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JIM: Van der Meer and Lloyd Critique International Consensus Criteria ME

Discussion in 'General ME/CFS News' started by Firestormm, Jan 23, 2012.

  1. Firestormm

    Firestormm Content Team Lead

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    With thanks to Anne for flagging this one: http://forums.phoenixrising.me/show...ectorate-Recommends-ICCME&p=235742#post235742

    I needed to reformat the editorial comment in order to better be able to read it and figured it warranted it's own thread.

    So far as I can recall, this represents the first critique of the 'new' consensus criteria:

    Journal of Internal Medicine Volume 271, Issue 1, pages 2931, January 2012:

    http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2011.02468.x/full
    http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2011.02468.x/pdf

    Editorial Comment

    A controversial consensus comment on article by Broderick et al


    'Recently, Journal of Internal Medicine published a consensus paper regarding chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) [1].

    Although trying to reach a consensus for improved diagnostic criteria for difficult medical disorders such as CFS?ME is commendable, this paper falls well short in many respects.

    It cannot be denied CFS?ME is a controversial condition. The controversy sometimes deteriorating into overt dispute is between those that believe that it is a nonexistent illness (maladie imaginaire); those that feel it is a psychiatric disorder; and the activists (comprising patients, doctors and even some scientists) who are convinced of a somatic disease all are unfortunately simplistic perspectives on a complex disorder.

    Separately, there are clinicians and scientists with an open mind, who recognize the disability associated with this enigmatic clinical illness, and who seek to engage scientifically in the challenge of defining the pathophysiology, and are therefore motivated to elucidate the biological basis of CFS in a systematic and unbiased fashion.

    This dispute between the various protagonists recently surfaced with the PACE trial published in the Lancet [2], which provided evidence for effectiveness of elements of cognitive-behavioural therapy (CBT) and graded exercise therapy (GET) for patients with CFS. This publication triggered unscientific and sometimes personal attacks on the researchers in both the scientific literature [310] and via the Internet [11].

    Similarly, the recent controversy on the role of the retrovirus, XMRV, in CFS [12] is a good example of how science and emotion (in this case mostly fear of contagion) commonly collide with regard to CFS [1320].

    Ultimately, only high-quality science will prevail. Quite a bit of mediocre research has been carried out in relation to CFS featuring poorly defined subject groups, inadequate sample sizes, utilizing non-validated assay systems, etc. Not unsurprisingly, much of that research is irreproducible when performed in a methodologically rigorous fashion. Overall, this implies that the database of solid scientific findings is rather small. Notably, no reproducible diagnostic test or even a consistently correlated biomarker has been unearthed.

    Designing diagnostic criteria is very difficult without such a marker, i.e. a gold standard [21]. In the absence of biomarkers, the resultant criteria are very prone to the individual biases of the group formulating them.

    One of the first questions in this process is: what is the purpose of the criteria? It makes quite a difference whether they intended for research in which case specificity is paramount (that is, do the criteria reliably identify only subjects with the disorder?). By contrast, if the purpose is epidemiological, for instance to understand the burden of disease in the community, sensitivity becomes paramount.

    Finally, if the intent is clinical that is to facilitate the diagnosis in individual patients a mix of these parameters is relevant. Regardless of the intent, once drafted, the criteria will only achieve validity by empirical testing in different health care and cultural settings [2224].

    In the consensus paper, these issues are discussed under Application of criteria, but the recommendations have no credible rationale for example, the recommendation in the application of the criteria in clinical settings is Determine whether symptom cluster patterns are congruent with those expected from dysfunction of an underlying causal system. Given that the underlying causal system(s) are unknown, this has no clinical utility.

    Similarly, in a research context, the authors suggest that the proposed criteria: focus on symptom patterns, which increase reliability. The International Symptom Scale ensures consistency in the way questions are asked and further increases the reliability of data collected in different locations. These statements are unreferenced, and the nominated scale is unpublished.

    By contrast, this approach has already been proposed and applied [25], in relation to the existing international criteria [26]. If the authors can be forgiven for omitting this essential starting premise, a more serious concern is that the paper is neither balanced in content nor does it represent a true consensus of the spectrum of credible scientific views.

