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

Discussion in 'Action Alerts and Advocacy' started by Tulip, Apr 9, 2011.

  1. Tally

    Tally Senior Member

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    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.
  2. biophile

    biophile Places I'd rather be.

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    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:

  3. roxie60

    roxie60 Senior Member

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    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.
  4. taniaaust1

    taniaaust1 Senior Member

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    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.

    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. .

    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.

    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.

    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.
  5. taniaaust1

    taniaaust1 Senior Member

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    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.


    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 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.

    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).
  6. Guido den Broeder

    Guido den Broeder *****

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    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.
  7. Guido den Broeder

    Guido den Broeder *****

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

    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.
  8. Tally

    Tally Senior Member

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    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.
  9. Guido den Broeder

    Guido den Broeder *****

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    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.
  10. Bob

    Bob

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

    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.

    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.)

    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.

    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'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

    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.
    Tally likes this.
  11. Bob

    Bob

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    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?
  12. Guido den Broeder

    Guido den Broeder *****

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    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.
  13. Guido den Broeder

    Guido den Broeder *****

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    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.

    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.

    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.

    You might want to read some publications by Chia.

    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.

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

    Bob

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    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?

    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 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.
  15. user9876

    user9876 Senior Member

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    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
  16. Bob

    Bob

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    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.

    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.
  17. Bob

    Bob

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    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.

    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.

    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.

    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.)

    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.
  18. CJB

    CJB Senior Member

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

    No.
  19. Guido den Broeder

    Guido den Broeder *****

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    Which ones?

    Er, no, that was not what I posted.

    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.

    What is your point?

    Why always this negativity? Evidence is never perfect. Doesn't mean we can't use it.
  20. user9876

    user9876 Senior Member

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    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.


    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.
    Bob likes this.

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