Invest in ME Conference 12: First Class in Every Way
OverTheHills wraps up our series of articles on this year's 12th Invest in ME International Conference (IIMEC12) in London with some reflections on her experience as a patient attending the conference for the first time.
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CMRC: Dr Lipkin, Workshops & wrap up

Discussion in 'General ME/CFS News' started by Simon, Oct 15, 2014.

  1. Simon

    Simon

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    Final set of reports from the CMRC conference, organised by Action for ME (see all reports) and written by various people (I wrote the report of Dr Lipkin's presentation, I think Clare Ogden at AfME wrote the rest of the material here).

    Workshop feedback
    Prof Stephen Holgate, CMRC Chair
    Prof Holgate asked participants from each of the previous day’s workshops to share some of the key points that had emerged.


    Workshop one: Working together for more and better research that benefits people with CFS/ME Facilitated by Sally Crowe
    See earlier report here


    Workshop two: Pain
    Facilitated by Prof Maria Fitzgerald

    “We had an excellent mix of people in this workshop, including a rheumatologist, a physiotherapist, and the parent of a child with M.E.,” reported Prof Fitzgerald. “We began by thinking what a typical patient question would be if they had pain, and agreed that it would be: why do I have pain, what is it for, when will it go away, and what are going to do to make it better?”

    The group discussed that it was necessary to move away from current answers to this – ie. you will just have to get used to it – towards measures that can be taken to increase function. The current situation is not helped by NHS constraints which send patients in particular directions.

    “We need to use our money in two directions,” concluded Prof Fitzgerald. “One is to usefully find out a lot more about pain and CFS/ME, looking for particular types of pain, and the relationship between fatigue and pain. We need to develop new clinical tools, because we can’t have outcomes for clinical trials unless we are confident in what we are measuring.

    “The second strand, but just as important, is to spend our money on patients who are severely affected. We would start with a small number across the UK, more qualitative but with an attempt at quantitative data, and investigate their pain. We’d have to work with carers and families, and we would use such a study as indicators for the future, to help us create hypotheses.”


    Workshop three: Sleep and fatigue

    Facilitated by Dr Sue Wilson

    This group agreed that sleep problems case a lot of distress in CFS/ME, and that an intervention to improve sleep would be beneficial.

    Recent reports of the high incidence of co-morbidity of CFS/ME and sleep disorders were also discussed. “We would like more clinicians to know about this and look for it,” said Dr Wilson.

    “The third key point was that other research councils have repositories for data, and we felt that all our data about people with CFS/ME should be held in something similar, to be accessed by other researchers. We didn’t know if the MRC would be able to do something about that.”


    Workshop four: What should we measure? Core outcome sets and PROMs

    Facilitated by Sarah Brookes

    Everyone in this workshop agreed that what we use to capture the impact of CFS/ME on patients, the heterogeneity of the condition, and particularly the degrees of severity, are inadequate.

    They explored the process that would needed to be develop some new core outcome sets, an agreed standardised set of measurable, recordable outcomes to be used in all clinical trials in a specific area.

    There are already tools to help with this process, for example the COMET initiative

    The group hoped that some of the mechanisms that had been elucidated in CFS/ME, and presented over the course of the conference, would eventually lead to therapeutic trials, hopefully using a set of core outcome measures and patient-reported outcome measures that can be used.


    Workshop five: Inflammation and infection

    Facilitated by Prof Hugh Perry

    This workshop discussed post-mortem tissue – what could be done with patients brains, for example – and how clinical phenotyping was essential if brains were to be examined.

    It was felt that there was a need for in vivo scanning of patients to try and understand what brain areas should be targeted.

    They also talked about:

    · characterising, rather than categorising, patients

    · the need to still recruit as many patients as possible, but more carefully

    · inflammation post-vaccination, and whether it would be possible to see what CFS/ME patients’ response would be to that sort of stimulation.
     
    Last edited: Oct 15, 2014
  2. Simon

    Simon

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    Microbiology & immunology of CFS/ME and other challenging disorders
    Prof Ian Lipkin, Columbia University


    Prof Ian Lipkin outlined 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. His presentation emphasised the use of high-tech methods and following the evidence wherever it leads, before outlining his CFS/ME research programme that takes a similar approach.