    The group that gathered to write this report appears to have carefully avoided many mainstream clinicians and scientists who, like the authors, have many years of both clinical and teaching experience, authored hundreds of peer-reviewed publications, diagnosed or treated.. thousands of patients but who hold divergent views. It is striking that the paper purports 100% consensus in a field where there are so many different opinions.

    Although it is a widely held view that a better name is needed [27], it is unfortunate that the authors propose to revert to the term myalgic encephalomyelitis (ME), abolishing CFS. By doing this, they ignore the fact that inflammation (-itis) has not convincingly been demonstrated in any organ [28].

    This labelling decision risks mistakenly giving patients the impression that the condition is because of inflammation and hence that anti-inflammatory medications may be curative, when clearly they are not [2932]; and biasing the research agenda at the potential expense of alternative biological hypotheses.

    Next, in a kind of Catch 22 scenario, the authors suggest that the currently accepted international diagnostic criteria, originally formulated by an expert group from several countries under the auspices of the Centers for Disease Control (CDC) [26] and subsequently modified by a further international group [33] are too broad (i.e. lack specificity) and allow patients with primary psychiatric disorders, notably major depression to be labelled with CFS?ME.

    Thus, the authors seek to discard the findings in published studies that have applied the existing international criteria, if the results do not fit with their notions of causation. As an example, if a study shows that CBT is effective, these authors suggest that the study actually included patients with psychiatric disorders, and not ME; hence, the positive results can be ignored.

    The same logic may hold if one cannot reproduce findings of alterations in immune or hormonal pathways, autonomic reflexes, etc. By contrast, if decreased grey matter in the brain is demonstrated (as we did [34]), the data are arbitrarily included, even though the same diagnostic criteria were used for inclusion.

    The literature cited in the paper is heavily biased towards positive findings (but sadly omitting the numerous failed replication studies), thereby creating a pseudo-science of the pathophysiology.

    A worrisome example is that XMRV is proposed without any mention of the host of scientific criticisms, failed replication studies and further investigations that have now led to the resolution of contaminating mouse DNA containing retroviral sequences as the culprit [1320].

    In a 21st-century consensus document, accounting in a balanced fashion for the strength of the evidence is an essential element. The current document is just a list of findings, most unconfirmed.

    Another major problem with the proposed criteria is the suggestive and misleading phrasing: when describing the criteria that assess fatigue, the label becomes post exertional neuroimmune exhaustion.

    Where is the Level 1 evidence for the neuro and for the immune? The same holds for neurological impairments all the listed items are subjective, none validated by objective abnormalities for example, muscle weakness and ataxia, which imply a demonstrable neurological deficit when one is present.

    Also, the labels for immune, gastrointestinal and genitourinary impairments and energy production/transportation impairments and the elements with in them are highly suggestive of a notional pathophysiology (although none is known, and many have been well-refuted see [11, 35, 36] for reviews).

    For example, a symptom of dizziness warrants a label of cardiovascular impairment of energy production. Yet no such deficit in metabolism is evident.

    We fear that with the publication of this report, that both the clinical and research agendas in relation to CFS will lose their credible scientific base, via introduction of yet another diagnostic criteria set.

    Under the auspices of the CDC-convened international expert group, we previously demonstrated that chronic fatigue states regardless of exactly how they are defined, share a common and relatively stereotyped set of symptom domains which can be readily identified in the community, at all levels of health care, and across cultures [24].

    We suggest that there is little to be gained by reshaping the diagnostic criteria. For the benefit of our patients, we should rather recognize the intrinsic heterogeneity in syndromal diagnoses [37], record and stratify by potentially relevant parameters in research studies [26], and continue to pursue evidenced-based treatment interventions and high-quality studies examining pathophysiology.

    Conflict of interest statement
    No conflicts of interest to declare.
    J.W. M. van derMeer1&A.R. Lloyd2
    1 From the Department of Medicine and Nijmegen Institute for Infection, Inflammation and Immunity (N4i) Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands and 2 Inflammation and Infection Research Centre, School of Medical Sciences, University of New South Wales, Sydney, NSW, Australia'
  2. Firestormm

    Firestormm Content Team Lead

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    Author Responds

    Author responds: http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2011.02499.x/full

    Dear Sir,

    First and foremost, we would like to thank Drs van der Meer and Lloyd [1] for their careful and thorough review of the International Consensus Criteria (ICC) paper [2].

