Is it worth explaining the difference between ME and CFS to the public??

[Tally]

I don't need anyone to hear their voices. Tell me what the cure is, and I will buy it on my own. Sadly, I seriously doubt you will be able to do that.

These are quotes from ME: ICC : "Myalgic encephalomyelitis (ME), also referred to in the literature as chronic fatigue syndrome (CFS)..."

also

"The label ‘chronic fatigue syndrome’ (CFS) has persisted for many years because of the lack of knowledge
of the aetiological agents and the disease process.
In view of more recent research and clinical experience that strongly point to widespread inflammation and multisystemic neuropathology, it is more appropriate and correct to use the term ‘myalgic encephalomyelitis’ (ME)..."

As you can see, they are talking about 'terms' and 'labels', not about two different entities.

 

[biophile]

It is unfortunate that the wealth of information on ME pre-1988 has essentially been ignored despite the assumption that ME and CFS are the same. But was the state of knowledge at that time really advanced to the point where the cause and cure were "pretty much known"? Would these be, combined enterovirus and herpes infection, then respective antiviral medications or adjunctants? I'm not sure if it is that simple, but Guido den Broeder does have a point that the voices of the few are being lost among the many, especially if only a small proportion of people meeting broad CFS criteria have ME and being obscured in the research results.

It appears to me that the ICC-ME does recognize that *others* use ME and CFS synonymously in the literature. The ICC is also heavily based on research using the Fukuda criteria for CFS. However, it is difficult to pin down where exactly they stand on ME vs CFS. They do take serious issue with CFS naming and criteria, and reject Reeves/NICE defined CFS. Perhaps they view CFS as a wastebasket which includes ME?

The Holmes et al 1988 criteria (CDC), which does not mention ME (and the CDC have even once stated that ME and CFS are not the same), was based on the Lake Tahoe epidemic. According to Hyde, this was another outbreak of ME (http://www.imet.ie/imet_documents/BYRON_HYDE_little_red_book.pdf). Regarding the incubation period and type of onset in general for ME, I did some digging:

On the basis of case to case contact, attempts have been made to fix the incubation period of the disorder. In the Iceland[6], Bethesda[15], Royal Free Hospital[27] and Punta Gorda[16] outbreaks the evidence indicated an incubation period of less than one week, probably five to six days. In Los Angeles[5] the information on this point is incomplete, but a few patients became ill four days after their first exposure, indicating the minimum incubation period. On the other hand, the Middlesex Hospital[8] and Durban[18] reports suggested a longer period of two to three weeks. An incubation period of fourteen days was present in the single case in which isolated contact occurred in the small second outbreak in the Royal Free Hospital in 1956[13].

"The clinical syndrome variously called benign myalgic encephalomyelitis, Iceland disease and epidemic neuromyasthenia." - Acheson 1959

http://www.meresearch.org.uk/information/keypubs/Acheson_AmJMed.pdf

A distinct prodrome occurred in 340/420 (81 %) patients, characterized by a respiratory/gastrointestinal or 'flu-like illness in 277/340 (81 %) and lymphadenopathy and summer/autumn onset in 218/340 (64%). Alternative prodromal presentations included: acute neurological, visual or psychotic episodes, myo/pericarditis, pleurodynia, exanthems, enanthems, thyroiditis, orchitis, and mesenteric adenitis. The remaining patients, 80/420 (19%) described an insidious onset, 105/340 (31 %) reported a similar illness in family or occupational contacts not invariably followed by ME. In eleven families, an incubation period of 2-5 days for the prodrome was noted, but subsequent recognition of ME varied from a few days to 6 months.

"Myalgic encephalomyelitis--a persistent enteroviral infection?" - Dowsett et al 1990

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2429637/pdf/postmedj00163-0031.pdf

Past case definitions are not consistent with regard to the type of onset involved in ME. Ramsay [41] described the onset of ME as acute and followed by persistent and profound fatigue, including other symptoms such as dizziness, muscle tenderness, headaches and pain. Ramsay used strict criteria to select those with a syndrome commonly precipitated by infection, though he included some patients reporting a more insidious onset [4]. In contrast, the London criteria specified that there needed to be an identifiable viral illness that preceded the development of ME [45]. Hyde’s Nightingale definition [16] specified that ME had a biphasic infectious onset. Moreover, it was suggested that ME had a primary infectious phase with a 4–7 day incubation period and a secondary chronic phase that occurred 2–7 days after the first phase, and it was this phase that most characterized ME. Hyde’s Nightingale definition also states ME could have a non-infectious onset that could be precipitated by toxic chemicals and referred to this as secondary ME [16]. Goudsmit et al. [11] supported this view by indicating that the onset of ME could be triggered by other factors such as immunizations, trauma, and exposure to other chemicals.