    Prof Lipkin is a renowned virus hunter who heads up the Center for Infection and Immunity at Columbia University. He has discovered more than 400 viruses, pioneered new molecular techniques for identifying pathogens and helped the World Health Organisation and Chinese Ministry of Health deal with the SARS outbreak.

    Prof Lipkin first studied CFS/ME in the 1990s, when he was asked to investigate a link between Borna disease virus (which he discovered) and the illness. He and Birgitta Evengard did a large study but found no link with the virus. However, the research highlighted that CFS/ME patients did have immune abnormalities. But there was no funding then to pursue further research in the field.

    Still, he retained his interest, and when he was asked a few years ago to look at a link between the disease and another virus, this time XMRV/PMLV, he jumped at it. Again the link was disproved for that specific virus, though he added they had “not ruled out viruses at all.” In fact, he’s continuing to hunt for them as part of his new programme of CFS/M.E. research.


    Where new human viruses come from

    Having devoted much of his life to hunting down viruses, Dr Lipkin knows just how far the task is from being done, and he is acutely aware of “all the infectious agents that are yet to be discovered.”

    Just how many unknown viruses are out there was highlighted by work Prof Lipkin did as part of the US Agency for International Development’s Predict programme, an ambitious effort to find the next Ebola lurking in nature before it spreads out of control. Most new human viruses start off life in wild mammals, and they often jump to humans via domesticated animals. New forms of flu, for example, often travel into humans from chickens that caught the virus from wild ducks. So one of Predict’s efforts was to estimate how many viruses there were in mammals – and they found a lot.

    Taking a single bat species as an example, Prof Lipkin and colleagues found 55 viruses, 50 of which were new discoveries. They found them by detecting their DNA or RNA in the blood using high-throughput sequencing techniques that Prof Lipkin helped pioneer.

    Extrapolating from this work and more on other mammals, he and his collaborators conservatively estimated that there are 320,000 different viruses in mammals, most of them unknown.

    That’s a pretty big pool of viruses that could produce the next human disease.

    Linking wild viruses to human disease

    The next step is to show that a particular virus causes a given disease. That requires detecting an immune response to the virus, particularly by finding the antibodies that help us fight off an active infection.

    Looking for antibodies has another huge advantage over looking for DNA or RNA, because they stick around long after the body has defeated the infection and the virus has vanished. The body retains a few ‘memory’ antibody-producing cells that allow us rapidly produce more antibodies if the microbe shows up again. Prof Lipkin has previously called this approach of focusing on antibodies as looking for “shadows of infection,” something he’d like to use in CFS/ME too.

    Just as there are microarray chips for detecting DNA or RNA of specific viruses, there are now ‘peptide microarrays’ that effectively allow researchers to check for antibodies against any virus. Peptides (ie. short protein chains) can mimic every possible viral protein that antibodies might bind to.

    “You can cover all vertebrate viruses in a single chip, which is amazing,” said Prof Lipkin. When blood is run across the peptide-studded chipped, the antibodies in the blood glom onto the peptides they’re associated with. And since each antibody was created in response to a particular virus, this reveals all the viruses that have ever infected the individual.

    Prof Lipkin used this method to great effect to study an outbreak of the MERS virus in the Middle East. He tested camel blood in Saudi Arabia with peptide microarray chips and found that the vast majority had at some point been infected with MERS. Added to other studies, this work showed that camels were the likely cause of the human MERS outbreak in the region.


    Some outbreaks are bug-free

    In late 2007 a slaughterhouse processing thirty thousand pigs a day reported an outbreak of a neurological disease and researchers began looking for a pathogen that caused it.

    Prof Lipkin and his colleagues realised that the patients worked at or near the section where workers blew brain tissue out of the pig skulls with a high pressure hose, a new technique that had been introduced when plant owners realized they could sell the brain matter.

    The result was a huge mess, including aerosolized bits of myelin, the fatty insulating sheath around nerve fibres. The workers’ immune systems, it turns out, were reacting hugely to this, triggering the paralysis or weak limbs and other neurological symptoms. The solution was simple: face masks, along with other protective devices.

