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(Ongoing UK study) "Investigating the epidemiology of CFS/ME in children using the ALSPAC cohort"

Discussion in 'Latest ME/CFS Research' started by Dolphin, Jul 5, 2014.

  1. Dolphin

    Dolphin Senior Member

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    I think it would have been much more interesting and the results would likely be more reliable if it involved some biological testing.

    Extract:
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    http://gtr.rcuk.ac.uk/project/92F6B9E6-B13E-4BC5-AD74-F2245F8B5D54

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    Last edited: Jul 5, 2014
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  2. alex3619

    alex3619 Senior Member

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  3. Esther12

    Esther12 Senior Member

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    Are they diagnosing CFS just on the basis of Chalder Fatigue Scores?

    The lack of specifics makes it hard to say much, but this doesn't look great.
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  4. Bob

    Bob

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    Can this study really determine the 'causes' of CFS/ME if no biological investigations are involved?
    As usual, they are conflating 'cause' with 'association'.
    No doubt they will report that certain cognitive and behavioural associations (i.e. "activity, patterns of sleep, anxiety and depression") are precipitating and perpetuating factors, which they will then claim are the 'causes' of CFS.

    Why, oh why, have the MRC given funds?
    Last edited: Jul 6, 2014
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  5. bambi

    bambi

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    :meh:
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  6. Bob

    Bob

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  7. user9876

    user9876 Senior Member

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    I'm pretty sure this doesn't make sense as the Chalder fatigue questionnaire is a random set of questions about fatigue rather than a scale. The questions themselves are quite confusing and there is an arbitrary weighting between mental and physical fatigue.

    But more importantly RoC curves are about classification but you can't classify someone as having ME or not based on a fatigue survey. A whole range of different things such as ruling out other diseases needs to be taken into account to perform a classification and say yes or no. I feel it is quite dangerous to suggest that the CFQ could be used as the input to a classifier.

    My guess is this is run a series of questionnaires about symptoms and see how they cluster. I don't understand how it helps to cluster symptoms from a questionnaire without an understanding of mechanism we have no idea whether they have any meaning. If they were to compare these to blood tests, b cell functioning, NK cells, response to exercise such as in the Light's study it might become interesting.


    They plan to use complex stats techniques to try and find stuff but without thinking about the basic structure of data from things such as the CFQ probably the sf36 and HAD scales. If your working that hard with complex stats tests you are probably not finding real cause and effect or confounding factors especially from relatively small datasets. Stats should be used to find interesting stuff that help generate models that can then be tested in further work they don't explain.

    I don't see how this research could help "improve the understanding of mechanisms" or even "improve sub-phenotypng" although this latter one is more arguable. Do the reviewers actually read stuff?

    The MRC could help children and carers make more informed choices by insisting White released the PACE data. And that wouldn't cost almost 300000.

    I believe aetiological refers to causal yet nothing in this study looks at causality its just playing with stats methods that show correlation. At best they may find leading and lagging indicators. Given EC tells patients that CFS is time limited and she can cure it with a coloring chart (even when a child is still ill) then I worry about her thoughts on maintaining factors. Maybe she is just looking for ways to justify recommending sick children are locked up in psychiatric wards.

    I suspect health resource use for ME are quite low. The significant impact on the nations wealth would be to do the pre-competative research into the biology of the disease so that patients can be treated and drug companies can look at making drugs. The problem is patients need to raise money for good research whilst the MRC fund this rubbish.
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  8. alex3619

    alex3619 Senior Member

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    On any large data set you can can find clustering by chance. It always needs further investigation. Of course the point made about association and causation is also critical - how many times must it be stressed that association does not equal causation?
  9. Sean

    Sean Senior Member

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    I got as far as Esther Crawley (Principal Investigator), and stopped. Told me all I needed to know.
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  10. Valentijn

    Valentijn Activity Level: 3

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    Yes, the conclusion had undoubtedly already been written. All that remains is to fill in the actual figures and find ways to make the data support that conclusion.
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  11. alex3619

    alex3619 Senior Member

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    The modus operandi of huge areas of psychogenic research is to find supporting evidence. Its not to test the hypothesis. Alternative explanations get ignored. This isn't even science when this happens, its called nonscience, and even pseudoscience. This methodology was mostly put to rest in the mid-twentieth century, with the demise of logical positivism, but not, apparently, in psychiatry.
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  12. Dolphin

    Dolphin Senior Member

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    I'm not that interested in symptom phenotypes without checking the underlying biology. The intensity of my individual symptoms fluctuate. I don't think clusters at any particular point in time likely are that solid/reliable. I remember Esther Crawley previously published a study based on phenotypes at one moment in time.
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  13. alex3619

    alex3619 Senior Member

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    There is unpublished research I was a part of, primarily as a test subject, which shows massive shifts in symptomology. These can be rapid. Indeed, we experience this from time to time. Snapshots have a purpose, but they don't capture the dynamics of what is wrong.
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  14. Simon

    Simon

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    I think the the idea of using a large prospective study, with a rich set of data, to investigate CFS is a good one. I'm a little concerned about how the study might be executed though. It's not clear that how they will confirm diagnosis of a difficult-to-diagnose illness, or whether they will make use of any of biosamples or physiological data collected by the ALSPAC cohort. And they appear to be looking at 'maintaining' factors in chronic fatigue rather than CFS.

    As others have pointed out, if the drivers of CFS are biological, and they don't collect biological data, they will end of sifting through a lot of data with only marginal relevance to the illness - which would be a lost opportunity.