The current definitions all seem to agree that most cases of ME have an acute onset; however, there are some disparities between the different definitions regarding the type of onset needed for diagnosis of ME. To stay consistent with the current definitions, we believe that there is a consensus for the onset of ME that can be categorized into three groups: ME-viral, ME-infectious non-viral, and ME-other. ME-viral can be described as onset precipitated by a virus, ME-infectious non-viral can be described as onset precipitated by infections such as a Lyme disease, and ME-other can be described as onset precipitated by chemical exposure or trauma. To be classified as acute, onset should occur within a one week period. In contrast, the recent ME-ICC [3] criteria indicate that onset can be acute or gradual.

"Myalgic Encephalomyelitis Case Definitions" - Jason et al 2012

http://www.ashdin.com/journals/ACPSF/K110601.pdf

 

[roxie60]

Another term that can be used in place of CFS is CFIDS. CFIDS is also on the CDC page as a disease. No idea how is compares to CFS when it comes to diagnostic criteria, but at least it sounds more serious.

CFIDS is what I first started calling what I have. It can be very confusing but I hope it does not divide us, we have enough going against us we dont need to tear each other down trying to pin down a proper name. I'm not sure after all this time we will get to chose. What is needed is a better understanding by the medical staff on how to diagnose ME/CFS/CFIDS.

 

[taniaaust1]

Thank you for your reply.
I wonder how many of us fit into this very strictly adhered definition of ME as described by Dr. Hyde.

I for example never had a spect scan done, therefore I don't know if there was injury to my CNS. I do have neurological symptoms but no confirmation that my CNS is damaged.
He also mentions Raynaud's Phenomenon where there is a change in color of the skin of the extremities when cold. - I don't have that.
He mentions there must be a vascular change with a decrease of blood volume. - never tested for that.
He talks about the fact that there must be cardiac irregularity. I just had an appointment with my cardiologist and everything is fine.
He said NO FATIGUE needs to be present, just the normal fatigue of being chronically sick.
He also yalks about POTS. - I think I have that
He talks about severe headaches. This I know I have.
He also talks about neck pain which I don't have.
He seems to say that you have to meet ALL his criteria to get a diagnosis of ME..

Why do you say that CFS is a made up disease? Every disease was discovered at some point then defined and named.
I agree that it's a crummy name but I would venture to say that very few of us can say that they meet ALL the criteria that Dr. Hyde describes.

nods crummy name too.. no one deserves to have their illness called that when so many other symptoms are present too. I say the name itself was made up.. something which CDC as far as Im aware just choose to call a ME outbreak and then water down the ME criteria till many other illnesses were also included (thing is it got so watered down that now even some ME cases dont fit and those ones cant then even get a CFS diagnoses). The Tahoe outbreak was not a newly discovered disease..but rather a missed (misdiagnosed) disease.

CFS is a mess of various illnesses lumped under one banner. The Lake Tahoe outbreak was a ME outbreak... (so it not being diagnosed as that, and given a different name was wrong).

There probably is under the banner of CFS, other unknown illnesses not yet to be discovered too. I think it is a generally known fact that many different things are coming under the banner of CFS. Its known patients arent all the same in their symptoms (hence why different subgroups are talked about etc)

Most of those at sites like this... probably dont have CFS but rather do have ME. How would one know for sure one dont have many of the ME abnormalities if certain tests arent done?? . Unfortunately most doctors are slack and do not do the tests which show up the ME abnormalities.

Is it that people want to disassociate to the name of CFS and it connotations that they want to form a new group "who are really sick" and call themselves ME?

I cant figure out why people think when a person is saying they believe the name CFS isnt correct for peoples illnesses, why then it is thought the person is also thinking about some being really sick and others not being really sick. All the people are obviously quite sick even if their symptom complexes are different.

Many of us who are very against ME being called CFS have that view cause we think it is wrong to be lumping different illnesses together, this affects research and so many other areas (having ME/CFS lumped together also hinders doctors being educated on the ME abnormalities and testing for them and also treating these.. Im a ME patient and get poorly treated for that as my specialists have been CFS ones so they dont understand what abnormalities are found in ME.. hence things like POTS went completely unlooked for an untreated).

Also research is affected when these illnesses arent separated eg CFS and ME research should get separate funding opportunties and studied separately. .

Do you think that the patients that Mr. Mikovitz studied were pure ME patients? She calls them CFS patients.