    We support this type of open discussion and strongly agree that only in this way will the basic and clinical science of myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS) evolve soundly.

    This being said the content of their feedback also leads us to believe that several elements have been taken out of context or that we may not have articulated these components as well as we had hoped. As a result, we fully appreciate this opportunity to rectify any such miscommunication.

    We certainly agree with Drs van der Meer and Lloyd that this is a controversial field of investigation into a very complex and poorly understood illness that also suffers from significant social stigmatization.

    Their statement that, Quite a bit of mediocre research has been done in relation to CFS is unduly harsh in our opinion; as with any field of investigation, the case definitions and laboratory assays evolve appreciably over time. We would argue that this field has advanced significantly over the past years and continues to do so, at least in part owing to this open exchange of views.

    Consistent with this, our ICC document was submitted as part of an ongoing development, which will include clinical guidelines and an International Symptom Scale (ISS). The ISS was not referenced because, as indicated, it is a future project.

    As stated in the paper, the primary goal of this consensus report is to establish a more selective set of clinical criteria that would identify patients who have neuroimmune exhaustion with a pathological low threshold of fatigability and symptom flare in response to exertion. Although, as indicated, the ICC is directed primarily at clinical assessment in its current format, we certainly look forward to the International Symptom Scale being fully developed so that these elements may be deployed in the selection of more homogeneous sets of research subjects.

    The International Consensus Panel clearly states that the scope of the paper entitled, Myalgic Encephalomyelitis: International Consensus Criteria (ICC) is limited to the criteria of ME and their application.

    A discussion of therapies such as cognitive behaviour therapy (CBT) and graded exercise therapy (GET) raised by Drs van der Meer and Lloyd was not within the scope of the ICC paper.

    The cardinal symptom of ME is a pathological low level of threshold of fatigability that is characterized by a specific pattern of inability to produce sufficient energy on demand associated with measurable, objective, adverse responses to exercise.

    This is a refinement of the much more inclusive criteria of fatigue that goes by the label of CFS and may or may not include ME. The panel did not intend to dismiss the broader range of components involved in fatiguing illnesses but instead focused on a patient population best described as having pathophysiological abnormalities that arise in response to exertion.

    It is precisely the issue of patient cohort heterogeneity raised by Drs van der Meer and Lloyd themselves that we hope to address with a more specific criteria and efforts such as this one directed at improving the clinical identification of ME patients specifically. One only has to question why 5 of 15 CFS patients in recent phase II clinical trials of rituximab were unresponsive to treatment to appreciate the need for more specific criteria [3].

    We believe that a prime cause of inconsistent and confusing research findings in this heterogeneous patient population has been the use of overly inclusive criteria for CFS such as the Oxford [4] and Reeves criteria [5], because each study may include very different patient sets.

    This dilutes the results, makes them difficult to confirm, leads to scepticism and thus inhibits progress. Jason et al. [6] found the Reeves empirical criteria to be flawed because it was possible to meet the CFS criteria without any physical symptoms, only 10% actually had ME/CFS and 38% of patients with Major Depressive Disorder were misclassified as having CFS.

    The increased estimates of CFS from 0.24% (Fukuda) to 2.54% (Reeves, USA) and 2.6% (UK) confirm that the Reeves and Oxford criteria select patient sets that are approximately ten times larger and more inclusive than those selected by the Fukuda criteria [7].

    Whilst some general information about fatigue may be ascertained using these inclusive criteria, it is not productive to try to study the mechanisms of ME if up to 90% of the research patient set do not meet the criteria for ME.

    The Fukuda criteria, in which postexertional malaise is an optional criteria, is based on what was known in the early 1990s and has been used in the majority of research studies. In comparison with the Fukuda criteria, the Canadian Consensus Criteria [8], which made postexertional malaise compulsory, differentiated ME patients from those who were depressed and selected patients with greater physical and cognitive functional impairments [9].

    Following the publication of the 2003 Canadian Consensus Criteria, studies confirmed their utility in this regard. The WHO International Classification of Diseases (ICD) 2010 further clarifies this issue of general fatigue. This falls under WHO ICD R53 malaise and fatigue.

    However, ME is classified as a neurological disease, ICD G93.3. The WHO stipulates that the same condition cannot be classified under more than one rubric because individual categories and subcategories must remain mutually exclusive by definition.

