M.E. caused by enterovirus?

[Hip]

According to Byron Hyde, funding stopped in about 1970 after the McEvedy and Beard paper which claimed ME was mass hysteria. Wessely was late to this bandwagon, but has been busy ever since he started, despite primises he no longer does CFS research.

Yeah, you are right, Wessely and Co got onto the bandwagon a bit later in the 1980s.

Though in fact the mass hysteria view of ME/CFS given by McEvedy and Beard in 1970 was already refuted before the 70s were out. Wikipedia says:

Epidemic cases of benign myalgic encephalomyelitis were called mass hysteria by psychiatrists McEvedy and Beard in 1970, provoking criticism in letters to the editor of the British Medical Journal by attending physicians, researchers, and nurses who fell ill.The psychiatrists were faulted for not investigating the patients they described, and their conclusions have been refuted. In 1978 a symposium held at the Royal Society of Medicine concluded that epidemic myalgic encephalomyelitis was a distinct disease entity.

In an article in the Journal of Clinical Pathology, Malcolm Hooper argued myalgic encephalomyelitis should be used in place of CFS, and that research in the UK has been hijacked by a "lobby of psychologists and psychiatrists" holding significant power within the medical fraternity, with a resultant "gross abuse/neglect of patients."

So since the McEvedy and Beard mass hysteria view of ME/CFS was refuted by the end of the 1970s, it is not clear how the erroneous psychiatric view of ME/CFS continued to be promulgated.

No doubt the nefarious activities of the disability insurance industry played a major role in continuing to promote the psychiatric view of ME/CFS in the next decade.

The 1980s saw the creation of the label "chronic fatigue syndrome" by the CDC — a label which defined ME/CFS as psychiatric, rather than the extant neurological definition of myalgic encephalomyelitis — and the 1980s saw the rise of the Wessely School pseudoscience, which cast the ME/CFS disease as a psychological condition, specifically, casting ME/CFS as a disease whose symptoms were caused by the fact that you held the belief in your mind that you were ill.

All this continued to distract the medical community away from researching the enteroviral etiology that was known already back in the 1950s.

Arguably, had it not been for the distracting pseudoscience promulgated by the psychiatrists, the pursuit of the enteroviral etiology of ME/CFS would have been far more advanced by now. These meddling psychiatrists have wasted decades on fruitless psychological research, and usurped much of the research funding from what was known, even as far back as the 1950s, to be viral disease precipitated by enteroviruses (coxsackievirus and echovirus).

 

[alex3619]

The claims it was refuted do not seem to be backed up by appropriate references. I think the wikipedia is wrong. One of those references was in fact from a paper by Wessely, and it was less a refutation than a restamping with his own brand.

I am aware that Ramsay, Hyde and Hooper all dispute the McEvedy and Beard claim. However it does not seem to have had much impact.

How many doctors actually read such papers? In particular, how many psychiatrists read biomedical papers? I don't think the disputation is widely known. The only one with substance was published in the South African Medical Journal. How many mainstream docs actually read that?

I think the McEvedy and Beard paper set things up for the railroading in the 80s. I think it had influence both in the UK and the US, but I still need to do a lot more research about this. It changed attitudes, and those attitudes made many vulnerable to the claims in the 80s.

Aside from enteroviral research, I think that from 1963 the technology was available, and in wide use, to properly assess ME patients. A combination of different issues of ignorance led this to being largely ignored till about 2007. I am referring to the 2 day CPET. CPET started in the 40s but became a standard protocol about 1963, in the Bruce protocol (though the modern protocol is better). Taking into account Ramsay's observations, and the (new in 1963) protocol to assess cardiopulmonary function, ME should have been validated before even 1970.

One of the issues, as we know well in ME research, is that published scientific papers seem to have little impact on a medical community that largely is too busy, too disinterested, and too sure they know what they are doing. Doctors often don't read science, they are often only interested on material with immediate clinical use, and they don't have time to research in obscure journals. Only dedicated doctors with a personal interest, or researchers, seem to take the time.