Some researchers/specialists have been forced to use the term CFS even thou they are probably studying more so ME patients, due to ME not being recognised in their countries.

I am gravely ill. Had sudden viral onset. I am exhausted most of the time. I have constant unbearable headaches. I have major sleep problems. I have many cognitive problems. I suffer from MCS. I suffer from POTS and PEM. According to the ME definition that I just read, I don not fit that "disease". I fit the "syndrome" of cfs that WAS MADE UP?
I have a major viral load in my system - EBV, HHV6, CMV and many others. My specialist diagnosed me as having CFS but, you are saying that CFS does not exist?
I don't get it.

Did you see a specialist who can tell the difference between ME and general CFS cases?
Ive seen 5-6 so called ME/CFS specialists but it turned out they only knew about CFS with none of them knowing about ME.. My CFS specialist even made a comment that a couple of my symptoms werent consistant to ME/CFS and those symptoms must mean i had something else going on... what he didnt realise is those symptoms I had which he were refering to.. as actually well known ME ones talked about by ones who studied ME epidemics!!!. As I said.. he's a CFS specialsit so dont know much about ME, so things in my case have confused him. This CFS specialists being not too familiar with ME, causes many of us not not be getting the treatments we need and may be endangering us.

What Dr Brian Hyde desribes, his defination, fits the illness I have far far better then the CFS definitions out there.

I wonder how many of us fit into this very strictly adhered definition of ME as described by Dr. Hyde.

I for example never had a spect scan done, therefore I don't know if there was injury to my CNS. I do have neurological symptoms but no confirmation that my CNS is damaged.
He also mentions Raynaud's Phenomenon where there is a change in color of the skin of the extremities when cold. - I don't have that.
He mentions there must be a vascular change with a decrease of blood volume. - never tested for that.
He talks about the fact that there must be cardiac irregularity. I just had an appointment with my cardiologist and everything is fine.
He said NO FATIGUE needs to be present, just the normal fatigue of being chronically sick.
He also yalks about POTS. - I think I have that
He talks about severe headaches. This I know I have.
He also talks about neck pain which I don't have.

Ive no idea how many of us would fit into Hydes defintion? (its been said that only one out of every 6 cases of CFs is probably ME hence why the different rates per pop given depending on what definition is being used)

My spect was normal but I suspect the ones reading it may of not known the ME abnormalities to look for so maybe there was stuff there which wasnt reported on. I show ME abnormalities in my EEGs but wasnt told as they were "non specific findings" so didnt find out i had abnormalities till I requested a copy of my test results.

I have had Raynauds, I have something on my foot which could be vascultitis?? (common in ME)
I have cardiac irregularity..but heart clinic says im fine, they missed it as it is an orthostatic issue and they didnt tilt table test. Maybe POTS too could be seen (and may of been by Hyde?) as a kind of cardiac irregularly.
I used to get the neck pain.. .. fatigue in my case isnt a huge thing. (hence how a ME patient who is now more POTsy so cant do enough to cause the fatigue well.. may not even fit the CFS definitions which keep being made up.. how many of those out now? The situation is crazy.

They are trying to use CFS to describe too many different illnesses in the one big group of illneses so there is so many definintions out there trying to cover it all.. It isnt about anyone being sicker then another group..but it is wrong for differnet illnesses to be lumped together as it affects patients and studies etc. ME is a certain illness.. an neurological diseease which also appears to be infectious, which has been around way before the 80s. It is a disease which does appear in outbreaks etc etc (does that truely sound like what the average CFs patient has, or does it sound like different disease entirely? I worry about infecting others.

The blending ME/CFS together is only some higher up attempt (gov?or insurance companies?) at trying to make ME vanish more. Not only that.. it also hides any other illnesses being diagnosed as CFS, be it disovered ones or undiscovered ones, it hides them in the pack too... It does no one a favour.

 

[taniaaust1]

M.E. did get some of it's recognition because of the research that has been done on CFS.

All that CFS research is worthless to those with ME due to the definations which were used.. different patient groups involved. Its like doing research on a group of people who just have sore fingers from all kinds of things.. and then say that research tells what is going on in Arthritis.

M.E. has always had some recognition.. some groups out there have never stopped fighting. Over time thou this battle is getting worst as things get more and more confused.

M.E. gets more coverage as a real illness since the American CFS has surfaced.
We have more members united. We can do more as a group.

ME actually in past times had its own medical journal.. yeah a ME medical journal which wasnt a CFS one (I really wish I could find out if any copies of that medical journal are about still hidden in library somewhere or something.. it would be invaluable ME info.. untampered by the CFS stuff). Ive forgotten why that journal stopped or if it was anything to do with what happened in America in the 1980s.. but ME was a real illness with coverage (its own medical journal!) before all that American CFS stuff happened.

