansing the air in the BioHome, imagine what they could do in your home!
by Cort via Phoenix Rising Forums
Published on July 15th, 2011 11:36 AM
In this three part series we looked at the Light's exciting work on ME/CFS. First - we looked at the Light's attempt to validate their gene expression findings, then we examined what they believe may be ground zero for CFS, and finally we brought their findings together with a theory paper by Shapiro which asserted that a different kind of herpesvirus is at work in ME.
In Part IV we give the quickie version of the three papers. Thanks to the Lights and Judith Shapiro for their willingness to answer questions and, as always, to Dennis for his invaluable help getting the research papers.
Part I: the Study
Drs. Alan and Kathleen Light in combination with Dr. Lucinda Bateman and others validate their prior findings that levels of receptors on white blood cells that pick up signs of muscle distress increase tremendously in people with CFS compared to healthy controls.
During their investigation they are able to pick out two subsets; a smaller group composed of about 30% of the study participants with a high incidence of ‘POTS’ (increased heart beat/dizziness, etc. after standing) and a fairly simple problem. A key gene that is supposed to transfer blood from non-working muscles to working muscles - does not get expressed during exercise - suggesting that further study could lead to a quick fix (if the drug companies get interested).
The problems in a larger group of ME/CFS patients is more problematic as exercise appears to throw their sensory, sympathetic nervous and immune systems into disarray. This group is more complex but a key receptor involved in both producing pain after exercise and causing inflammation stands out and the Lights hope, at some point, to find a drug company that will build a drug to block this receptor - thus hopefully turning off some of the pain, fatigue and inflammation occurring after exercise in ME.
Big Study - The Lights have been able to snag a Pfizer funded study that will examine if their unique approach to gene expression works. In this study they’ll follow CFS patients in severe pain to see how they react to Lyrica. If those patients who get better find that their gene expression levels are declining as well - the Lights have proven that they’ve found biomarkers for pain and fatigue in chronic fatigue syndrome - thus setting the stage for more studies and, hopefully, more drug company involvement.
Part II - Ground Zero for ME/CFS - the Dorsal Ganglia?
The Lights believe the receptor upregulation they’re seeing in white blood cells is mirrored in central gathering places for nerves called the dorsal root ganglia (DRG) that occur just outside the spinal column. These nerve centers relay information from sensory nerves to the brain and have been implicated in a variety of neuropathic conditions.
The Lights believe an that injury to these centers is causing them to put the sympathetic nervous (‘fight or flight’) system on alert constantly and to ramp up the pain and fatigue levels in patients. This constant state of alert has an extra cost, however and that cost is the tendency of the sympathetic nervous system to begin to ignore signals for more action.
The SNS may be turned on constantly but when it’s asked to do more - ie to send more blood to muscles during exercise- it refuses to do so - thus causing the acidic conditions in the muscles that cause pain and fatigue and and propel people with ME/CFS quickly into a state of anerobic energy production.
Other factors such as receptor upregulation in the immune cells in the brain and a gene which puts the ‘fight or flight’ system more quickly into play in people with CFS may play a role as well.
The Lights will begin to test their dorsal root ganglia theory in a study to commence soon.
Part III - A Different Herpesvirus for ME/CFS?: Varicella-Zoster, Shingles the Dorsal Root Ganglia and ME
But what is actually causing the purported dorsal root ganglia dysfunction? It could be a variety of things but one may stand out. It turns out that the dorsal root ganglia aren’t just gathering places for sensory nerve cell bodies; they’re also, due to a leaky nerve/blood barrier, gathering places for herpesvirus infections.
Judith Shapiro argues in a 2009 theory article that herpesviruses attracted to the nervous system such as varicella zoster virus (VZV) (the herpesvirus that causes chickenpox and shingles) are a more likely candidate for ME/CFS than more commonly studied herpesviruses. She proposes that a varicella-zoster infection of the dorsal root ganglia or other peripheral ganglia could readily account for a number of factors in CFS the acute onset, the wide variety of symptoms, the high misery/low fatality index and the post-exertional relapse found.
