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Dr. Kerr's 7 Subtypes of CFS

Discussion in 'General ME/CFS News' started by starryeyes, Feb 23, 2010.

  1. starryeyes

    starryeyes Senior Member

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    Over in the XMRV UK test thread oerganix wrote:

    "The 7 subtypes are:

    * Subtype 1
    This is one of the more severe subtypes. Effects are cognitive, musculoskeletal, sleep-related and anxiety/depression.

    * Subtype 2

    This is one of the more severe subtypes. Effects are musculoskeletal, pain and anxiety/depression.

    * Subtype 3

    This subtype has the mildest symptoms.

    * Subtype 4
    This subtype is dominated by cognitive issues.

    * Subtype 5
    Effects are musculoskeletal and gastrointestinal.

    * Subtype 6
    This subtype is dominated by post-exertional malaise (extreme crash after exercise or exertion.)

    * Subtype 7
    This is one of the more severe subtypes. Effects are pain, infections, musculoskeletal, sleep-related, neurological, gastrointestinal, neurocognitive and anxiety/depression.

    Dr. Kerr emphasizes that each subtype is a distinct condition. This is the first study to identify these genomic subtypes and it will need to be verified by more research before the information is put to use in diagnosing or treating people with the disorder.

    Other findings:

    * Many of the abnormal genes are ones that researchers know can be affected by viral infections, which they believe are a predominant trigger of many ME/CFS cases.
    * Drugs that are already on the market for other diseases target five of the 88 genetic abnormalities, meaning potential treatments for some subtypes may already be available.
    * The team is now looking into whether the abnormal protein levels are detectable in the blood, meaning they'd be considered biological indicators of ME/CFS and could be used for diagnostic tests."


    Personally, these subtypes don't resonate with me. I believe he is categorizing people with CFS according to his genomic findings but I don't know if that really translates to real life cases. I'd say many of us start out with milder symptoms which generally progressively get worse but I don't see PWC neatly fitting into these subtypes and these types themselves overlap each other a great deal.

    To me, this "research" is very confusing. Personally I don't exactly fit into any of them. The best I can say is that I mostly fit one or another at different times during the 25 years I've had CFS. How about the rest of you?
  2. Jenny

    Jenny Senior Member

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    I agree teejkay. I think we discussed this some time ago somewhere else on this board (what are we going to do when the number of threads gets too big to cope with?!)

    For me too these link to the stages I've gone through with this illness - for example I had more gastro symptoms early on but now have more pain and neurological symptoms.

    Jenny
  3. flybro

    flybro Senior Member

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    Same here, I've been in and out of most of the subsets.
  4. Advocate

    Advocate Senior Member

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    Some of the subsets don't seem to have much relationship to CFS. If he related the subsets to particular genes, that would be interesting. Not that I'd understand it. :rolleyes:
  5. oerganix

    oerganix Senior Member

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    He did another study and came up with a new set of subtypes, called a thru h, so as not to be confused with the first study.

    I like the approach, but like you all, don't totally fit into any of the first study's types. I'd like to see this followed up and refined.
    Previous thread on this forum: http://forums.aboutmecfs.org/showthread.php?1332-New-Dr-Kerr-Gene-Expression-study-published/page3

    One important finding was that, genetically speaking, those with major depression had gene profiles dramatically different from those of CFS patients, which is worth the study in and of itself.
  6. George

    George Guest

    Barking up the wrong tree?

    teejkay great post. I agree that this subtyping just sounds off somehow. I mean I don't know, if we did a poll right now and everybody picked one of the 7 then we might get a sense that subtyping works. However, I would bet dollars that it would be way more interesting to read the comments or see how many checked the . . .none of the above box.

    This is speculation on my part backed up by what I've read. I think two things are happening; one is that if you say something often enough then people really believe it's gospel. The saying I'm referring to is the one that "CFS is a heterogeneous illness". I don't agree. I think it's the same disease for everybody. This whole thing about it being a heterogeneous illness got started because of crappy criteria in the first place. So some of the people who have a CFS diagnosis may end up with MS, or Cancer or another illness down the road.

    If I have the flu and I have to pee all of the time and you have the flu and don't pee at all does that mean that we have two different flu's??? No it means that everyone's bodies are diffrent and deal with the same virus differently.

    The second thing is that I believe that the answer to the difference in gene expression is caused by retroviral interference. As the viral load elevates in the body and depending on the persons genes XMRV or another retrovirus bonds with enough cells to change the gene expression and create symptomatically in the given area, or what Jenny said (grins)

    Course is just the way I'm interpreting the information.
  7. Esther12

    Esther12 Senior Member

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    I'd be interested to knw how this compares to the gene expression of other illnesses. Has anything similar been done with MS? AIDS? Eating disorders?

    Looking at this work in isolation, it doesn't seem that important, but I don't have any understanding as to how it compares to other conditions.
  8. Katie

    Katie Guest

    I agree with this, we need a gene expression database, every little thing measured on it's own and comorbidly too. Does anyone think that we might be a front runner for most genes misbehaving?