A group is only good and strong if they all agree..unfortunately there is no way as a group this stuff can be agreed on. As some will always believe they are different things.. while things who havent been around so long..often think they are the same things. Some also have fears that they may be seen as having a "fake illness" due to the biased towards CFS, if ME and CFS are separated. That fear of separation from ME alone will keep many patients supporting to have them together.

I haven't been tested for blood volume (maybe it is written in my file and I don't remember)

I dont know anyone who's been tested for that (its only done in research i think)... so all people can go by are signs of that probably being the case eg Taking Florenif which helps low blood volume helping a person etc etc.

I believe my spect scan was normal.

the spect ME abnormalities may not be paid any attention to to doctors who arent specialising in ME. Also often non specific abnormalies info arent passed on to the patient. Always ask for a copy of your test results. (something i learnt the hard way..when so many of my abnormalities I didnt find out about until i started requesting copies of my tests).

 

[Guido den Broeder]

Many patients with e.g. Lyme or Hashimoto also get diagnosed with CFS, after which all investigation stops. Indeed, the concept of CFS does nobody any good.

The treatment of ME seems fairly straightforward. Get rid of the herpes virus, and with the false signals gone the body will rebalance (any active infections should also be treated though). Some damage remains - loss of gray matter, stress response - but a near complete recovery is currently possible, and has been for some time.

See, for instance:

Lerner M, Beqaj S, Fitzgerald JT, Gill K, Gill C, Edington J (2010), "Subset-directed antiviral treatment of 142 herpesvirus patients with chronic fatigue syndrome", Virus Adaptation and Treatment, mei, Volume 2010:2, p.47-57

Lerner uses strong antivirals. Rituximab can work as well, because it kills the B-cells where the herpes virus is hiding.

 

[Guido den Broeder]

I don't need anyone to hear their voices. Tell me what the cure is, and I will buy it on my own. Sadly, I seriously doubt you will be able to do that.

See above. Let me know as soon as you are able to buy Valaciclovir or Rituximab somewhere.

These are quotes from ME: ICC : "Myalgic encephalomyelitis (ME), also referred to in the literature as chronic fatigue syndrome (CFS)..."

also

"The label ‘chronic fatigue syndrome’ (CFS) has persisted for many years because of the lack of knowledge
of the aetiological agents and the disease process.
In view of more recent research and clinical experience that strongly point to widespread inflammation and multisystemic neuropathology, it is more appropriate and correct to use the term ‘myalgic encephalomyelitis’ (ME)..."

As you can see, they are talking about 'terms' and 'labels', not about two different entities.

They are talking about what other people are saying. Note that further down, they write:

"In a study of the Reeves empirical criteria [16], Jason et al [18] reported that (...) only ten percent (10%) of patients identified as having CFS actually had ME."

Expressions like 'also referred to', 'also known as' etc. do not indicate synonymity but rather the awareness of the author that there is an issue there.

 

[Tally]

See above. Let me know as soon as you are able to buy Valaciclovir or Rituximab somewhere.

I fully intend to try both of those drugs.

But they have not been proven to be cure, not yet. Both of them worked only on a subset of patients. Both preliminary studies have been done on a tiny number of patients. Dr. Montoya's study has still not been published yet, and Rituximab patients, if I understood correctly, mostly relapsed. In addition, most of the patients that were helped by those drugs just moved a few points up the Energy Index Point Score. it is a glimmer of hope we all need, but it is not a cure.

 

[Guido den Broeder]

142 patients (Lerner) is not tiny, and they did not 'move up a few points'.

The Rituximab results are also far better than you are saying. But the treatment may need to be repeated because there is a chance of reinfection. Phase 2 studies are currently being conducted in Norway.

But all this research could and should really have been done many years ago.

 

[Bob]

Then the CDC went to investigate an outbreak area in the 1980's, and they invented the 1984 Fukuda 'CFS' description of the illness, based on what they say they saw in the patients.

The first definition of CFS is Holmes 1988. It is fairly narrow and about 80-85% of that group has ME. Then the psychiatrists stepped in and new, wider definitions were invented, of which Fukuda 1994 (not 1984) is the one most used in CFS research. Only about 40-50% of the Fukuda group has ME.

Thanks. I said my memory is unreliable. I didn't think it was that bad though!

However, Fukuda is a broad definition, so it includes patients with just long-term 'fatigue', and doesn't specify any distinct symptoms.