Confirmation of Shapiro’s theory will be difficult given the potentially severe consequences of interfering with the DRG but new herpesvirus drugs due to come on the market in the next couple of years, some of which are specifically targeted at VZV and the Lights focus on the dorsal root ganglia, should spur more interest into this intriguing theory of ME/CFS.
 Toni Bernhard at the doctor's office From the Psychology Today blog
A debilitating illness leaves me no-win choices in the doctor's office.
Published on April 10, 2011 by Toni Bernhard, J.D. in Turning Straw Into Gold
I've been sick since 2001 when I failed to recover from what appeared to be an acute viral infection. It has left me mostly house-bound, often bed-bound. In effect, I've had the flu without the fever for almost ten years: the aches and pains, the dazed sick feeling, the low grade headache, the severe fatigue. It cost me my career as a law professor; it cost me the ability to be active in the lives of my children and grandchildren.
Because I meet the Centers for Disease Control (CDC) case definition, I've been given the diagnosis, Chronic Fatigue Syndrome (CFS). Although there have been some promising developments (a possible connection to a retrovirus; the presence of unique proteins in the spinal fluid of CFS patients), as of this writing, there's no proven cause and no cure. This is not surprising, given that so little money is allocated for research into this debilitating illness. Why? One reason is the absurd name. As others have pointed out, calling it, "Chronic Fatigue Syndrome," is like calling Emphysema, "Chronic Cough Syndrome," or Alzheimer's, "Chronic Forgetfulness Syndrome."
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On October 15, 2009, Dr. Nancy Klimas of University of Miami's Miller School of Medicine spoke about the lack of research money to The New York Times:
My H.I.V. patients for the most part are hale and hearty thanks to three decades of intense and excellent research and billions of dollars invested. Many of my C.F.S. patients, on the other hand, are terribly ill and unable to work or participate in the care of their families. I split my clinical time between the two illnesses, and I can tell you, if I had to choose between the two illnesses in 2009, I would rather have H.I.V.
When doctors ask what's wrong with me, I can give one of two answers, neither of which is satisfactory in the context of obtaining quality health care for myself and others with CFS. That leaves me in a no-win position in the doctor's office.
Option #1: If I say, "I have Chronic Fatigue Syndrome," I'm likely to be discredited as a witness to my own condition. I've had doctors tell me there's no such thing as Chronic Fatigue Syndrome. One doctor said: "Just drink some coffee."
Option #2: If I say, "I contracted a serious viral infection and never recovered," it goes down better, but by saying this, I'm undermining the effort to bring legitimacy to the illness. Legitimacy means research money. By avoiding the phrase, Chronic Fatigue Syndrome, I'm also undervaluing the lifelong work of many doctors, including Nancy Klimas, Dr. Anthony Komaroff of Harvard Medical School, Dr. Charles Lapp of the Hunter-Hopkins Center, and Dr. José Montoya of Stanford University School of Medicine, all of whom have dedicated their careers to CFS research and patient care.
A few weeks ago, I had an appointment with a doctor regarding something unrelated to my illness. The New Patient Form asked, "Are you in good health?" I checked "no." Next question: "If you checked ‘no,' please explain." How many times have I faced "please explain" on a medical form and had to choose between those two unsatisfactory options? I've lost count. I needed the best care I could get from this doctor so, playing it safe, I reluctantly took option #2 and wrote, "Contracted a serious viral infection in 2001 and never recovered."
On the back side of the form was a list of symptoms with instructions to put a check in the box next to any that applied. Looking down the list, I reached: "Fatigue." What's a person with CFS supposed to do with that choice? Most of the people I know say they're tired. But the fatigue of Chronic Fatigue Syndrome? The CFIDS Association of America calls it bone-crushing fatigue. I call it bone-crushing and sickly fatigue—that flu without the fever. Laura Hillenbrand, bestselling author of Seabiscuit and Unbroken, and a CFS sufferer herself, put it this way: "This illness is to fatigue what a nuclear bomb is to a match. It's an absurd mischaracterization."