 

[Hip]

Chronic enteroviral infection is not just associated with ME/CFS; it is also linked to type 1 diabetes:

Enterovirus infection and type 1 diabetes mellitus: systematic review and meta-analysis of observational molecular studies

In particular, it is again this hard-to-detect enteroviral RNA infection (the non-cytolytic enterovirus) that may be involved in type 1 diabetes. A non-cytolytic enterovirus infection in the insulin producing beta cells of the pancreas may be precipitating the destruction (by apoptosis) of these beta cells, leading to diabetes. Ref: here.


Wikipedia provides a list of other diseases that are linked to enterovirus:

• Amyotrophic lateral sclerosis
• ADHD
• Autoimmune diseases
• Carcinoid tumors
• Chronic fatigue syndrome
• Crohn's disease
• Diabetes mellitus type 1
• Diabetes mellitus type 2
• Dilated cardiomyopathy
• Guillain–Barré syndrome
• Myocardial infarction
• Schizophrenia

 

[Hip]

The claims it was refuted do not seem to be backed up by appropriate references. I think the wikipedia is wrong. One of those references was in fact from a paper by Wessely, and it was less a refutation than a restamping with his own brand.

The 3 June 1978 article "Epidemic myalgic encephalomyelitis" in the British Medical Journal (cited in Wikipedia) seems to refute McEvedy and Beard quite strongly. To quote this article:

Some authors [McEvedy and Beard] have attempted to dismiss this disease as hysterical, but the evidence now makes such a tenet unacceptable. Some purely psychiatric symptoms may well occur, particularly in patients entering the chronic phase. No doubt too, in an epidemic some hysterical persons will simulate these symptoms of the disease. Nevertheless, the organic basis is clear — from the finding that the putative agent can be transferred to monkeys; the detection of an increased urinary output of creatine; the persistent finding of abnormal lymphocytes in the peripheral blood of some patients; the presence of lymphocytes and an increased protein concentration in the cerebrospinal fluid of occasional patients; and the neurological findings.

 

[alex3619]

I agree that McEvedy and Beard are untenable. I am not sure it had an impact on the medical community. In my view McEvedy should not have been awarded his PhD for his study. I cite some of the same examples as the BMJ article, I found the 1955 Australian paper that the agent is blood transmissible quite interesting, especially the animal autopsy findings.

It was a nice find @Hip, I haven't seen that particular paper before.

I think we still have a tendency to think of this whole psychobabble process as rational, and scientific. I am currently of the view that its more sociological, political and in many ways a cult. The way it seems to work is not rational. If it was then psychogenic medicine would have been rejected long ago. Ris* Simon would not have his influence, at least not on this subject. Governments would not be rolling out biopsychosocial policy either, to the great detriment of the people.

As I look more and more at this, I see more and more evidence of extreme, pervasive, socially and politically and economically reinforced irrationality.

*Ris is not a typo. It spells something backwards, something that for political reasons I refuse to say or write. So its an anti-something. It was suggested on another thread, and I would like to see us adopt it.

 

[Roy S]

I agree that McEvedy and Beard are untenable. I am not sure it had an impact on the medical community. In my view McEvedy should not have been awarded his PhD for his study. I cite some of the same examples as the BMJ article, I found the 1955 Australian paper that the agent is blood transmissible quite interesting, especially the animal autopsy findings.

It was a nice find @Hip, I haven't seen that particular paper before.

I think we still have a tendency to think of this whole psychobabble process as rational, and scientific. I am currently of the view that its more sociological, political and in many ways a cult. The way it seems to work is not rational. If it was then psychogenic medicine would have been rejected long ago. Ris* Simon would not have his influence, at least not on this subject. Governments would not be rolling out biopsychosocial policy either, to the great detriment of the people.

As I look more and more at this, I see more and more evidence of extreme, pervasive, socially and politically and economically reinforced irrationality.

*Ris is not a typo. It spells something backwards, something that for political reasons I refuse to say or write. So its an anti-something. It was suggested on another thread, and I would like to see us adopt it.

