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Hunting down the cause of ME/CFS & other challenging disorders - Lipkin in London
In a talk to patients in London on 3rd September, Dr. W. Ian Lipkin described the extraordinary lengths he and his team are prepared to go to in order to track down the source of an illness, with examples ranging from autism to the strange case of Kawasaki disease.
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A Tale of Two Viruses: Why AIDS Was Pinned to HIV, but CF Remains a Mystery

Discussion in 'Media, Interviews, Blogs, Talks, Events about XMRV' started by Jemal, Jan 12, 2012.

  1. Jemal

    Jemal Senior Member

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    This was posted by XMRV Global Action on Facebook. It's a column by Prof. Racaniello.

    This is the conclusion:

    http://blogs.discovermagazine.com/c...-deduce-what-does-and-doesnt-cause-a-disease/
     
    justinreilly, Waverunner, CJB and 4 others like this.
  2. Mark

    Mark Acting CEO

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    I think it's a good analysis, there is much that is very positive here and that we should applaud. For example:

    That's getting to the heart of so many of the core issues that we would wish to highlight as campaigners, and so much better than the average article, that IMO we should be enthusiastic in our support for Dr Racaniello's analysis here - it's a breath of fresh air.
     
  3. Mark

    Mark Acting CEO

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    Also, the article links to a very interesting-looking article from 1959, by Henderson and Shelokov:

    http://www.nejm.org/doi/full/10.1056/NEJM195904092601506

    Evidence from this time period is of great interest to me, because i generally find these accounts to be substantially free from the political spin that surrounds modern accounts, and thus, I believe, more objective in their description of the raw data. I am also intrigued by the comments from this time period where the authors tend very much to describe the outbreaks and the illness as a new phenomenon with which they were previously unfamiliar. I think that such evidence points clearly towards the conclusion that ME/CFS is primarily a modern phenomenon, which must be crucial in considering its aetiology. I'm not convinced by the common argument of (pseudo)sceptics that this illness has always existed but was previously unremarked; accounts like this which view the emergence of ME/CFS from within the historical context of their time strongly suggest that a new phenomenon is being described.

    Does anybody know how I can view this article without paying for it? It's from 1959 and an important historical document; it's disappointing if it is still not publicly available.
     
  4. Firestormm

    Firestormm Guest

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    Totally agree Mark. Very good coverage and summary there from Prof Racaniello. I shall have a read of that link in due course. Thanks.
     
  5. alex3619

    alex3619 Senior Member

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    I posted this on another thread but it belongs here too. One person had a comment saying that AIDS is real, CFD is not a disease. My reply, awaiting moderation, is:

    11. Alex Young aka alex3619 Says: Your comment is awaiting moderation.
    January 12th, 2012 at 9:14 pm

    In reply to: . Jon Says: January 12th, 2012 at 2:27 pm There is only one difference between AIDs and CFS. AIDs is a real disease that results in death if not treated. CFS is not a disease at all.

    This is a technicality. CFS is a syndrome and a number of definitions describe a heterogenous patient mix. The core disease that has occured in many geographical clusters (epidemics) is Myalgic Encephalomyelitis. The number of biophysical abnormalities is huge (thousands), but not routinely tested for indeed most pathology labs do not even have the required tests.

    Let me give some examples of these things to give an idea of the issues:

    1. Many with long term ME have heart damage. It is now apparent that this kind of damage might be unique to the disorder, but for most of the last ten years this was confused with regular diastolic heart failure/dysfunction. Heart biopsies frequently find viral infection when the biopsy is done, but biopsies are rare.
    2. Abnormal immune chemistry abounds. Take for example 37 kDa RNase L. It is found in most ME patients. It is also found in MS and Rheumatoid Arthritis patients, so it is not diagnostic. Most of the abnormal chemistry is shared, and so not diagnositc.
    3. Three abnormal findings have high diagnostic value and await validation: spectral coherance EEG (Komaroff); post exertional pathophysiology (Pacific Labs, Lights) and severely decreased NK cell function with a low bright cell to dim cell ratio (Bond University).