Given no alternative but "Fatigue," I checked the box and moved on.
In the exam room, the doctor looked at my form and asked: "What's this viral infection you never recovered from?" Without using the phrase Chronic Fatigue Syndrome, I succinctly explained the different theories regarding the cause of my continued illness. He listened and then said: "What's the diagnosis?" I was cornered. "Chronic Fatigue Syndrome," I said. I watched him disengage from me. He swiveled on his stool, put his note pad down, turned back to me as if we'd just met and said: "What have you come to see me about today?"
On March 3rd, Dr. Montoya said in a talk at Stanford University that it was his dream that the medical community would someday produce a formal apology to patients for not believing them all these years when they said they were facing a real illness.
Millions of us share your dream, Dr. Montoya.
 Severe ME/CFS: Emily Collingridge From The Telegraph, By Elizabeth Grice10 Dec 2008
A succinct article on how ME/CFS manifests and changes lives in those who have very severe cases.
12:46AM GMT
This is only the third telephone conversation Emily Collingridge has been strong enough to receive this year.
She can manage to hold the phone but it is painful against her ear and her mental processes are stretched to the limit to sustain a conversation. Either her brain is racing far too fast, or running too slow, she explains. “It is as if there is a huge wall in my head. I am on one side and all my mental skills are on the other. I hope one day I will scrabble up and climb over the wall…”
Losing her cognitive ability is only part of it. Collingridge has been bedridden for three years and ill for as long as she can remember.
At 27, she is in nappies, totally dependent on her mother and is fed mainly through a peg in her stomach. She looks at the door of her darkened bedroom in Dulwich, south London, wondering if she will ever be able to walk out of it – or even towards it.
With help, she can now sit up for a few minutes a day but her legs feel dead. She asks: “Will they ever be able to support my weight?”
Her hearing has become so hypersensitive that the faintest noise registers like a fracas. Her mother brushes the carpet on her hands and knees because the sound of a vacuum cleaner is torment.
Even the hum of the central heating makes her feel ill. When Emily was at her worst, skeletal through lack of food and in terrible pain, she says that to hear people breathing in the same room was akin to being beaten up. “It was like an assault on the body.”
Unknown to them, she could hear doctors talking in whispers on the other side of her hospital room. “They were saying they thought my heart was going to fail.” For a while, she was blind because her eyelids would not open and the eye muscles were too weak to focus.
Somehow or other, Emily pulled back from the brink to which myalgic encephalomyelitis (ME) had driven her. But for two weeks last summer, unable to speak, eat or move, and feeling as though someone had slit open her back with a knife and poured acid inside, she contemplated assisted suicide.
“Every few minutes, there seemed to be a new symptom until I couldn’t stand any more. I’d read about euthanasia and wondered what it would be like, but I was incapable of asking my parents because I had no voice.
“Then by a miracle, when I was at my lowest, it started to let up a little. I turned the corner. It was truly the darkness before the dawn. If that dawn hadn’t come...”
Some years ago, when she was working for the Association of Young People with ME (AYME), Emily heard of the case of Lynn Gilderdale, the East Sussex girl bedridden for 17 years whose mother, Kay, has now been arrested on suspicion of helping her to die.
“I feel so lucky compared with her,” she says. “I had three years of nothingness, of hell, but this slight improvement has given me hope. The first time I washed my face, it was as big an achievement as when I was two years old. I can clean my teeth again.
Once it was too painful and made me sick. But I can live only in the here-and-now. If I look backward, it’s hell and if I look forward, the future is uncertain.”
Her mother, Jane, understands the Gilderdales’ hopeless anguish because she and her daughter have come close to it themselves.