    On a more serious note of the subtypes, I find them confusing as ME is remitting and relapsing and I had gotten the impression that the subtypes were related to trigger more than what the illness was actually doing because of it's variable nature. I'm not sure how I fit, my ME was also different in my teens which was probably down to hormones. Curious.
  9. oerganix

    oerganix Senior Member

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    Ummm, isn't that exactly what he did, relate the various 88 abnormal genes in CFS to the subsets he came up with? That he found CFS has those 88 abnormal genes is worth something, it seems to me and that they can be roughly grouped could be useful in future treatments and possibly diagnosis. Just excluding depression would be worth a lot. And he might, in future, determine that a patients abnormal genes could indicate what stage a person is in, if there turn out to be stages, as it seems to happen. He also found geographical subsets, which might be subsets of subsets and further cloud the initial picture, but might be useful later.


    Dr. Jonathan Kerr's work[​IMG] Microbial infections in eight genomic subtypes of Chronic Fatigue Syndrome / Myalgic Encephalomyelitis (CFS/ME)

    Lihan Zhang1, John Goudh1, David Christmas2, Derek Mattey3, Selwyn Richards4, Janice Main5, Derek Enlander6, David Honeybourne7, Jon Ayres8, David J Nutt2, Jonathan Kerr1,*
    1 St George's University of London, United Kingdom;
    2 University of Bristol, United Kingdom;
    3 Staffordshire Rheumatology Centre, United Kingdom;
    4 Poole Hospital NHS Trust, United Kingdom;
    5 Imperial College London, United Kingdom;
    6 New York ME / CFS Service, United Kingdom;
    7 Birmingham Heartlands Hospital, United Kingdom;
    8 University of Birmingham, United Kingdom

    Correspondence to: Jonathan R Kerr, Dept of Cellular & Molecular Medicine, St George's University of London, Cranmer Terrace, London, SW17 0RE, United Kingdom; jkerr@sgul.ac.uk

    Accepted November 3, 2009
    Abstract

    We have previously reported genomic subtypes of CFS/ME based on expression of 88 human genes. In this study we attempted to reproduce these findings, determine specificity of this signature to CFS/ME, and test for associations between CFS/ME subtype and infection.
    We determined expression levels of 88 human genes in blood of 61 new patients with idiopathic CFS/ME (according to Fukuda criteria), 6 patients with Q-fever associated CFS/ME form the Birmingham Q-fever outbreak (according to Fukuda criteria), 14 patients with endogenous depression (according to DSM-IV criteria) and 18 normal blood donors. In patients with CFS/ME differential expression was confirmed for all 88 genes. Q-CFS/ME patients had similar patterns of gene expression to idiopathic CFS/ME. Gene expression in endogenous depression patients was similar to that in the normal controls, except for upregulation of five genes (APP, CREBBP, GNAS, PDCD2, PDCD6).
    Clustering of combined gene data in CFS/ME patients for this and our previous study (n=117 CFS/ME patients) revealed genomic subtypes with distinct differences in SF-36 scores, clinical phenotypes, severity and geographical distribution. Antibody testing for Epstein-Barr virus (EBV), enterovirus, Coxiella burnetii and parvovirus B19 revealed subtype-specific relationships for EBV and enterovirus, the two most common infectious triggers of CFS/ME. http://jcp.bmj.com/content/early/2009/11/26/jcp.2009.072561.abstract
  10. Gerwyn

    Gerwyn Guest

    I wonder what the genetic abnormalities were and did the genes have any regulatory function in common--could they have involved polymorphisms were they switched on or off etc.Very diverse symptoms can be caused by the expression of very similar proteins XMRV can influence gene switches all over the body particularily in the brain CNS and the autonomic nervous system this in turn can regulate the expression of other genes creating at least an impression of subtypes
  11. Angela Kennedy

    Angela Kennedy *****

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    A big issue here is: what does Kerr mean by 'anxiety/depression'? Reactive anxiety and depression (especially intermittently) seem to be banal and understandable reactions to having a serious illness that is psychogenically dismissed, i.e. they occur because of the impact of the illness and mistreatement by others. Eleanor Stein has written on this issue before.

    I do have my doubts that Kerr has elucidated in his study the status of any 'anxiety/depression' (i.e. whether reactive or not). The reason I believe this is possible is because, in his "Parvovirus 'stress' is involved in 'CFS'" study, he based his claims on the RETROSPECTIVE self-reports of just 5 'CFS' sufferers, of which there was a WEAK correlation (the 'CFS'ers had a statistically significant but very small increase in 'stress' measurement).

    This sort of problem is endemic in 'CFS' research. The ubiquity in humans of psychological 'symptoms' doesn't help of course! : )
  12. muffin

    muffin Senior Member

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    Dr. Kerr's subtypes make no real sense to me. I fit into many of these subtypes and yet he has not really captured the most severe cases of CFIDS/ME in one of those categories. I thought Kerr was a smart guy. Seems he must still be in the learning phases of ME/CFIDS and all the symptoms that are really involved. Better he stick with genes and stay away from the subtypes for a bit.