    Therefore, ME (ICD G93.3) must be removed and kept separate from the overly inclusive criteria for chronic fatigue and malaise (ICD R53), which actually states that G93.3 is an exclusion of R53.

    The 2011 ICC for ME continues the direction of refinement undertaken in the Canadian Consensus Criteria and incorporates more recent knowledge and understanding. More specifically, the rationale of the ICC document advances the successful strategy of the Canadian Consensus Criteria of not viewing symptoms isolated in a nominal list, but rather as coordinated patterns of symptoms that directly reflect the regulatory interactions of the underlying systems involved.

    If the same symptoms consistently flare in response to exertion, they are more likely to share a common cause. For example, if a patient consistently experiences flu-like symptoms, sore throat and tender lymph nodes in response to exertion, it suggests that immune activation is a component of their underlying pathophysiology, which then can be studied scientifically.

    Given that the Oxford criteria are based on general chronic fatigue and it is possible to meet the Reeves criteria without having any physical symptoms, it is surprising that the ICC was admonished for its use of subjective symptoms.

    Symptoms by definition are subjective; however, the clinician can observe visible signs that accompany symptoms such as swollen lymph nodes, crimson crescents in tonsillar fossae, abnormal accommodation responses of the pupils, abnormal body temperature or blood pressure, abnormal tandem gait and positive Romberg test, thus confirming symptoms.

    In most neurological clinics, muscle weakness and ataxia are valid symptoms/signs that are used as part of a diagnosis for a variety of conditions. Further, objective serial stress tests recorded by heart monitors and magnetic resonance spectroscopy (MRS) can confirm many symptoms, e.g., postexertional exhaustion and pain, decreased cerebral oxygen and significantly reduced anaerobic threshold heart rate, VO(2) peak and peak work, prolonged recovery period, and loss of capacity to recover from acidosis [1019].

    Tilt tests can identify orthostatic intolerance (OI) [2022]. The use of 24-h Holter heart monitors and cardiac MRS can identify abnormalities in heart function [2326]. SPECT scans can identify cerebral hypoperfusion, and other brain imagery tests can identify additional brain abnormalities [2731].

    The ICC identify patients who have measurable and reproducible pathophysiological abnormalities in response to exertion, which people with general fatigue or depression do not have.

    In contrast, the Reeves and Oxford criteria do not require postexertional malaise or exhaustion in their definitions, and it is optional in the Fukuda criteria. The more general and stereotypic the criteria, the less useful they become because lumping together patients whose chronic fatigue is an integral part of many other diseases skews both clinical and research findings.

    It is prudent to study patients who have various kinds of adverse pathophysiological reactions to exertion to isolate various pathogeneses responsible for them and determine appropriate treatments. The use of patient sets selected by relevant, well-defined and consistent ICC for ME in research will thus advance science, provide greater clarity of understanding and elicit more reproducible scientific results.

    This will also allow a selection of more homogeneous sets of ME patients, given the current knowledge, which can then be compared with other populations. Whether patients with less severe conditions represent a continuum, faulty diagnosis or different disease entities can only be determined by future studies.

    Another element of debate concerned the use of the name myalgic encephalomyelitis. We submit that this name had been in existence for decades before the coining of the label of chronic fatigue syndrome. The suffix itis has not resulted in research being restricted to inflammatory mechanisms and the efficacy of various anti-inflammatory drugs.

    Although the name myalgic encephalomyelitis may not be perfect, it is the most accurate and appropriate name available and indicates underlying pathophysiology. Obviously, the ethical implications and medical risks prevent brain and spinal biopsies, thus limiting direct evidence.

    However, spinal autopsies have identified neuroinflammation of the dorsal root ganglia (Chauduri A. Royal Society of Medicine Meeting 2009). There is simply too much evidence of pathophysiologic neurological and immune dysregulation, immune activation and an imbalance between inflammatory and anti-inflammatory mediators to be ignored [3256].

    Unfortunately, the name CFS and its hybrids ME/CFS and CFS/ME have been used to refer to both ME and general chronic fatigue. The best way to end the resulting confusion is to only use the name ME for those who meet the more restrictive ICC criteria for this very serious disease, which is consistent with the WHO ICD neurological classification.

    The significant misalignment between the focus of this consensus paper, which is limited to ME, and the commentary of Drs. van der Meer and Lloyd appears to be centred on the use of the much more inclusive criteria for CFS or general fatigue.