“They were a brave mother and daughter and what they went through is just awful,” she says. “I have myself sat with Emily when she could do nothing and was in great pain and, for a short time, I thought her life was not worth living. It seemed so relentless. At times she did not even recognise me.
“This is such a poorly understood condition. It’s not just chronic fatigue and extreme pain, but it embraces cognitive problems, too. Emily feels as though she has lost a grasp on expressing herself. It is painful for her to be touched but I find it awful not to be able to give her a cuddle.”
Emily probably contracted ME when she was seven and started to suffer a sequence of minor illnesses, but she was not diagnosed until she was 14.
At school, she struggled and eventually had to be educated at home. Three years ago, she suffered a major relapse.
She is 5ft 8in tall but her weight had dropped to six stone because she could no longer swallow. When a feeding tube was inserted in her stomach through which she could be fed, her body went into violent spasms.
“It was terrible to see her in that degree of pain,” says her mother. “She suffered post-traumatic stress as a result.” She also contracted septicaemia and there were fears for her life.
The ability of ME to defy definition and treatment and to manifest itself in ways unimaginable to non-sufferers has made it one of the most intractable of modern illnesses.
It is a condition that still baffles and divides doctors. Emily describes how she was visited by her GP, the doctor who delivered her, when she had relapsed and his response frightened her.
“I could see I was unrecognisable to him. I could sense the fear in him. When your doctor is afraid, what can you do?”
As Dr Max Pemberton explains above, the term Chronic Fatigue Syndrome (CFS) has gradually replaced ME and the perjorative term “yuppie flu”.
But, according to Katie James, of AYME, the underlying cause of the condition has split the medical profession, patients and support groups. But there is at least no longer any doubt about its existence or its “devastating and debilitating effects”.
Sylvia Penny, who is her daughter Michelle’s sole carer, was a victim of this professional division when a paediatrician in her home city of Cardiff, and another in Durham, could not agree on her treatment.
Michelle was subjected to Graded Exercise Therapy (GET), one of the two treatments with scientifically proven value for ME (the other is cognitive behavioural therapy) for six months in 1999. But in her case, it was disastrous and her mother says she has never really recovered. She is unable to hold a pen, or feed and dress herself properly.
A widow, Sylvia looks after her 24-year-old daughter without medical or social services support. “Michelle is isolated. She has lost her youth and lost her friends. She is exhausted by visits. She used to get through five novels a week but now she struggles to read what I call trashy magazines. Her concentration has gone. This is a very cruel illness because it takes your life away and your family’s life away. It is like living in limbo.”
In most cases, parents ungrudgingly give up their lives to help their stricken children in the hope that there will be remission or even, one day, a cure.
With no self-pity, Jane Collingridge remarks in passing that she and her husband cannot travel or have holidays or even go out together as other retired couples do. That doesn’t concern them.
“The very worst thing,” she says, “is seeing Emily suffering. Life’s out there and she can’t live it.”
ProHealth.com
by Mark J Pellegrino, MD*
July 6, 2011
Dr. Pellegrino is a leading fibromyalgia specialist and author who has had FM himself since childhood. His observations of familial fibromyalgia patterns and permutations such as "the aging threshold" reflect more than 20 years' experience treating patients at the Ohio Pain & Rehab Specialists Center. Basic knowledge to help genomic researchers sort things out as we move closer to understanding and control.
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THE PROBABLE CAUSES OF FIBROMYALGIA
All of us involved in fibromyalgia, either by treating it or having it, have come to appreciate how complicated this condition is…. Most important, there is more than one way to get fibromyalgia; it is an “end point” condition with multiple ways leading to it.
One of my pet peeves is that I continue to read in the scientific literature statements such as “the cause of fibromyalgia is not currently known,” or "future research will hopefully discover the cause of fibromyalgia." This implies that we don't know anything about the causes. I have had some doctors and attorneys suggest to me that if the cause is unknown, then perhaps we are not even sure that fibromyalgia exists.