Now, Alex.. Just lie on the couch and tell me how you "feel" about all of this. ;-)

http://en.wikipedia.org/wiki/Richard_Webster_(British_author)#Why_Freud_Was_Wrong

 

[alex3619]

Now, Alex.. Just lie on the couch and tell me how you "feel" about all of this. ;-)

http://en.wikipedia.org/wiki/Richard_Webster_(British_author)#Why_Freud_Was_Wrong

Oh dear, I don't know if I can put it in words! Maybe this:

(PS Webster is a very long book, but very readable.)

 

[end]

I would like to know what are people doing about there Enteroviral infection who tested Positive via Dr Chia's Lab?

Especially the Australians?

I just tested strongly Positive on all four charged slides

Although the report does not specify exacterly which Enterovirus's I am infected with....

Will start a thread maybe...

 

[Ema]

My mild (by PCR) Coxsackie virus (an enterovirus) and equally mild parvovirus B19 (not an enterovirus) cleared up within 3 months with only 1 Equilibrant daily. I did feel noticeably, but not hugely, better.

I stopped taking E after 9 months but when I began having regular flu-like symptoms again I went back on E. For me it seems to help at a low dose.

It has not been a cure, or even a really big improvement like Valcyte, but has been effective as one of many treatments that give noticeable improvement.

Worth noting-- I'm fighting back from bed bound, severe ME so what seems a smallish improvement on my scale of need could feel like a big improvement to someone with mildish ME.

Also, I've only taken 1 E daily because my enterovirus infection appears mild. Higher doses might be more effective for more serious infections.

Did you take the Equilabrant at the same time as the Valcyte?

 

[Ema]

So what testing is currently recommended to look for enterovirus?

Is the stomach biopsy still in favor?

Coxsackie A only? Or B too? Antibody tests or only PCR?

VP1? DsRNA? These aren't listed on Labcorp's menu...

Is this the ARUP test?

http://ltd.aruplab.com/Tests/Pub/2003259

Would you test for enterobacteria at the same time too? Do they often occur together?

If it makes any difference, I'm thinking of a friend with Crohn's that has failed all immunosuppressive therapies. Infection would be a good reason why...

Although I'd also be interested in an updated list just for my own interest as well.

 

[SOC]

Did you take the Equilabrant at the same time as the Valcyte?

Most of the time I was on E I was not taking Valcyte. However, I did take them together for about 6 weeks last Jan with no trouble.

 

[end]

So what testing is currently recommended to look for enterovirus?

Is the stomach biopsy still in favor?

Coxsackie A only? Or B too? Antibody tests or only PCR?

VP1? DsRNA? These aren't listed on Labcorp's menu...

Is this the ARUP test?

http://ltd.aruplab.com/Tests/Pub/2003259

Would you test for enterobacteria at the same time too? Do they often occur together?

If it makes any difference, I'm thinking of a friend with Crohn's that has failed all immunosuppressive therapies. Infection would be a good reason why...

Although I'd also be interested in an updated list just for my own interest as well.

The VP1 is the method EV Med(Dr Chia's Lab)use. Which does not determine species of EV/parvovirus from what I have infront of me

The antibody plasma test I THINK he said isn't very sensitive compared to the biopsie as there's very low infection markers in blood

Prelim reading seems to suggest ARUP leads to specificity of infection/s??

With suspected Lyme a PPTU rogue parasite/s also being factor's with myself there's a lot on my plate ATM ie lots of reading

Hip might chime in and clarify things for us re EV's

 

[end]

So what testing is currently recommended to look for enterovirus?

Is the stomach biopsy still in favor?

Coxsackie A only? Or B too? Antibody tests or only PCR?

VP1? DsRNA? These aren't listed on Labcorp's menu...

Is this the ARUP test?

http://ltd.aruplab.com/Tests/Pub/2003259

Would you test for enterobacteria at the same time too? Do they often occur together?

If it makes any difference, I'm thinking of a friend with Crohn's that has failed all immunosuppressive therapies. Infection would be a good reason why...

Although I'd also be interested in an updated list just for my own interest as well.