    There was an outbreak of disease, but, it turned out, pathogens had nothing to do with it.


    Hunting down microbes with planes

    Kawasaki disease occurs in outbreaks, affects mainly children and is sometimes fatal. It’s named after the Japanese physician who described it in the 1960s.

    Inflammation of blood vessels causes symptoms including rashes, swollen hands and feet and ‘strawberry tongue.’ Sometimes it affects the heart too, a problem that kills in around 1% of all cases. People have being trying to figure out what causes Kawasaki disease for years, Prof Lipkin’s group included: they detected Bornaviruses and other microbes, but none proved to be the cause of Kawasaki disease.

    Then a few years ago, a researcher noticed a remarkable association: the outbreaks coincided with changes in wind direction several kilometres up in the atmosphere. Planes with filters flew high into the atmosphere to collect samples. They found very little, and most of what they did find was, apparently, methyl bacteria.

    It turned out that tiny amounts of these bacteria were contaminating the commercial kits they were using to test for microbes – which became a big problem when they had so little ‘real’ sample – and the contaminating bacteria dominated results.

    Researchers had to develop tools to remove the contaminants to see what was really going on: “We went from 73% methyl bacteria to 4%,” said Prof Lipkin. “And suddenly we began finding things we had never seen before.”

    Above all they found the fungus Candida, which might yet prove to be the trigger of Kawasaki disease. Intriguingly, a forgotten study from the 1970s showed Candida can cause a Kawasaki-like disease in mice.

    Autism: from viruses to gene defects and bacteria

    A new focus of Prof Lipkin’s work is the microbiome, the ecosystems of microbes that colonise our body from gut to mouth to skin.

    The work began when the CDC asked his laboratory to investigate the possible link between measles RNA from vaccines and children with Autism Spectrum Disorder (ASD) plus gastrointestinal (GI) problems. In blinded studies they found no link, but Prof Lipkin was intrigued by those gut problems. “Some of these kids may have an infection, some may have a genetic defect,” he says.

    They compared these ASD/GI children with non-autistic children who had similar gut problems. This work revealed that the ASD children had dramatic reductions in the gene expression of enzymes needed to break down carbohydrates in the gut, as well as of the transport proteins that carry digested carbohydrate across the gut wall.

    Prof Lipkin’s team went on to look at the microbiome in the gut and found a relatively obscure bacterium, Sutterella, in the microbiome of around half of patients – but not in controls. What’s more, these patients also produced antibodies against the bacterium Sutterella, suggesting it had penetrated the gut wall and was provoking an immune response. It’s possible too, said Prof Lipkin, that the bacterium produces something that ultimately goes into the brain and causes disease.

    So a study investigating a link with a vaccine found none, but researchers kept looking and instead discovered defects in key gut enzymes as well as unusual bacteria in the microbiome that may have resulted in an infection. These findings might explain why some ASD children respond to antibiotics or changes in diet and probiotics.

    Prof Lipkin briefly mentioned another study, where they found that a particularly aggressive form of colon cancer was linked to a microbiome that produced low levels of a chemical called butyrate. Butyrate, produced by some gut bacteria, can have a tumour-suppressing effect.

    Microbiome medicine

    While HIV infection rates are falling in most parts of the world, they continue to rise in Southern Africa, and one of Prof Lipkin’s studies revealed a surprising role of the vaginal microbiome in the spread of HIV.

    An anti-retroviral gel helps prevent HIV infection in many women, but some women remain susceptible, and these women have high levels of cytokines in vaginal tissue. Many of them also had high levels of a bacterium called Prevotella in their microbiomes, which was probably driving the high cytokine levels and susceptibility to HIV infection. Treating these women with antibiotics could reduce their level of Prevotella and cytokines and, in conjunction with the anti-retroviral gel, help protect them from HIV infection.

    So in these three studies Prof Lipkin and collaborators have found evidence that the microbiome might play a role in autism, colon cancer and HIV infections.

    CFS/ME research programme

    Prof Lipkin outlined his extensive CFS/ME research programme which, because of his expertise, inevitably started with a pathogen hunt: he called it “Bugs R Us.” So far they have drawn a blank.