You are confusing Fukuda with the Oxford criteria which indeed require only prolonged fatigue.

Yes, I wasn't accurate there, but Fukuda does not require post exertional malaise.
So CFS can be diagnosed with fatigue and just these additional symptoms, for example: unrefreshing sleep, headaches, muscle pain and joint pain.
So it's not particularly selective, but does go further than just fatigue.

Now the new International Consensus Criteria (ICC) purports to define a disease called 'ME'.
So we seem to have gone in a full circle, from ME to CFS and back to ME.

There is no such circle. ME did not become CFS (there is no mention of ME in Holmes 1988 or Fukuda 1994) and CFS did not become ME. What happened was that for some time ME was considered by some to be obsolete and that all research funding went to CFS instead.

But Fukuda was based on the patients in an ME outbreak. (Or was that the Holmes criteria?) (My memory seems to have short-circuited this week!) Whichever it was, it was supposed to describe those patients in the outbreak area. (I think I'm referring to Dr Peterson's patients in Lake Tahoe.)

The ICC is quite different to the old definitions of ME, if my memory serves me correctly (again).
So I question whether the ICC describes the same disease as the old descriptions of ME from the outbreaks.
But I don't think it's the most important issue, as decades have gone by, and we need to move forwards from where we find ourselves today, and with our current knowledge and understanding.

The ICC is more detailed, but it is intended for the same disease.

But the ICC describes quite a different illness to some of the early descriptions of the outbreak areas, so I question whether it does describe the same disease or diseases. I acknowledge the theory that different enteroviruses were implicated.

I'm not sure how many patients fitting the ICC would be from outbreak areas these days (not sure if there are any stats), but my guess is that it would be a minority from outbreak areas.

Nearly all of them, rather.

And where is the evidence for this please?
I've never seen any stats on this at all.
So I'd be very grateful to see them.

My guess is that 99% of patients on this forum are sporadic cases, and not from outbreak areas. So are all these 'sporadic' cases not 'ME' patients, even if they fit the ICC? If so, then we need the ICC to diagnose for a disease with a new name, and not for 'ME'. In this scenario, 'ME' needs to be diagnosed for separately, with something like Byron Hyde's definition, as the ICC clearly diagnoses for something other than 'ME', and then there needs to be a third category for people who don't fit the ICC's atypical ME diagnosis.

I'm not sure how many patients fitting the ICC would be from outbreak areas these days (not sure if there are any stats), but my guess is that it would be a minority from outbreak areas.

Nearly all of them, rather. (Criteria are not the disease itself, so it's never 100% but it can be 99%.) There has been a slight change in symptoms since the enterovirus triggering ME often used to be a poliovirus, which is now rare. With other enteroviruses, there is generally no paresis.

I've yet to see convincing evidence that ME is always caused by, or triggered by, enteroviruses.
I'd be grateful to see it if there is any.

Byron Hyde doesn't seem to think that the evidence is convincing, or conclusive (my emphasis):

"Doctors A. Gilliam, A. Melvin Ramsay and Elizabeth Dowsett (who assisted in much of his later work,) John Richardson of Newcastle-upon-Tyne, W.H. Lyle, Elizabeth Bell of Ruckhill Hospital James Mowbray of St Mary’s and Peter Behan all believed that the majority of primary M.E. patients fell ill following exposure to an enterovirus. (Poliovirus, ECHO, Coxsackie and the numbered viruses are the significant viruses in this group, but there are other enteroviruses that exist that have been discovered in the past few decades that do not appear in any textbook that I have perused.) I share this belief that enteroviruses are a major cause. Unfortunately, it is very difficult to recover polio and enteroviruses from live patients. Dr. James Mowbray developed a test that demonstrated enterovirus infection in many M.E. patients but I do not believe he qualified his patients by acute or gradual onset type of illness. In my tests in Ruckhill Hospital in viral infection only in acute onset patients and not in any gradual onset patients. Few physicians realize that almost all cases of poliovirus recovered from poliomyelitis victims came from cadavers. At the very least, these enteroviruses must be recovered from The Nightingale Definition of M.E. patients during their onset illness and this has rarely been done..."

http://www.nightingale.ca/documents/Nightingale_ME_Definition_en.pdf

Some people also question whether slow-onset ME is the same as fast-onset ME.

There is no slow-onset ME. The incubation time of ME is that of the triggering enterovirus, typically 4-7 days.

Even Byron Hyde recognises a gradual-onset version of ME, as a result of a chemical trigger. He calls it "Secondary ME" and "Non-Infectious M.E. Type Disease". Does the ICC mention sudden onset vs gradual onset?