I think we can say that a number of causes of fibromyalgia are known at the present time. And I think one of our problems is that we try to be too scientific, when we really need to be more practical and logical. One difficulty is determining the difference between cause and pathological mechanism. In fibromyalgia the cause would be WHY fibromyalgia developed. The pathologic mechanism would be HOW fibromyalgia developed.
I have compiled a list of probable causes of fibromyalgia.
This list is based on my experiences and understanding of the current literature. My opinions on these probable causes may not be shared by everyone. My list of probable causes is as follows:
1. Genetics
2. Trauma
3. Connective tissue disease
4. Infection
5. Catastrophic stresses
6. Chemical exposure.
Probable FM Cause #1: GENETICS
These observations support the notion that fibromyalgia can be inherited, or at least the tendency to develop fibromyalgia is inherited:
• Physicians who see patients with fibromyalgia can recall a number of patients who are relatives.
• I have seen numerous family members,mother-daughter, sister-sister, sister-brother, etc., who have the typical symptoms and findings of fibromyalgia.
• Several members of my family have fibromyalgia through four generations!
• I also see numerous patients who tell me they have family members known to have it (their family history is positive for fibromyalgia).
• Many adult patients state they had pain as a child.
Several studies on the hereditary aspects of fibromyalgia have been published. Dr. George Waylonis and I published a study in 1989.(1)
We studied 17 families and as many first-degree relatives as we could gather up (sibling, parent, child), and concluded that:
• A number of family members had fibromyalgia in a pattern that suggested an autosomal dominant mode of inheritance. This means that if one parent has fibromyalgia, then 50% of the offspring have a chance of getting fibromyalgia, whether they are male or female.
• There also appeared to be a variable latent stage, which means that the fibromyalgia could develop at different ages in different offspring.
• There also appeared to be variable transmission (i.e., it could skip a generation).
My study found a high percentage of fibromyalgia in men with a positive family history, nearly equal to the women.
This is much different than the people who present to the doctor’s office, because among these people more than six times as many women as men will be diagnosed with Fibromyalgia. Men DO have Fibromyalgia, but they take a different course than women. Sometimes we have to go out and look for them because they do not tend to come to us to be diagnosed.
Dr. Dan Buskila from Israel performed a study looking at 60 children of 21 mothers with fibromyalgia.(2)
He found that 23% of the offspring, most of them female, have fibromyalgia. When he looked at the males with fibromyalgia, he found that the ones who were under 18 had fibromyalgia almost as frequently as the women under 18. He concluded that fibromyalgia had a major genetic component that possibly fit the autosomal dominant mode of inheritance (50% of children who have one parent with FM will have FM, whether male or female) - especially among males and females under age 18.
Dr. Buskila did another study looking at people with fibromyalgia, and many of their relatives.(3) He found that 45% of the relatives reported widespread musculoskeletal pain resembling fibromyalgia.
Other studies have supported an inherited pattern to fibromyalgia.
Dr. Muhammad Yunus performed Human Leukocyte Antigen (HLA) studies in fibromyalgia. HLAs are genetically determined molecules that are found in virtually all cells. HLA genes can be markers for certain diseases, and the results of Dr. Yunus’ HLA study suggests a genetic role in fibromyalgia.(4)
I believe that the literature, combined with accumulated clinical experience, supports a genetic cause of fibromyalgia.
A “common sense” approach would be to recognize that fibromyalgia is so common in the general population of the entire world that there must be some type of common genetic make-up that leads to it. Another logical conclusion from all of the available information is that people are genetically predisposed to getting fibromyalgia.
I think a number of people are programmed genetically to develop fibromyalgia over time, probably independent of the environment. However, for a number of others, an environmental trigger must occur (i.e., the other causes listed here and perhaps others yet unknown) for the fibromyalgia to develop.
Who Is at Risk Genetically to Develop Fibromyalgia?