Re enterobacteria he uses rifampin along with Oxymatrine for a seven day stint as he thinks the EV's are an underlying cause for the small bowel bacterial overgrowth often seen in CFS/ME other forum member's have stated he seems to think EV's are responsible for other bowel issues including bowel pockets etc http://forums.phoenixrising.me/index.php?threads/equilibrant.15839/page-10

 

[Hip]

Yes, what you said @end is right:

The enterovirus antibody tests (micro-neutralization tests) at ARUP Lab (for coxsackievirus B and echovirus) do determine which species of enterovirus you have.

However, this antibody tests are not as sensitive as the enterovirus VP1 protein stain test (aka immunohistochemistry test), which tests a biopsy tissue sample from your stomach for the presence of enteroviruses.

More info about this here:
Enterovirus Foundation

 

[wastwater]

Ive given up with the whole is it a ME a cfs a cf or a fatigue illness,but I was thinking strictly speaking you should have to be part of a cluster outbreak to have ME as that is where it derived its name from.It has also been called atypical ms and encephalomyelitis,i don't mind the name encephalopathy but Its doesn't really tell you anything about the illness.

 

[heapsreal]

good name would be STUFFED UP (sleep, thinking, brain fog, fatigue, pem, pain, shit, crap, buggered,) just a short name.

 

[end]

Ive given up with the whole is it a ME a cfs a cf or a fatigue illness,but I was thinking strictly speaking you should have to be part of a cluster outbreak to have ME as that is where it derived its name from.It has also been called atypical ms and encephalomyelitis,i don't mind the name encephalopathy but Its doesn't really tell you anything about the illness.

A little of topic -

I beleive KDM's identification of Sub-Groups is important and lends to a clearer definition for each of us??

Although, do not think ANY NAME can describe the suffering we endure

I have watched people die from Cancer's(one of them being very close to me)which has led me to believe WE have more of a raw deal then they do

A term that makes sense at least someone else mentioned on this forum:

Multi-System Dysfunction Syndrome

 

[philpot]

Let me clarify something. There are NO known causes of ME. There are known triggering events, that is initial infections or injury. We do not know, for sure, than any are causal, though I think a strong case might be made they are co-causal. While many were ruled out over the decades, now we know the bases on which they were ruled out relied on flawed scientific interpretations, largely due to the immaturity of the science. Hence many are back in, and herpes and enteroviruses are back in with a vengeance.

However there was a paper published a few back that showed that all (most?) of the infections associated with ME or CFS have a similar lifecycle, with similar tissue tropisms (that is they infect similar tissues). I do not think that is coincidence. In particular they all affect the gut, and can exist inside B cells.

Enteroviruses have a marked affinity for the muscle, and herpes viruses for nerves.

Its also not ruled out that what I call the multiple hit hypothesis is involved. It could be several different infections or other processes combining to cause ME, and someone might not need to have these happen all at once, they might happen over years or decades.

I still think enteroviruses are the number one potential cause though.

Interesting comments. I think ME will end up being along similar lines to cancer in that there can be multiple reasons why it starts but which all end up with the diagnosis they call cancer. The human body by default is born with a variety of defects, and in fact it is in many cases those defects and that we are all different which stops viruses wiping us all out in one go, and in addition as we age so we accumulate many more defects.

In my opinion and based on my own data keeping ME/CFS is primarily caused by a virus but as with many things there needs to be a series of steps in order for that virus to lead to ME. Rather like a serious accident where there is found to be a string of events, remove any one and the accident does not happen. Most people who walk the planet are exposed to the same viruses but do not get ME, many get other illnesses whilst others of course remain healthy.

You make a statement that there is no known cause for ME which is correct; however there are causes and it's just that we do not know them yet. So this of course gives us hope and the day will come when we make that breakthrough. I think the research is too fragmented and someone needs to connect all the dots.

Regards.

 

[Hip]

You make a statement that there is no known cause for ME which is correct

I am not sure this is correct: it depends on how you interpret the definitions of ME, such as the Canadian consensus criteria (CCC).

Certainly it is known that some infectious agents, such as parvovirus B19 and the bacterium Chlamydia pneumoniae, do produce an disease state that satisfies the CCC.

So the issue here is whether we call this disease state ME or not.