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

Edited: I've added extra paragraphs and info.

 

[Bob]

The treatment of ME seems fairly straightforward. Get rid of the herpes virus, and with the false signals gone the body will rebalance (any active infections should also be treated though). Some damage remains - loss of gray matter, stress response - but a near complete recovery is currently possible, and has been for some time.

See, for instance:

Lerner M, Beqaj S, Fitzgerald JT, Gill K, Gill C, Edington J (2010), "Subset-directed antiviral treatment of 142 herpesvirus patients with chronic fatigue syndrome", Virus Adaptation and Treatment, mei, Volume 2010:2, p.47-57

Lerner uses strong antivirals. Rituximab can work as well, because it kills the B-cells where the herpes virus is hiding.

The problem with this is that there isn't enough convincing evidence to be sure that it is definitely Herpes viruses that are causing the problem in all patients. The success using anti-virals is limited and has worked on only a subset of patients, and they haven't yet successfully defined the subset, as far as I'm aware.

We do not yet know how, or why, Rituximab improves symptoms.

How do Herpes viruses fit in with the Enterovirus theory?

 

[Guido den Broeder]

The herpes virus interferes with the immune response to the enterovirus.
What Rituximab does is well known.

There is lots of research into herpes viruses outside the field of ME/CFS.

The succes of antivirals is limited because so often the wrong antivirals are used. Each herpes virus requires a different antiviral. That is why Lerner has far better results than Montoya.

 

[Guido den Broeder]

But Fukuda was based on the patients in an ME outbreak. (Or was that the Holmes criteria?) (My memory seems to have short-circuited this week!) Whichever it was, it was supposed to describe those patients in the outbreak area. (I think I'm referring to Dr Peterson's patients in Lake Tahoe.)

These criteria were not based on any research into the US outbreaks of that time. There was never a proper analysis. Peterson collected data, but nobody wanted to analyse them.

But the ICC describes quite a different illness to some of the early descriptions of the outbreak areas, so I question whether it does describe the same disease or diseases.

Not all outbreaks were studied in depth, so it is possible that some were not ME. But the ones that were studied, had so much in common that there was a worldwide consensus - in the 1950s and again in the 1970s - that they were all the same disease. The ICC is more detailed than most of the early descriptions, but it does not contradict them.

My guess is that 99% of patients on this forum are sporadic cases, and not from outbreak areas. So are all these 'sporadic' cases not 'ME' patients, even if they fit the ICC?

Outbreaks are no longer consistently recorded, so there is no way of knowing for sure. Epidemic research shows a degree of clustering. ME is more frequent in some regions of e.g. the UK than in others.

Today, ME occurs both in clusters and endemically. This may not always have been the case. The first known outbreak is that of Los Angeles in 1934, while sporadic cases of ME have been reported only since WW II.
The number and percentage of sporadic cases increased significantly when polio vaccination was introduced.

But it is a safe bet that not everyone on these forums has ME.

I've yet to see convincing evidence that ME is always caused by, or triggered by, enteroviruses.
I'd be grateful to see it if there is any.

You might want to read some publications by Chia.

Byron Hyde doesn't seem to think that the evidence is convincing, or conclusive (my emphasis): (...)

That statement is not exact. Rather, Hyde introduces non-enteroviral ME as an additional group. This is not in accordance with the WHO classification and IMHO there is no value in it. Although some complaints are the same (but not all, see Kerr), ME-like conditions caused by pesticides, metal poisoning etc. have a different pathology (including gradual onset) and a different treatment.

Does the ICC mention sudden onset vs gradual onset?

The article does, but there is nothing about onset in the criteria proper.

 

[Bob]

The herpes virus interferes with the immune response to the enterovirus.

So I'm confused... Are you saying that it is a herpes virus or an enterovirus that is causing ME? Or both? Or that a herpes virus perpetuates an enterovirus infection? In which case, is it a symbiotic relationship? And how can you tell which causes the illness, and which perpetuates it?

What Rituximab does is well known.

We know Rituximab kills B cells, but we don't know why or how it improves ME symptoms.
Rituximab might have other immune-modulating actions, or hitherto unknown actions, that contribute to an improvement in symptoms.
I can't see how killing B cells fits in with the enterovirus, or herpes, model of illness. It doesn't make any sense. Killing B cells wouldn't increase the body's ability to eliminate enteroviruses, but it would decrease it. Killing B cells would not necessarily eliminate enteroviruses, or herpes viruses, from the body, but could hypothetically, temporarily increase the number of viruses in the plasma, and could hypothetically allow the viruses to flourish in other tissues.