    And oh yea, I have never had anxiety or depression related to CFIDS. Knocks out his most severe subtype right there, doesn't it?
  13. Angela Kennedy

    Angela Kennedy *****

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    He does seem wedded to stress and depression EXPLANATIONS for 'CFS' - this is evident on one of the dvd's of a conference he presented on, and, by his reactions I've seen, seems unable to grasp why this is a problematic idea SCIENTIFICALLY.

    He did say 'stress' was part of the 'pathogenesis' of CFS (indicating a causation explanation on his part) in the parvo/CFS/'stress' study as well.

    The issue of so-called 'co-morbid' psychiatric disorders' is a massive problem in CFS research. ANY feeling of 'depression' or 'anxiety' can get press ganged into a causation claim, and of course feelings of depression and anxiety at some time is a ubiquitous human phenomenon. As is 'stress' for that matter! And do not get me started on the 'childhood trauma' claims and what's wrong with them...!
  14. Gerwyn

    Gerwyn Guest

    The action of XMRV on multi site crim " switches" MIGHT cause the observations re gene expression seen by dr Kerr.Stress might well be an infection enabler allowing our fiend to get such a hold in the first place given it has so many nueclotide sequences in common with the human genome.Chilhood trauma affects the development of the mind leading to a disorganised attachment schema.This is a relatively simple thing to ascertain yet they refuse to use this method I wonder why?It would actually be a simple and relatively cheap trial as we have all the raw material to hand
  15. Marco

    Marco Old blackguard

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    I'm really not sure where he's coming from with this research.

    The proposed sub types seem to me like an example of nominal fallacy. He has detected differential expression of certain genes in ME patients and then describes certain largely overlapping sub groups which appear to typify that particular gene expression pattern. That sounds a rather circular line of reasoning to me.

    I'm also not sure whether he is suggesting that these patterns are innate or acquired; i.e. are we pre programmed to be vulnerable to illness or has an infection switched the genes?

    I'm not convinced that gene expression is significant to ME per se. There's a theory that people have a 'preferred expression' of illness regardless of the particular illness. Some tend to 'express' illness through gastro problems, some musculoskeletal etc.
  16. Gerwyn

    Gerwyn Guest

    endo retroviruses commonly modulate gene expression either upwards or downwards in different areas of chromosomes which are capable of producing symptoms apparently originating in different parts of the body.I think this is what Dr Kerr is picking up but i dont think his subtypes theory is correct just the same bug causing diff problems depending where it binds on crib sites in our genome.One cause different genes regulated different symptomonology my THEORY of course
  17. V99

    V99 *****

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    What's impression did anyone have on his recent gene expression study looking at the viral trigger of ME?
  18. starryeyes

    starryeyes Senior Member

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    Yes. I think it does. I never had either of those two.. what are they? Emotions? Dysfunctions? States of mind? I mean occasionally but nothing to write home about. I don't like seeing those as any part of CFS diagnosis either because of the history and politics of our illness.

    V99, I haven't seen that but it sounds vaguely familiar.

    I don't trust Kerr. A lot of people say he's got our back but I don't see it.
  19. Angela Kennedy

    Angela Kennedy *****

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    Hi Gerwyn

    My problem with the 'childhood truama causing the development of CFS' is firstly, the vague definition of 'childhood truama'. The Heim et al papers, for example, are so vague, that ANY distressing childhood experience can be classed as 'trauma', and how many people (including the healthy) escape childhood without distress? Again - retrospective reporting of people under stress NOW can lead to introspection not present so much in the so-called 'unstressed'.

    Secondly, whatever experiences affect the development of MIND- exactly HOW do they lead to a specific, serious Central Nervous System and other physiological dysfunction from an infection? I contend this has not ever been verified or even tested properly, and possibly never will.

    If 'stress' is an 'enabler', it would be occurring for all other disease- because ME/CFS sufferers are not the only people to have had 'stress' in their lives! But with ME/CFS there is a special pleading on sufferers are somehow more 'stressed' and that this CAUSES the illness.

    Plus- the emphasis on psychological distress as THE putative 'stressor' ignores that human (and other animal) bodies experience all sorts of physical stress on them.

    On top of that - 'stress' theory is now being replaced with 'Negative Affectivity' stories, where people's negative personalities and psychological 'maladaptive' responses to 'stress' are postulated as causing 'CFS'. Kerr's 'stress index' utilised that assumptions as well as 'stress'. There are so many flaws and problems in those theories.

    And lastly - even with all these problems, on top of them, childhood trauma/stress/cfs papers have terribly weak correlations at best, and so are massively subject to the logical fallacy of correlation equals causation. PLUS - the cohorts are CDC defined! Just to add another problem into the mix...
  20. muffin

    muffin Senior Member

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    TEE: "I don't trust Kerr. A lot of people say he's got our back but I don't see it" As much as I hate to say this, I think I may be watching Dr. Kerr more closely as well. Stress is a human condition and we KNOW that diseases are affected by stress - nothing new there. So why push stress/anxiety so hard in CFIDS? I don't get this? Has Kerr been gotten to by that creepy looking Weasel Wessely and his stupid mental weakness issues?

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