    This latter makes ME a type of non-HIV AIDS affecting NK cells and not T cells different, but not entirely different. ME has much lower mortality in the medium and short term, but the long term is questionable it doesnt kill as fast, but it does kill. Lymphoma is very common in ME patients, and some cases of Karposis sarcoma have been claimed, normallly found in HIV AIDS. However, ME morbidity is similar to HIV AIDS morbidity shortly before death ME is much more disabling during most of the disease history. Imagine feeling like an AIDS patient weeks before death, but it goes on and on and on for years and decades.

    Bye, Alex

    PS, not part of the reply to the article, I had to be highly selective in my examples. There were so many I could have talked about, but I wanted a one page reply not a book.

    PPS I can't get the Henderson article but two similar articles are here, download the pdf:
    http://journals.lww.com/smajournalonline/Citation/1959/06000/Epidemic_Neuromyasthenia.27.aspx
    http://journals.lww.com/smajournalonline/Abstract/1959/10000/Epidemic_Neuromyasthenia.6.aspx
     
  6. Firestormm

    Firestormm Guest

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    Of course 'Jon' could have been making the point that as far as he is concerned 'CFS' is a construct and not a disease per se I suppose...

    Either way there are some good and not so good comments after that article. You reckon L. Hart is that lawyer Mikovits once had? Louise Hart I recall from Cohen's article was commenting quite 'vigorously' at one point.

    Anyway, I digress and I can't sleep so am tired and I have a stack of papers to read... ho hum.. diversion therapy is required methinks...

    Sorry!
     
  7. alex3619

    alex3619 Senior Member

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    Hi Firestormm I thought of that interpretation, then had to decide that most will not see it that way and I should be addressing them. I am not really addressing Jon. Its the wider audience that has to be reached, not one individual. I too have been doing diverstion therapy - I have been rewatching the old TV show Dark Angel. Bye, Alex
     
  8. Ember

    Ember Senior Member

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    Prof. Racaneillo correctly implicates the failed consensus on a case definition in the failure of CFS research:

    But he side-steps the CDC's role in the ongoing research problem. In his November article on Prof. Racaneillo's blog, David Tuller more accurately describes the CDC's role in designing a Tower of Babel for us:

    I wonder if Prof. Racaneillo is reluctant to draw a political conclusion. He writes, While the path to understanding CFS has been clouded by non-scientific issues, in the end the main reason why we do not understand this disease is because it is extraordinarily complex. Then he undermines his own conclusion by adding, But that never stopped a good scientist.

    David Tuller, on the other hand, in describing the impact of the CDC case definitions, quotes Prof. Racaneillo:

    Tuller also quotes Lenny Jason, who himself implicates the failed consensus on a case definition in the failure of CFS research:

    This morning, Prof. Racaneillo chooses to blame the politics surrounding the ongoing research problem on the failed research itself: The amount of money spent on a disease for research is driven in large part by how much progress is made (comment #21). David Tuller concludes differently, For the most part, the elements of the CFS program that Dr. Reeves championedthe empiric criteria, the name of the illness, (most of) the disputed website information, etc. remain in place under Dr. Unger (http://www.virology.ws/2011/11/23/chronic-fatigue-syndrome-and-the-cdc-a-long-tangled-tale/).
     
  9. alex3619

    alex3619 Senior Member

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    I have added another reply, in response to a comment by in vitro infidelum:

    35. Alex Young aka alex3619 Says:
    January 14th, 2012 at 8:46 am

    I am the other Alex, there are two on this page.

    I am in partial agreement with in vitro in post 33. There is still insufficient evidence to equate post viral fatigue with ME. They may not be the same thing. This is one of the problems we face. Are we talking about one or several discrete but similar diseases? Are we talking about one disease with a spectrum of manifestations? Are we talking about as subset of post viral fatigue becoming ME? (I think this latter case is the most likely at this point.) Without reliable biomarkers the research can never really address these questions.

    Confusion between PVFS and ME may also be responsible for much of the uncertainty over prognosis. For example, most cases of PVFS resolve themselves in a few months to five years at the outside. Looking at data over the five year mark, most long term ME patients never recover. If the under five year data is a combination of ME and PVFS this would explain the discrepancy. Since most people see those with PVFS recover, it would also explain why they do not understand why those with ME do not. But is this explanation correct? We need biomarkers to proceed.