The succes of antivirals is limited because so often the wrong antivirals are used. Each herpes virus requires a different antiviral. That is why Lerner has far better results than Montoya.

I haven't seen any comparisons between Lerner's and Montoya's antiviral research.

But I've read that the leading researchers (doing the antiviral trials - names fail me - my brain seems to have given up this week) are attempting to base their subgroups, for antiviral treatment, on patients who are testing positive/negative for Herpes viruses, and not on types of Herpes virus.

 

[user9876]

The problem with this is that there isn't enough convincing evidence to be sure that it is definitely Herpes viruses that are causing the problem in all patients. The success using anti-virals is limited and has worked on only a subset of patients, and they haven't yet successfully defined the subset, as far as I'm aware.

We do not yet know how, or why, Rituximab improves symptoms.

How do Herpes viruses fit in with the Enterovirus theory?

I think its far from clear that Rutuximab is working to remove a virus. It is used for this purpose but seems to work quite quickly. For example its used to reduce EBV virus in patients who have had a bone marrow transplant.
http://www.nature.com/bmt/journal/v31/n11/full/1704061a.html
See Fig 1 where they are getting a reduction in the virus (and b cells) very quickly. The timing with Fluge and Mella's study seemed to take a lot longer and this ties in with comments from Jonathan Edwards around timing for RA

http://www.plosone.org/annotation/listThread.action?root=6147

 

[Bob]

The problem with this is that there isn't enough convincing evidence to be sure that it is definitely Herpes viruses that are causing the problem in all patients. The success using anti-virals is limited and has worked on only a subset of patients, and they haven't yet successfully defined the subset, as far as I'm aware.

We do not yet know how, or why, Rituximab improves symptoms.

How do Herpes viruses fit in with the Enterovirus theory?

We know Rituximab kills B cells, but we don't know why or how it improves ME symptoms.
Rituximab might have other immune-modulating actions, or hitherto unknown actions, that contribute to an improvement in symptoms.
I can't see how killing B cells fits in with the enterovirus, or herpes, model of illness. It doesn't make any sense. Killing B cells wouldn't increase the body's ability to eliminate enteroviruses, but it would decrease it. Killing B cells would not necessarily eliminate enteroviruses, or herpes viruses, from the body, but could hypothetically, temporarily increase the number of viruses in the plasma, and could hypothetically allow the viruses to flourish in other tissues.

I think its far from clear that Rutuximab is working to remove a virus. It is used for this purpose but seems to work quite quickly. For example its used to reduce EBV virus in patients who have had a bone marrow transplant.
http://www.nature.com/bmt/journal/v31/n11/full/1704061a.html
See Fig 1 where they are getting a reduction in the virus (and b cells) very quickly.

Ah, thank you... that's very interesting.
I haven't seen that paper before, and it seems to address some of my questions.
I was struck by this comment in the paper: "None of our patients developed opportunistic infections during the observation period", because I had assumed that Rituximab would seriously compromise the immune system.

Interesting that EBV levels in the plasma are quickly reduced after administration of Rituximab.

The paper says that Rituximab (indirectly or maybe directly?) eliminates the EBV found in B cells and reduces EBV in plasma. I wonder if that's the reason for it's success, or is its success based on Rituximab eliminating the early cases of malignant B cells, thus avoiding proliferation? I'll have to read the paper again, to understand it better.

The timing with Fluge and Mella's study seemed to take a lot longer and this ties in with comments from Jonathan Edwards around timing for RA

http://www.plosone.org/annotation/listThread.action?root=6147

But the reaction times in this study are not based on symptoms (as the ME study is), but are based on copy numbers. If there are viruses involved in ME, we don't know how quickly the copy numbers are reduced.
In any case, viruses other than EBV might be involved with ME, which might take longer to be eliminated or it might just mean that ME is the result of a more complex disorder of the immune system. Or the action of Rituximab in ME might not be virus-related.

 

[Bob]

But Fukuda was based on the patients in an ME outbreak. (Or was that the Holmes criteria?) (My memory seems to have short-circuited this week!) Whichever it was, it was supposed to describe those patients in the outbreak area. (I think I'm referring to Dr Peterson's patients in Lake Tahoe.)

These criteria were not based on any research into the US outbreaks of that time. There was never a proper analysis. Peterson collected data, but nobody wanted to analyse them.

Like I said earlier, the early CFS criteria were supposed to be based on the patients in the outbreak areas.
I agree that a full and proper analysis was not carried out by CDC officials, but they were supposed to investigate the outbreak.

But the ICC describes quite a different illness to some of the early descriptions of the outbreak areas, so I question whether it does describe the same disease or diseases.