    This poignantly establishes the urgent need to clarify this issue by distinguishing patients who meet the ICC criteria for ME from those that satisfy the broader and more inclusive Oxford, Reeves empirical criteria and the NICE criteria.

    Not only it is common sense not to mix diseases classified under various rubrics in one heterogeneous pot, but it is in keeping with the WHO classification rule that a disease cannot be classified under more than one rubric.

    Research on other fatiguing illnesses, such as cancer or multiple sclerosis (MS), is carried out on patients who have those diseases. It is imperative that research for ME be carried out on patients who actually have ME.

    When advances in scientific technology are applied to patients who meet the more specific case definition of the ICC for ME, the current urgent need for identifying and confirming specific biopathological mechanisms and biomarkers will be facilitated, and our improved understanding of the pathophysiology can then be directed towards enhancing treatment efficacy.

    Scientific debate about the relative merits of various hypotheses is constructive and healthy. However, it is important to avoid confusing patient stratification with scientific bias. To do so is to ignore a well-justified and extensively used strategy for the study of complex disease populations.

    The distinguished clinical, research and pedagogical status of our panellists has been clearly laid out in the document. Clinicians and researchers who had extensive experience in this area were asked to donate their time and expertise to the panel, and they in turn were asked to suggest others.

    The authors opinions did vary in some areas, opinions were discussed, and only those criteria that were agreed upon by all authors were included in the final manuscript.

    The panel does not claim to represent the entirety of the field. However, we suggest that consensus amongst a panel of investigators of this size, geographical distribution and diverse specialties and backgrounds has merit and represents a valuable contribution to the field.

    Conflict of interest statement

    No conflict of interest was declared.

    G. Broderick

    From the Division of Pulmonary Medicine,Department of Medicine,
    Faculty of Medicine and Dentistry,University of Alberta, Edmonton,
    Canada

    http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2011.02499.x/pdf
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  3. Esther12

    Esther12 Senior Member

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    3
    Feehan SM. The PACE trial in chronic fatigue syndrome. Lancet 2011; 377: 18312.



    4
    Giakoumakis J. The PACE trial in chronic fatigue syndrome. Lancet 2011; 377: 1831; author reply 45.



    5
    Kewley AJ. The PACE trial in chronic fatigue syndrome. Lancet 2011; 377: 1832; author reply 45.


    6
    Kindlon T. The PACE trial in chronic fatigue syndrome. Lancet 2011; 377: 1833; author reply 45.



    7
    Mitchell JT Jr. The PACE trial in chronic fatigue syndrome. Lancet 2011; 377: 1831; author reply 45.



    8
    Shinohara M. The PACE trial in chronic fatigue syndrome. Lancet 2011; 377: 18334; author reply 45.



    9
    Stouten B, Goudsmit EM, Riley N. The PACE trial in chronic fatigue syndrome. Lancet 2011; 377: 18323; author reply 45.



    10
    Vlaeyen JW, Karsdorp P, Gatzounis R, Ranson S, Schrooten M. The PACE trial in chronic fatigue syndrome. Lancet 2011; 377: 1834; author reply -5.


    11
    Prins JB, van der Meer JWM, Bleijenberg G. Chronic fatigue syndrome. Lancet 2006; 367: 34655.


    Hmmm.
  4. Sean

    Sean Senior Member

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    "unscientific"? "personal attacks"?

    Oh the irony.

    Their propaganda really is getting desperate of late. We must be scoring a few uncomfortable bulls eyes.
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  5. biophile

    biophile Places I'd rather be.

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    Some initial thoughts on the van der Meer & Lloyd comments before I read Broderick's reply (I'm already risking a crash so maybe later) ...

    I won't argue that the ME-ICC has limitations, there could have been a stronger emphasis on a systematic review of the literature, but no definition has ever done that, and if there are fundamental questions surrounding the criteria then what reliable literature can be reviewed without risking GIGO? The authors are attempting to establish a new definition based on a careful selection of previous research and their own clinical experience.

    No, the "controversy" also involves biopsychosocialists who, like yourselves(?), believe CFS is a "complex" functional somatic syndrome perpetuated mainly by cognitive and behavioural factors relating to "abnormal illness beliefs" rather than organic disease processes. Some people may have simplistic perspectives, but regardless of the underlying etiology and pathophysiology, people are also resisting for good reason the spin and overemphasis on flawed cognitive-behavioural research that is being pushed on us as something we should swallow uncritically lest we be accused of being recalcitrants.