I think the following can be considered at risk:
1. A child with one or both parents with fibromyalgia.
2. A child of one or both parents with a connective tissue disorder such as rheumatoid arthritis or lupus.
3. A child with a sibling who has fibromyalgia.
4. A child with a first-degree relative (parent or sibling) who has fibromyalgia.
Just because someone is a risk does not mean he or she will automatically get fibromyalgia. The right “trigger” may never happen. If a child at risk does become symptomatic with fibromyalgia, there’s a lot that can be done. (See
"Fibromyalgia in Children and Teens - Risk Factors, Symptoms, and Treatment"). Don’t assume that someone will get fibromyalgia or that it will be bad if he or she does.
Genetics Play a Role in Pain Sensitivity
Dr. George Uhl (a neurologist at Johns Hopkins) found that differences in pain perception were due to variations on the surface of nerve cells, specifically on the molecule called the mu opiate receptor. The mu receptor works by bonding with natural chemicals called peptides that help diminish the sensation of pain. Individuals who have lots of these receptors (too few mu’s!) cannot diminish the pain as well, and even small stimuli can cause severe pain.
The number of these receptors is controlled by the action of the mu opiate receptor gene. Those with fibromyalgia, or at risk for it, may be genetically mu deficient.
I believe with additional research we will be able to further clarify specific genes causing pain, identify gene expression profiles of specific subtypes of fibromyalgia, and develop genetic-specific medicines to control pain and reduce the effects of fibromyalgia.
[Note: just weeks ago, a pioneering study involving whole genome sequencing of identical twins with a rare condition found that they had inherited a "double dose" of such a gene variant, one from each parent; a "dramatic manifestation" of what in single copies the researchers believe may explain a recognized pattern of fibromyalgia symptoms among other family members.(5)]
Genetics and the “Aging Threshold”
A common story I hear from patients is that their pains gradually developed without any obvious or precipitating event. We mentioned earlier that genetics may cause some people’s fibromyalgia to develop randomly at some point, and once the pain starts it’s always there and can get worse over time. But is this process random, programmed, or subject to environmental factors? Probably a combination is involved.
I see many children and teenagers with fibromyalgia, but I see more adults in their 30’s or older when they first developed fibromyalgia symptoms. If genetics were the only factor in developing fibromyalgia, I would expect more younger patients with chronic pain complaints.
Genetic expression of a condition may take years to happen, so some people who first develop FM symptoms in their 30’s or later may have programmed genes causing the delayed expression.
Although genetics are a factor, I think there might be additional factors causing the “delayed” development of fibromyalgia; factors that I refer to as the “aging threshold.”
The aging threshold implies that as a person gets older, the threshold is lower for developing fibromyalgia. The person may be more vulnerable to getting fibromyalgia from various causes in the [probable cause list], but the aging process is also a risk for getting fibromyalgia, especially in women.
• Both men and women are found to lose their ability to inhibit chronic pain signals as they get older, and normal women already have a “defective” pain inhibitory system to begin with. Thus, any vulnerable person (who inherited fibromyalgia genes) would be less able to inhibit pain signals as he or she aged, and would become more susceptible to developing amplified pain (women more than men).
• Also, wear and tear changes on the body over time may contribute to the aging threshold. As we age, inevitably our muscles, tendons, ligaments, discs and joints show signs of deterioration accumulated micro-trauma. These deteriorating tissues may form painful areas, i.e., pain-generation. In a vulnerable person, the development of painful areas may trigger the “amplified pain” cascade.
• Additionally, hormonal changes over time can increase the risk for developing pain. For example, early menopausal women are more likely to report increased fibromyalgia pain.
If we combine these different factors, we can appreciate how the pain / fibromyalgia threshold lowers as one ages, and it appears that by the 4th or 5th decade (30’s and 40’s) the aging threshold has reached a “predictable” level - where fibromyalgia can take hold. Hence the increased frequency of fibromyalgia complaints in this age range.
Once the pain threshold drops below the body’s ability to inhibit potential / random chronic pain signals, the threshold is “breached.” Now, chronic pain signals have a better chance of propagating the amplified pain cascade of changes and lead to Fibromyalgia. (To read more on this cascade of changes, see “Fibromyalgia - Ultimately a Disease of Amplified Pain.")