    Bye, Alex
     
  10. Firestormm

    Firestormm Guest

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    Ember,

    Great post. I think though it should always be remembered that Vincent Racaniello is a virologist. That's his interest and that's his principal motivation for writing.

    Edit:

    Found his comment now:

    21. Vincent Racaniello Says:
    January 13th, 2012 at 7:35 am

    The amount of money spent on a disease for research is driven in large part by how much progress is made. When HIV-1 was discovered, huge amounts of money were allocated for its study because there were so many clear paths. At one point there were seven study sections at NIH reviewing AIDS grants, and one study section for the rest of virology. That caused consternation as you might imagine. If XMRV had panned out as a CFS cause, you would certainly seen much more money poured into CFS research. Its a chicken-and-egg problem, but that is the way science works. When you get an NIH grant, you are expected to use some of the money to explore other areas, and if you get interesting results, they can be used to secure additional funding.
     
  11. Firestormm

    Firestormm Guest

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    IVI's comment:

    '24. In Vitro Infidelium Says:
    January 13th, 2012 at 12:46 pm

    VR wrote: Hoever, there is plausible evidence for an infectious etiology, including observations that the disease is known to occur in outbreaks. Furthermore, in many cases the onset of symptoms appears to begin with a flu-like illness.

    There is a double dose of a priori reasoning being applied here. There is no secure epidemiology that can reliably demonstrate commonality of illnes either within reported outbreak cohorts, or between outbreak cohorts; in addition the linkage of symptom onset is a feature wholly of patient report, not of any validated assessment. That is not to say that outbreaks are not representative of occurences of highly localised epidemilogical features of M.E/CFS, nor that M.E/CFS is not characterised by an acute onset, but at this stage these remain speculative features, not definitive descriptions.

    While an event characterised by multiple individuals displaying symptoms of a communicable infection which is followed by a chronicity of symptoms that are typical of M.E/CFS is clearly suggestive of an involvement of infection within the aetiology of M.E/CFS, there are simply too many confounding factors to allow a conclusion that M.E/CFS is unequivocally explained by an infection mediated aetiology. It must be asked that if the assumed infectious agent is active in a given population, then what proportion of that population will becom infected, what proportion of those infected will display acute symptoms and what proportion of those who are a) infected and asymptomatic b) infected and display an accute symptomology go to develop a chronic condition that is describable as M.E/CFS ? If we were talking about HIV, the answer to the third part of the question is would be something close to 100% for both a) and b), yet we have no such evidence in the M.E/CFS that infection necessarily equates to chronic disease. In the case of M.E/CFS infection appears only to be associative, not directly causative, something which is echoed in one of the few epidemiologically consistent observations of M.E/CFS patients, that is, there is a strong imbalance in gender representation women being diagnosed at a much higher rate than men. Unless a very unusual exposure process is in play, then the gender imbalance issue is a major stumbling block for any hypothesis of M.E/CFS that is founded on a purely infectious causation.

    The patient reported association with acute onset coincident with a viral infection is also problematic. It is of course axiomatically impossibe to have planned a prospective test of a patients health prior to their reporting illness, and the patients observations may well be important evidence. However it can not be discounted that there may have been low level symptomology present prior to an acute infection, with that symptomology being entirely independent of any infection, or alternatively that an infection may be a trigger for an underlying but asymtomatic condition. Given the level of disbelief which has histerically met M.E/CFS patients encountering medical services, there may be very strng predisposition for patients to locate the commencement of chronic illness at point that is coincident with an accepted state of illness in the very natural attempt to provide validity for their very real chronic illhealth.

    M.E/CFS is a complex illness that demands significant commitment of research effort, that effort can not be short cut by poorly stated hypotheses, and only through research which is conducted in relation to the known characteristics of the illness can real progress be made. M.E/CFS most certainly is not like HIV, it is nevertheless a debilitating illness and the lack of progress in understanding it undoubtedly raises questions about the perspectives of the medical profession, the research fraternity and polititions.'