    Perspectives I've read on the "controversy" written by proponents of the biopsychosocial approach to CFS, portray their own ilk as the most objective/reasonable while critics are too wrapped up in Cartesian dualism etc to understand the enlightened BPS approach. It is never admitted or grasped that the critics have genuine reasonable arguments, it is usually implied that criticism is based all on emotion and entrenched beliefs, and the criticisms are rarely addressed properly.

    Little doubt they would see themselves in the latter enlightened group which is supposedly above and beyond the controversy of the simpletons? Although from what I've read of van der Meer's work, perhaps it would be a stretch to say he is "motivated to elucidate the biological basis of CFS". And people have different interpretations of what is meant by a "biological basis", for some a biological basis means deconditioning and the reversible/functional consequences of psychological factors and behavioural deviances, while for others it means organic pathophysiology.

    Which group of "protagonists" do the PACE authors belong? Anyway, the dubiousness of making these statements based on the citations given is worthy of a separate post on a pre-existing thread dedicated to misleading claims unsupported by the references (http://forums.phoenixrising.me/show...ychosocialists&p=235811&viewfull=1#post235811). To summarize that briefly: van der Meer & Lloyd cite the 8 Lancet letters to the editor (and related authors' reply?) on the PACE Trial for the claim of "unscientific and sometimes personal attacks on the researchers". However, these letters were not "unscientific" and no "personal attacks" were made within them. Further, the reference used for the claim that this also occurred "via the Internet" appears to be a citation error because it is a paper from 2006 and therefore irrelevant to an event that allegedly happened in 2011.

    Another allusion that PACE vs criticism, like the issue of supporting XMRV/HGRV, was all about "science vs emotion".

    LOL. We can only hope so! Do van der Meer & Lloyd accept Wiborg et al 2010 as "high-quality science" which found that in 3 trials CBT has no effect on objective activity levels which remain abnormally low in CFS?

    True, but broad criteria also casts a net so wide that psychobabble will end up being applied to large epidemiological studies and swallowed as fact, like those "depression and stress are risk factors but we didn't evaluate any patients for diagnosis" national birth cohort and twin registry studies.

    Feeling left out eh? Why would they consult people who, like yourselves, don't accept that the specific condition being written about (ME-itis) even exists or is separate from "CFS", as is implied in the following paragraph? This group is about consensus for ME, not CFS, and perhaps they also weren't interested in biopsychosocial-babble from known biopsychosocialists about vague idiopathic "chronic fatigue states"?

    The next few paragraphs is about cherry picking, as if nearly every CFS paper ever published including their own doesn't do that to some degree. It isn't meant to be a systematic review of all the literature, its a consensus document. Sometimes cherry picking also omits bad cherries for good reason.

    All the reviews cited are over 5 years old, perhaps there has been new evidence published since then?

    They mention that "we previously demonstrated that chronic fatigue states regardless of exactly how they are defined, share a common and relatively stereotyped set of symptom domains which can be readily identified in the community, at all levels of health care, and across cultures" (http://www.ncbi.nlm.nih.gov/pubmed/19085525) This study is useful, but then they use it to justify "We suggest that there is little to be gained by reshaping the diagnostic criteria. For the benefit of our patients, we should rather recognize the intrinsic heterogeneity in syndromal diagnoses [37], record and stratify by potentially relevant parameters in research studies [26], and continue to pursue evidenced-based treatment interventions and high-quality studies examining pathophysiology."

    However, the ME-ICC was itself based on a large study into symptom frequency/patterns (De Becker et al 2001). Yes, more work needs to be done on patterns of symptoms, but the ME-ICC is an attempt to clarify a distinct condition without all the confusion arising from broad umbrellas and paradoxical heterogeneity.
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  6. Nielk

    Nielk

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    My Scientific unbiased take on J.W.M. Van der Meer and A.R. Lloyd? Their ego's are hurt by the fact that they were not asked to participate in the authorship of this ICC.

    They show their true colors when they mention the avoidance of the authors to include mainstream specialist clinicians. Where is the hard evidence of this? And the back up reference?
    They included people who were willing to donate their time freely to work on this. The 100% concensus was of the authors not the world. Even a "simpleton" like me understood that.