    They used a technique he developed called Mass Tag PCR to search for specific pathogens in blood plasma including enteroviruses, influenza A virus, herpes virus and Borrelia bacteria, but found no significant differences between patients and controls.

    Then, working with Dr Jose Montoya, Prof Lipkin moved on to high-throughput sequencing that can detect any pathogen, but again they found no specific microbes linked to CFS/ME. They did find that a large but poorly-understood group of viruses – torque viruses – were less common in patients than controls, but the significance of this is unclear.

    Prof Lipkin explained they had profiled cytokines in CFS/ME patients, as had several other groups. They found differences between those patients who had only been ill for a short time (under three years) and patients who had been ill for longer. Prof Lipkin also reported some intriguing findings from Dan Peterson’s Cerebrospinal fluid samples. Cerebrospinal fluid bathes the brain and spinal column, giving a window on what’s happening in the brain, which emerged as a key area of interest in this conference. Cytokine patterns were different in patients and controls, and Prof Lipkin hopes this research will be published fairly soon, but the unpublished results can’t be shared here.

    Metabalomics: chemical clues in the blood

    Prof Lipkin, like many other researchers, believes the emerging field of metabolomics has the potential to reveal a great deal about diseases. Metabolomics is the study of the complete set of small chemicals in any tissue or the blood. These chemicals (or ‘metabolites’ as they are all the result of metabolic processes) include molecules such as amino acids and hormones like testosterone.

    Diseases may have particular chemical fingerprints that will give clues about what’s gone wrong in the body, which is why Prof Lipkin is keen to develop his work on this in CFS/ME.

    He pointed out that the blood metabolome includes many molecules made by the gut microbiome, as a lot of small molecules cross the gut wall to the blood. For example, some gut bacteria can convert chemical found in beans and fish into tryptophan which is actively transported across the gut into the blood. The body needs tryptophan to make the neurotransmitter serotonin.

    The gastrointestinal microbiome’s potential to send chemicals into the body is a big reason Prof Lipkin wants to focus on it: “I think it produces compounds which traffic through the body or into the brain and cause all sorts of curious diseases”. He added that infection can lead to changes in the microbiome, which could influence the illness. And the microbiome also has the capacity to turn on and turn off the immune system. So the microbiome could be playing a role in CFS/ME in several different ways.

    Prof Lipkin is crowdfunding (www.microbediscovery.org) for his microbiome work after twice being turned down by the National Institutes for Health for strange reasons (reviewers of his application said the illness was either psychosomatic or down to a herpes virus infection in white blood cells).

    Prof Lipkin wrapped up by outlining the key ways in which he’s trying to understand CFS/ME. As well as the microbiome and metabolomic work, he’s planning:

    · further pathogens searches, this time in white blood cells (where herpes viruses, for instance, can hide out)

    · gene expression studies to see if patients have different genes active to healthy controls, which could help show what’s going wrong

    · proteomics, which is the ‘protein fingerprint’ of the blood much like metabolomics is the chemical fingerprint; again, differences between patients and controls might reveal clues about what’s going wrong in the illness

    · functional immunology with the National Institute of Allergies and Infectious Diseases.

    Add these to the completed cytokine study and earlier pathogen hunts and you have a comprehensive programme of research into the possible causes of CFS/ME.
     
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  3. Sasha

    Sasha Fine, thank you

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    Thanks, @Simon. You've been hard at work!

    A question: did anybody end up 'owning' any of the actions recommended by the workshops in terms of getting them implemented?
     
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  4. aimossy

    aimossy Senior Member

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    Thanks @Simon - great reading :)
     
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  5. Simon

    Simon

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    Taking collaboration forward: next steps
    Prof Stephen Holgate, CMRC Chair



    “Yes,” was the resounding answer from delegates when Prof Holgate began his closing address by asking if they would like the Collaborative to continue.

    Referencing William Osler, the father of modern medicine, Cofounder of the Johns Hopkins Medical School in Baltimore and later Regius Prof of Medicine at Oxford, and the author of The Principles and Practice of Medicine first published in 1892, Prof Holgate commented that we had practiced medicine in this way ever since.