    "Children of the 90s" /ALSPAC cohort
    It's worth looking at the cohort they used:
    There were clinic visits by participants at approximate ages 7,8,9,10,11,12,13,4,16 &18. Not all children attended all clinics, with 8,000 making the first one down to 5,000 by age 18+. They also have DNA for 10,600 children and cell lines (immortalising the DNA to enable more sampling) for 7,100 children.

    upload_2014-7-7_19-6-39.png

    Since they are looking at 16/17 year olds, they have a maximum sample of 12,500 people (data). Assuming 1% of these have CFS (or had it at 13) that would give a sample of 125 patients, approx 13 of whom would have been bedbound/very severe [using their estimates of 1% prevalence, 0.1% too ill to attend at all). That would actually be a pretty respectable sample.

    Diagnosis
    Since the children were born in 91/92, they would be 16 in 2007/9. I'm not sure how they the CFS diagnosis will be asssigned eg if this was recorded at a clinic or if they will use questionnaires to retrospectively ask if they had CFS (the approach used by earlier birth cohort studies).

    It's possible that some patients were diagnosed in CFS clinics were operating in Avon at that time (it's an Avon cohort), but given the emphasis in the study proposal on measuring 'recovery without treatment', it looks like most are not expected to have attended a CFS clinic.

    The problem is that CFS is a diagnosis of exclusion, and if patients haven't been properly tested/assessed to rule out other illnesses that puts the findings in doubt too as they may not relate to CFS. Maybe the study has a way to provide clear diagnosis, but there is nothing in the information here that says so.

    Chronic Fatigue vs CFS

    This does seem to be confusing chronic fatigue with CFS.

    A Simon Wessely study on chronic fatigue in adults found that most adults attending GP surgeries with chronic fatigue attributed their fatigue to psychosocial factors

    A chronic fatigue sample is likely to be made up of overwhelmingly non-CFS patients, so it's hard to see the relevance of 'maintaining' factors for Chronic Fatigue to CFS.

    The study says they will use the Chalder fatigue scale. The questionnaires used (which ones not stated) covered fatigue at age 13 and 16 ie just 2 time points, so it's not clear how they will do this:
    But then it is just a brief description of the study.


    Biology vs psychological/behavioural factors
    The ALSPAC cohort has a lot of physiological data as well as biosamples [as above] and presumably clinical data on other illnesses subjects have too. Yet the proposal seems to focus on those factors studied in previous birth cohorts, primarily behavioural/psychosocial factors eg activity (though it appears they used activity monitors at ages 13 & 16, as well as an activity diary at age 10 which should reduce self-report bias).

    Might have been nice to draw in, say, immunologists and endocrinologists, neurologists even ahead of obesity researchers. It looks unbalanced to me, for a study that puts so much weight on mechanisms:
    Other biological data they might like to include:
    - Sudden vs gradual onset
    - Any illnesses/vaccinations etc that appeared to trigger the illness
    For adolescents, I would have thought glandular fever would be a key one to investigate, as something like 10% of adolescent glandular fever cases go on to CFS - and GF diagnosis would be documented in medical records for verification.
    - while the sample is probably too small to do much in the way of DNA studies, it might be interesting to follow-up the Dubbo study findings of that those who developed CFS post GF were more likely to have highly-active versions of interferon-gamma genes. This would be a relatively easy way to follow-up on the Dubbo findings, the sort of collaborative work that would allow this new study build on existing research on biological findings in CFS.

    What is 'better'/'recovery'?
    That's very true, but what definition of 'recovery' or 'better' will the study used? The principal investigator erroneously claimed the PACE trial showed a 40% recovery rate, but even the 22% recovery rate later claimed by the PACE trial doesn't match real world recovery (13% of PACE participants met either fatigue or function 'recovery' criteria - or both - before receiving any treatment).
  15. seanpaul

    seanpaul

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    This study is a waste of money - spending scare resources on a psychiatric study of prevalence and risk factors whereby the study will be biased by the bias of the investigators who will use an out-dated Oxford Criteria , risk factors will be drawn from biased previous studies done by psychiatrists, and data collection will be biased by how risk factors are understood and defined.

    Knowing how many children suffer pain or fatigue wont reveal much - and we may just find that due to the biases of this study far more children are deemed CFS patients requiring CBT then first thought.

    Patients and ME supports groups MUST make their voice heard by writing to the MRC to object to this use of funds when biological factors are not funded.

    30-40 years of psychiatry has not helped us understand ME/CFS much - indeed its diverted attention away from biological and immunological factors that require careful study.

    No point complaining on here: action must be taken to show the MRC patients are not happy with how tax payers money is spent.
  16. user9876

    user9876 Senior Member

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    I was wondering how they can possibly spend nearly £300,000 crunching a bit of data using standard techniques.
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  17. Dolphin

    Dolphin Senior Member

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    10-15 years ago, I remember some individuals and patient groups in the UK were calling for epidemiological research. I'm not saying this had anything to do with this study, but I thought I'd make the point now I made then that epidemiological research is very often done by those of the CBT/rehab school of thought.

    One of the reasons people seemed to want epidemiological research is because it would demonstrate the scale of the problem and the need for biological research. However, it is well-accepted that a condition like Fibromyalgia is quite common, probably affecting in the region of a million people in the UK (possibly a lot more), but that doesn't mean it gets a lot of biomedical research in the UK. We already have an idea of the scale of the problem.

    Some of these people and other people said it was hard to plan services without knowing exactly how many people have it. However, epidemiological research in CFS tends to involve questionnaires and so doesn't necessarily give us very accurate figures. If one develops some diagnostic tests first, it makes looking for cases much easier (don't just work by exclusion) and it should make it more accurate.
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