    They don't want to rock the boat we are in - even though it's sinking! Why confuse ineffective meaningless criteria with more scientific experienced facts?
    They would rather that we stay in the dark ages. Unless, of course, we would listen to them two.

    "Criticizing others is a dishonest way of praising ourselves." - I'm not saying that the ICC is beyond criticizing but, come up with some positive changes that can actually improve on it, not take it back a century.
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  7. alex3619

    alex3619 Senior Member

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    Hi biophile, just to pick up on a point you made I agree with, on cherry picking supporting info: this is not only widely done but inevitable in any complex topic. Its not like you can reference all 5000 papers on ME and CFS in any publication, you have to use selection criteria. In this sense the cherry picking of the biopsychosocial proponents is justifiable. However, there are larger and overlapping issues. When faced with specific scientific challenges, especially those that go the the very foundation of the biopsychosocial hypothesis, what you use to support argument is much more critical. It has to address the issue at hand, and do so in a rational and data supported way. Typically this is not the case. For the PACE trial this is not the case. Instead we get multiple claims of violent patients, unscientific attacks, and so on. Arguing the man: a logical fallacy. They rarely address the complaints and issues, many of which come from respected scientists and clinicians: instead they divert attention to those hysterical patients again.

    This is politics and spin, not science. I think the problem stems from the historical situation. For decades they have not been substantially challenged. Nobody took them seriously, and they were in their own little isolated area: people outside this area just ignored them for the most part. Now more and more people are realizing just how foundationally baseless and methodologically flawed the biopsychosocial research is. BOOKS are being written about it by medical academics (I have one on order). The charge is not being led by hysterical patients, its being led by medical academics, including other psychiatrists. They have never had to face this level of criticism, and it is getting worse as more and more wake up to what they have been saying and doing. They need a scapegoat, a straw-man, and they selected us, either consciously or unconsciously - I am in no position to infer motive or whether its intentional, but I can point to the fact of it happening.

    Bye, Alex
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  8. SilverbladeTE

    SilverbladeTE Senior Member

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    Somewhere near Glasgow, Scotland
    Cut to the chase:
    When scumbags start to get noticed and investigated for the vermin they are and crimes they have commited, they always throw up a smokescreen of bullshit to try and avert attention, and curry sympathy as the "victims".
    BOLLOCKS! :D

    All the Weasle's are in deep SHIT and they know it and are bleating like sheep.
    HA BLOODY HA! Screw the lot of them to Hell, or rather scientific proof they are quacks and charlatans and nice, long jail terms for fraud and criminal abuse!

    Verbose dialectics doth not a compassionate nor honest physician make.

    Revenge is a dish best served cold: ah, how true, gotta luv ratbags wriggling on the hook they made for themselves, muhaha!! :victory:
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  9. Nielk

    Nielk

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    Hi Silver,

    I needed your writing a post to make me smile! I am in so much pain that even smiling hurts.

    Seriously, on second thought - I think that this is good news for us:

    #1- It brings attention to our illness

    #2 - It brings attention to our illness by "very esteemed members of the medical field?

    #3- They obviously put in a lot of effort in dissecting and slicing and "referencing" the ICC which itself was authored by the big names around the globe.

    #4- Why even bother if one really thinks that this ilness is somatic or doesn't exist?

    #5- In the future, we'll be able to rub this in their faces when more tangible evidence (backed up by referenced studies) will show them wrong.

    #6- We have a new topic to be angry about. (instead of being angry about our situation.

    #7- Silver made me smile! (almost laugh) ha
  10. SilverbladeTE

    SilverbladeTE Senior Member

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    Somewhere near Glasgow, Scotland
    Nilek,
    *bows with a theatrical flourish!*

    As always, ribbed for your pleasure! :D
    Nielk likes this.
  11. oceanblue

    oceanblue Senior Member

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    I agree with the many of the criticisms here of the van der Meer & Lloyd editorial, and I especially liked this one-liner from Broderick:
    I could go on about how absured it is to label as an 'activist' anyone who pursues biomedical research, but not those with the same approach to biopsychosocial research - but that and many other valid points have been made already.