Probable FM Cause # 2: TRAUMA
(See “Fibromyalgia as a Complication of Injuries.”)
Probable FM Cause # 3: CONNECTIVE TISSUE DISEASE
Many people get fibromyalgia associated with another disease, particularly rheumatic and connective tissue diseases. After genetics and trauma, I believe this type of disease is the most common cause of Fibromyalgia. Conditions in this category that can lead to reactive fibromyalgia include rheumatoid arthritis, lupus, polymyalgia rheumatica, and autoimmune disorders such as thyroiditis and Sjogren’s syndrome. Fibromyalgia does not turn into rheumatoid arthritis, lupus, or other inflammatory conditions, however.
Probable FM Cause # 4: INFECTION
(See “Infection as One Possible Cause of Fibromyalgia.”)
Probable FM Cause # 5: CATASTROPHIC STRESSES
These are synonymous with emotional trauma. These are not your everyday stresses. Rather they represent more severe stresses which can cause fibromyalgia. The mechanism is probably very similar to a physical trauma, only instead of a tissue injury, there is a stress injury that may disrupt the hypothalamic-pituitary-adrenal hormone regulation (the stress hormones).
Probable FM Cause # 6: CHEMICAL EXPOSURE
I’ve seen a number of patients who have developed fibromyalgia after chemical exposure. Usually they have inhaled fumes from offending chemicals which include petroleum oils, paint thinners, cleaning solvents, dyes, or gasses/fumes from burning products. Most of the time these patients are treated at the hospital, but have lingering symptoms and ultimately develop fibromyalgia. The mechanism whereby these chemical exposures cause fibromyalgia appears to be an allergic and/or autoimmune response that escalates and sets off the fibromyalgia cascade. Many people with fibromyalgia are sensitive to chemicals, drugs, and environmental allergens like pollen, dust and molds. A condition known as chemical sensitivity syndrome occurs when one becomes chronically fatigued and ill from exposures to various substances.
* * * *
Future Research
We may not know the specific cause for a particular individual, but every single person with fibromyalgia has a cause, and ongoing funding and research of this complicated condition will result in further understanding. Future research will continue to shed light on these factors:
1. More specific identification of Fibromyalgia subgroups and better delineation of the overall Fibromyalgia Spectrum (See “The Fibromyalgia Spectrum - Part of the Big Picture in Understanding Fibromyalgia.")
2. Better understanding of the actual pathological mechanism, and learning what specifically triggers fibromyalgia from a microscopic or cellular level.
3. The ability to predict who will get fibromyalgia and what happens over time, and to understand the risks.
4. Additional genetic research to identify specific gene markers or specific neurobiological factors that contribute to fibromyalgia. Genetic research could also identify healing factors or specific gene therapy.
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Sources:
1. "Familial occurrence of primary fibromyalgia," Archives of Physical Medicine and Rehabilitation, Jan 1989.
2. "Mechanisms of Disease: Genetics of Fibromyalgia," Nature Clinical Practice, Rheumatology, 2006.
3. "Epidemiology of Fibromyalgia," Current Pain and Headache Reports, 2003; "Genetics of Chronic Pain States," Best Practice & Research, Clinical Rhematology, 2007.
4. "Genetic linkage analysis of multicase families with fibromyalgia syndrome," Journal of Rheumatology, 1999.
5. "Will Gene Variant Discovery Explain Fibromyalgia?"
* Note: This article is excerpted with kind permission from Dr. Pellegrino’s book, Fibromyalgia, Up Close & Personal © Anadem Publishing, Inc. and Mark Pellegrino, MD, 2005. You may purchase a copy of this highly recommended book by contacting Dr. Pellegrino's office at the Ohio Pain & Rehab Specialists Center (Phone: 330-498-9865, Toll-Free: 800-529-7500).
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