    “But, as I’ve said repeatedly, we are now the threshold of something completely different, and this is what’s exciting,” he continued. “It has two components to it, both beautifully brought out in this meeting.

    “The first is that we put the individual patient at the centre of our science; the second is that we use new technology to identify new pathways relating to, in this case, CFS/ME using integrated scientific approaches.”

    He then drew out highlights from the conference, the first being the importance of viewing CFS/ME as a multisystem disease(s), and looking at the disease more holistically thereby avoiding a dualistic understanding of the illness as being either physical or mental, when the research literature finds associations with biological, psychological and social abnormalities.


    Clear biological basis

    The second thing was the clear biological bases to this disorder. “I think there has been a mismatch between what patients think we think, and what we think they think,” he said, to considerable murmurs of agreement

    “And that’s a massive issue. I think we need to do something about this, and shouting about the fact that we believe that CFS/ME has a biological basis. We have heard about important gene by environmental interactions (e.g. microglia in the central nervous system, skeletal muscle, sensory neurones) which help reinforce this.”

    He then moved onto heterogeneity, and the fact that CFS/ME is most likely to be “multiple forms of a complicated set of interacting causal pathway, involving disordered immunity and central sensitisation.”

    He referenced inflammation, accompanying stress responses, and multiple organ responses. “I was particularly struck today buy the re-emphasis on brains, the spinal cord and microglia,” he said.

    He talked about triggers, and the possibility that what starts CFS/ME might be different from what maintains it. “We have to think about the biology of those separate process, and identifying endophenotypes; those different causal pathways in the different organs or systemically, that might be causal”.

    Connecting biological and behavioural sciences was also important, urged Prof Holgate, if the patient is going to be at the centre. “Without this, we are going to go nowhere, because much of the symptomatology is expressed through the behavioural sciences.”

    Prof Holgate described how CFS/ME fits the new medical paradigm of stratified medicine (also called personalised, or P4 medicine), and how this could open new doors to unpick its complexity. This in turn could lead to new diagnostic tests, new treatments and improved clinical care.


    Speaking with one voice

    By working together and speaking with a single voice, he said, we could increase patient confidence and propagate research in a different way by pooling expertise.

    “I think we’re going to have to go back to prioritising, to see what is tractable to make a difference early on” said Prof Holgate. “We also need to focus on early career researchers – I think it was great that we had so many PhD and medical students here, because capacity building is what growing a scientific discipline is all about.”

    He moved onto practical steps, setting out what his suggestions for what the CMRC might do next. These were to:

    · Penetrate the medical scientific hierarchy to get CFS/ME more recognised: this is an integrated spectrum of disorders with high medical and socio-economic burden. The conference could be a springboard to launch a major report with the Academy of Medical Sciences, the Royal Society, or Academy of Royal Colleges which brings together experts not only from the UK but also overseas.

    · Involve patients and carers in helping to set the research agenda, starting with feedback from the Associate Member workshop that took place on the first day of the conference and looking at the possibility of developing a patient register for ease of involvement.

    · Work towards a sustainable model to keep the CFS/ME Research Collaborative going: “We can’t go backwards now,” urged Prof Holgate.

    · Being more outward-facing and improving international links to further strengthen and validate our approach to CFS/ME research

    · Capitalise on the coming together of interdisciplinary researchers to develop national protocols for biobanking, phenotyping and applying the new ‘-omics’ technologies to large numbers of patients across the full disease spectrum.

    “Over these past few days, the considerable endorsement of having you all here gives me the energy and enthusiasm to help move this whole field forward and to turn attitudes about the disorder around,” concluded Prof Holgate. “We have to think about what we need as a community to maximise the interactions the Collaborative is trying to promote.”


    End of conference summary

    Prof Hugh Perry, University of Southampton

    Declaring his intention to add only a few things to what Prof Holgate had highlighted in the preceding presentation, Prof Perry said that thought the conference had been hugely successful.

    “When I first met Stephen in the context of a CFS/ME meeting, a number of years ago, I remember being appalled at the quality of the science delivered there,” he recalled. “I could not believe the science community could not do a better job. And now here we are, some years later, and it’s abundantly clear that the science community can do something completely different, and really make a significant difference.

    He ended by drawing attention to “two things that I think are really important.”