    Instead, I'm going to put on my flak jacket and say that I think the editorial authors made a valid criticism of the ICC by pointing out that it places a lot of emphasis on symptoms reflecting an underlying causal physiology, without the evidence to back up that claim, as in:
    As Lloyd & van der Meer point out, the underlying causal system(s) are unknown which makes the logic of the diagnosis questionable. I don't think Broderick's response for the International Consensus Panel adequately addresses this criticism. He starts off by saying:
    Personally, I think the pathological low threshold of fatigability and symptom flare in response to exertion is key, but the neuroimmune claim is less than robust, as the editorial points out. (The editorial also claims that many [biomedical] findings have been 'well-refuted', but that's not true either; there are a lack of robust findings either way.)

    Broderick quotes a long list of studies in support of abnormalities but I don't think any of them have been robustly replicated, and that's true generally for biological abnormalities in CFS, with the notable exception of reduced Natural Killer cell cytotoxicity which was demonstrated in a large sample by Fletcher & Klimas and subequently confirmed in an independent sample by Brenu. If there are robustly replicated abnormalities out there, please tell as I've read a lot of papers fruitlessly searching for them (lots of fascinating findings, little robust replication).

    Also, many of the findings cited by Broderick seem to be based on the Fukuda criteria - since that's been the main criteria in use, and the ICC has not yet been used in any research studies. So it's hard to see the basis for his claim that:
    Then Broderick rather undermines his own case, in the penultimate paragraph, by pointing to how the ICC will help 'identify and confirm specific biopathological pathways' which implicitly acknowledges the evidence right now isn't so hot:
    I agree the ICC is, as Broderick writes, 'a valuable contribution to the field'. I think this more specific case definition has the potential to identify a relevant group of patients with distinct disease pathophysiologies, but I wish they wouldn't claim that the pathophysiologies had already been established and were the basis for diagnosis. Above all, I think we need more data to show which of the criteria are most effective in identifying patient groups with common underlying disease mechanisms.

    Over on the other forum, Dr Yes made this suggestion about the way forward:
    I've no idea if Dr Yes agrees with me in general about the ICC, but I think his/her suggestion is a good one.

    OK, flak jacket and hard hat on...
  12. Dolphin

    Dolphin Senior Member

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    Link to 8 Lancet letters said to be "unscientific and sometimes personal attacks"

    The 8 Lancet letters said to be "unscientific and sometimes sometimes personal attacks" by van der Meer and Lloyd can be read at: http://forums.phoenixrising.me/show...ublished-and-authors-response-(and-editorial) .

    I don't think that is a fair way to characterise them at all.

    ----
    ETA: I see biophile has dealt with this in another post in another thread: http://forums.phoenixrising.me/show...ychosocialists&p=235811&viewfull=1#post235811
    Wildcat likes this.
  13. Esther12

    Esther12 Senior Member

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    No. I think they've opened themselves up a to a testy reply on that one. I don't know who a lot of the letter writers are, but many of them made good and important points.

    Surely they were trying to be funny here, but I don't see how they could think that this bit was a good idea (or funny).
  14. oceanblue

    oceanblue Senior Member

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    Wildcat likes this.
  15. Sean

    Sean Senior Member

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    ie propaganda.

    Yep. The reality of all this is starting to hit them hard, and they do not like it. And they are looking for somebody else to blame.
  16. alex3619

    alex3619 Senior Member

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    Logan, Queensland, Australia
  17. Dolphin

    Dolphin Senior Member

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    Just a FYI: "Somatic" means "of the body".

    See, for example, their line:
  18. Nielk

    Nielk

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    Just a FYI: "Somatic" means "of the body".

    You are right, Dolphin. I was thinking of"Psycho-somatic".
    It's a wonder that I can think or write at all today so please forgive for the inaccuracy:)
  19. Dolphin

    Dolphin Senior Member

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    No problem. You are not the only person who I have seen misuse it (have seen lots) so thought I'd correct.
  20. Ember

    Ember Senior Member

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    By adding emphasis without noting that it's yours, you may inadvertently be misquoting the ICC. Try reading this sentence as it may have been intended: "Determine whether symptom cluster patterns are congruent with those expected from dysfunction of an underlying causal system (emphasis mine).

    The authors of the ICC include Nancy Klimas, Alan Light and Stacy Stevens. Would they have measured and reproduced pathophysiological abnormalities in response to exertion in ME patients?

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