Not all outbreaks were studied in depth, so it is possible that some were not ME. But the ones that were studied, had so much in common that there was a worldwide consensus - in the 1950s and again in the 1970s - that they were all the same disease. The ICC is more detailed than most of the early descriptions, but it does not contradict them.

I haven't studied them for contradictions, but the ICC does not include some of the symptoms seen in some of the early outbreaks, and I don't recognise some of those symptoms as being a symptom of ME that any of us experience.

And where is the evidence for this please?
I've never seen any stats on this at all.
So I'd be very grateful to see them.

My guess is that 99% of patients on this forum are sporadic cases, and not from outbreak areas.

Outbreaks are no longer consistently recorded, so there is no way of knowing for sure.

Well, you posted with such certainty that all ICC-diagnosed patients are from outbreaks areas, that I assumed there might be some evidence that I didn't know about. But, as I thought, there is no evidence.

I've yet to see convincing evidence that ME is always caused by, or triggered by, enteroviruses.
I'd be grateful to see it if there is any.

You might want to read some publications by Chia.

Well, that's precisely my point, because Chia's research does not support your case. Chia has done some good research, but his work only applies to a subset of his patients, and he is unable to easily test for viruses in those patients who he treats. (And maybe he is not even able to successfully test for enteroviruses in his entire subset of supposedly infected patients? But I can't remember the details here.)

Byron Hyde doesn't seem to think that the evidence is convincing, or conclusive...

That statement is not exact. Rather, Hyde introduces non-enteroviral ME as an additional group. This is not in accordance with the WHO classification and IMHO there is no value in it. Although some complaints are the same (but not all, see Kerr), ME-like conditions caused by pesticides, metal poisoning etc. have a different pathology (including gradual onset) and a different treatment.

I don't think you can have read the quote. Hyde is very clear that the evidence for enteroviral infection is only partial, and explains why. He isn't referring to what he calls "Secondary ME", but he is discussing the historic and current inadequacy of viral tests.

 

[CJB]

...................................................................................................................

For an explanation of what this thread is about, please go HERE

The history of M.E. please go HERE

In answer to your question - is it worth it explaining the difference?

No.

 

[Guido den Broeder]

I haven't studied them for contradictions, but the ICC does not include some of the symptoms seen in some of the early outbreaks, and I don't recognise some of those symptoms as being a symptom of ME that any of us experience.

Which ones?

Well, you posted with such certainty that all ICC-diagnosed patients are from outbreaks areas, (...)

Er, no, that was not what I posted.

Chia has done some good research, but his work only applies to a subset of his patients, and he is unable to easily test for viruses in those patients who he treats. (And maybe he is not even able to successfully test for enteroviruses in his entire subset of supposedly infected patients? But I can't remember the details here.)

Best read up on the details, then. Whether the test is easy is irrelevant here, I think, but few tests score 100%. I am satisfied with the 98% he reports.

Hyde is very clear that the evidence for enteroviral infection is only partial, and explains why. He isn't referring to what he calls "Secondary ME", but he is discussing the historic and current inadequacy of viral tests.

What is your point?

Why always this negativity? Evidence is never perfect. Doesn't mean we can't use it.

 

[user9876]

Ah, thank you... that's very interesting.
I haven't seen that paper before, and it seems to address some of my questions.
I was struck by this comment in the paper: "None of our patients developed opportunistic infections during the observation period", because I had assumed that Rituximab would seriously compromise the immune system.

.

Don't take that as a comment that the immune system is not compromised, its just an observation I assume to suggest other things weren't happening. Not only would the patients be on Rituximab but also immune supressants and there immune system will be seriously compromised. They may well be in an iscolation unit or if not at home and not allowed out in public places, this is normal for a bone marrow transplant patient.

I wonder if that's the reason for it's success, or is its success based on Rituximab eliminating the early cases of malignant B cells, thus avoiding proliferation?

Seems to be a standard treatment now for a bmt patient who has EBV. They do testing for malignant cells (including bone marrow tests, scans of lymph nodes) and even when negative they still do preventative treatment with Rituximab to reduce the EBV via b cell depletion. There are quite a few papers on the subject, I liked the graphs in that one since they show time. I suspect there are some interesting papers since haemotologists seem to love testing hence they will collect a lot of data about what is happening with the blood as well as looking for infection markers etc.

I don't think they believe that the EBV is removed. They say that the original problem is probably that the EBV virus is dormant in the body and that something stimulates it. With a new bone marrow you have unlearned the antibodies for the virus and it spreads quickly especially with the immune suppressants.