The CCC definition of ME involves certain exclusions, which are given as follows:

Canadian Consensus Criteria — Exclusions
Exclude active disease processes that explain most of the major symptoms of fatigue, sleep disturbance, pain, and cognitive dysfunction. It is essential to exclude certain diseases, which would be tragic to miss: Addison’s disease, Cushing’s Syndrome, hypothyroidism, hyperthyroidism, iron deficiency, other treatable forms of anemia, iron overload syndrome, diabetes mellitus, and cancer. It is also essential to exclude treatable sleep disorders such as upper airway resistance syndrome and obstructive or central sleep apnea; rheumatological disorders such as rheumatoid arthritis, lupus, polymyositis and polymyalgia rheumatica; immune disorders such as AIDS; neurological disorders such as multiple sclerosis (MS), Parkinsonism, myasthenia gravis and B12 deficiency; infectious diseases such as tuberculosis, chronic hepatitis, Lyme disease, etc.; primary psychiatric disorders and substance abuse. Exclusion of other diagnoses, which cannot be reasonably excluded by the patient’s history and physical examination, is achieved by laboratory testing and imaging. If a potentially confounding medical condition is under control, then the diagnosis of ME/CFS can be entertained if patients meet the criteria otherwise.
Source: here.

As you can see, the CCC excludes "infectious diseases such as tuberculosis, chronic hepatitis, Lyme disease, etc".

This exclusion is necessary because the long term prognosis of conditions like tuberculosis and chronic hepatitis is different to ME (untreated TB is fatal; and late stage chronic hepatitis C leads to a huge ballooning of the abdomen).

However, the tricky word in that sentence is "etc".

I would argue that "etc" does not refer to infectious agents such as parvovirus B19 and Chlamydia pneumoniae, and does not refer to enteroviruses.

If we exclude enterovirus infection, how can researchers like Dr John Chia ever hope to one day prove that enteroviruses are the cause of ME? So clearly infections with enteroviruses, and other agents like parvovirus B19 and Chlamydia pneumoniae, must not be excluded from the CCC definition of ME.

Therefore, we should call parvovirus B19 and Chlamydia pneumoniae known causes of ME.

 

[Firestormm]

No. They are considered to be triggers of ME. There is a difference. Until such time as they can be identified as causing the disease itself, they remain triggers along with other known triggers.

There is something else occurring, other than the infections themselves. Not everyone who has glandular fever goes on to develop the symptoms and prognosis associated with ME. There elusive connections are between the infection and the disease state.

Why do some who have the infection, not develop the disease state that is known as ME? ME occurs after a period of time has elapsed during which a recovery would be deemed likely. It is part of the reason - I believe - why you cannot diagnosis ME from day one: but diagnosis only occurs after several months (ideally) following the trigger and this lack of recovery.

We are now at a different place in our understanding from that of the ME outbreaks where it was thought that some common but unknown 'agent' might have been responsible. In history there have been many incidences of people not recovering well - as others might - from an infection and it didn't matter what the infection might have been.

If Chia can demonstrate that enteroviruses are somehow being reactivated by something in only certain people and leading to the disease state known as ME: then that might prove part of the puzzle for some.

Why he hasn't tried to apply to NIH or elsewhere for a grant to carry out a proper controlled trial I do not know: but maybe if patients were willing they could persuade him to make an application.

He still needs to demonstrate a pathological link and to try and show what is causing this reactivation of a virus that can only be found in the gut through biopsy, and only then is reactivated in some patients.

Why don't one of you simple fire a question off to Lipkin or Mady Hornig, and ask if it is even possible for a virus to hide in the stomach, and be reactivated, and if so by what, and then if it could go on to present as ME symptoms?

You guys know this stuff better than me, but has it even been demonstrated that 'something' can reactivate enteroviruses or that they can hide in tissue?

Maybe if you asked the relevant question of Lipkin and his team, he might then approach or invite Chia for a chat and a review of his research?

If you want, draft something, and I will forward it to Columbia. We are developing quite a good rapport with the Microbiome study campaign. Just keep it brief and to the point.