    The article has certainly led to an interesting exchange of comments I think. Kinda cuts to the chase in many respects, doesn't it?

    Personally, I still feel that 'CFS/ME' is too big a 'pot' and that research will only progress if that 'pot' can become smaller 'pots' whose patients fit more relevant and testable criteria.

    Even the ICCME doesn't go far enough - even if it does progress to testing. If we are considering 'viral causation' then we need to consider better testing at the point of diagnosis.

    This idea of leaving it until it develops - which can be six months or more from the point of acute infection (assuming there is such a point of course) - seems to me to be too late.

    But, if you don't test and find what that infection is in the first place.... what's the point of moving the diagnosis point forward e.g. from 6 months to 1 month if indeed this is even prudent for a condition that at present depends on our inability to 'recover' post-infection?

    So you could - in theory - be looking at a total reorganisation of the way in which people are investigated and treated when reporting symptoms of viral infection. That each and every person is thoroughly tested to find what that virus is - not as at present when one is diagnosed generally with 'a viral infection'.

    And what do you do with folk whose diagnosis is 'a viral infection' but whose virus cannot be found? This is assuming of course that a virus is responsible and I don't personally believe it is.

    So define 'it' and how 'it' might infect and cause CFS/ME (whatever) in such a seemingly random (but more female orientated) group people. I don't think you ever will.

    Indeed, I would rather (as I have said countless times before) they look at our immune systems - and although you still run into the same problems as above and in the article - I do believe that it is predominantly 'immune dysfunction' (even perhaps some autoimmune thing) that is preventing me from 'recovering' and indeed 'relapsing' when a(nother) virus takes hold - as has happened in my case.

    As far as I am concerned there is no 'one virus' responsible and that includes retroviruses. It just doesn't make sense. But I remain open-minded when it comes to published research of any description of course - I just don't 'buy' into the speculation or indeed vaccine causation either by the way and just for the record.
     
  12. alex3619

    alex3619 Senior Member

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    Hi Firestormm, historically I have had the perspective (since 1993) that ME (CFS to me back then) had many triggers but was actually a heterogenous mix of immune and biochemical malfunctions, but that most CFS patients (Holmes definition) had the same disorder, with a minority having other similar disorders. There is not much doubt about viral triggers. There is not much doubt about immune dysfunction. The arguments are all about where the pieces fit, how many pieces there are, and which are the most important. For that we need science, but for good science we need funding and biomarkers (probably more than one). Bye, Alex
     
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  13. Firestormm

    Firestormm Guest

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    Agreed. And 'liked'.
     
  14. alex3619

    alex3619 Senior Member

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    On the same article comments I have added:

    I suspect that for many drugs and therapies that are applied to ME patients there is a huge gap between the evidence base and actual results. Patients often respond far differently to the norm, especially for drugs that involve serotonin or vasoregulation chemistry. Similarly many of the CFS studies are a mixture of psychiatric fatigue, idiopathic fatigue, PVFS and ME. In addition, using the ICC ME severity scale, most patients in such studies are mild patients, with maybe a few moderate patients thrown in. I am at the severe end of moderate but could not get into a local study due to the issues that only moderate ME cause, particularly with capacity to travel. So there is almost NO evidence base at all for severe and very severe ME patients, and very little of relevance to moderate patients. So when someone says a treatment is based on "evidence based medicine" what they mean is they are using evidence that applies to someone else if you are moderate or worse.

    As a result most doctors are experimenting on ME patients with every therapy. Patients are also experimenting on themselves. This is due to the severe underfunding of quality science over many decades. This experimentation appliesto "evidence" based approaches as much as others, perhaps more so since they have an unvalidated standard of evidence.
     
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  15. justinreilly

    justinreilly Stop the IoM & P2P! Adopt CCC!

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    I thought this was a very good article, 'considering'. He was wrong in concluding the main problem was the complexity, though that is a big problem. Otherwise, excellent. My badgering got him to finally read David Tuller's guest post on his blog and now, to his credit he has given a shout out to it here. Overall, I think he is a good guy and fair, but he does need to be led to the truth, as many others must, so don't give up!
     

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