    “This cannot fall on the shoulders of a small number of people. I say to the community as a whole: this has to be a shared journey. If we want sustainability, we have to get young researchers to join in, and draw in members of the patient community. This linkage between the science, the charities and so forth, is absolutely essential.

    “Some of our scientific peers have been unwilling to engage in a productive conversation about what CFS/ME is. By encouraging more interest, I hope the ripples in the pond will spread out from this meeting, at every different level.”

    “I thank everyone who has been involved for their huge amount of work to make this conference happen. I have learnt a lot, and I hope you go away with these words: sustainability is important, and this is a science that needs to be done."
     
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  6. A.B.

    A.B. Senior Member

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    I'm glad that Lipkin is involved. His previous work is certainly impressive.

    Holgate's comments come across as psychobabble interpreted through biology (and I had previously a good impression of him)
    Central sensitization: hysteria. The patient perceives things to be worse than they are.

    "what starts CFS/ME might be different from what maintains it" fits perfectly into the BPS model.

    Behavioural sciences: because behaviour is one of the maintaining factors in this condition, right?

    Use of the word "holistic" is usually a red flag and means pretending to treat physical symptoms with psychotherapy.
     
  7. Sean

    Sean Senior Member

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    Thanks for the reports. :thumbsup:

    But I thought we scared them all off? :nervous:

    :p
     
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  8. Esther12

    Esther12 Senior Member

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    Thanks Simon.

    I need to go back and look at the earlier conference reports too.

    PACE PACE?

    TBH I really didn't like the sound of what Holgate was saying eg:

    Given the problems in this area I think that patients have too much confidence in researchers, and that's partly because there's not been enough of the brutal criticism which is needed.
     
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  9. Sidereal

    Sidereal Senior Member

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    Some pretty telling comments by Holgate there.
     
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  10. Sean

    Sean Senior Member

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    A.B.

    The outcome of all this remains to be seen, but the critical change that has taken place is that other areas of medical science, including some very senior players in the biology based disciplines, are starting to take a closer look.

    Somehow I don't believe that the whole of the rest of medical science is going to so easily fall for rhetorical froth whipped up by the CBT/GET school.
     
    Last edited: Oct 15, 2014
  11. A.B.

    A.B. Senior Member

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    Yes, we will see what happens. My comment was pessimistic because someone had to say it. There is also the possibility that Holgate hasn't yet realized how nonsensical the BPS model is (we all have to start from somewhere). I think it would be good if he spent time talking with patients.

    It's also possible that Holgate is trying to appear non-threatening to the BPS establishment. The language is a bit vague and allows multiple interpretations.
     
    Last edited: Oct 15, 2014
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  12. alex3619

    alex3619 Senior Member

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    Any work towards standardized assessment that captures the heterogeneity and full range of symptoms, and especially standardized outcome measures that are objective and reflect the full range of symptoms, gets my support. Much of the bad science out there gets through because there is no accepted standard. Its not that we can have any perfect outcome standard until we really understand what is going on, but some kind of comprehensive standard may be better than a lot of what we see. Then we can improve on it over time.
     
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  13. alex3619

    alex3619 Senior Member

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    To be fair, quite a few models imply this, not just psychogenic models. Indeed if the work showing a clear biochemical change at about year three is right, then this might be a critical part of a biomedical model. The difference between science and nonscience is that science is about things that can be objectively measured, and science makes predictions that can be objectively tested.

    The problem with the BPS model is its so broad it describes almost everything. Its like fatigue in that respect. Hmmm, I wonder if a lesson can be drawn there. This is in part why the BPS model (in general, I am not referring to CFS or ME here) has been labelled as almost useless by some. Its too vague and all encompassing to be really useful.

    Oh, one caveat. As I have commented before, some think that BPS should be BPSE, even more encompassing, with E as environment, such as the physical world we live in and all its perils including toxins etc.
     
  14. Simon

    Simon

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    Throughout this process, Stephen Holgate has worked very hard to keep everyone on board, and that might be behind his ambiguous comments.

    I'd recommend watching his talk to EdMesh, a patient group in Edinburgh (one of several talks he's given to patients around the country). There's fascinating stuff about the use of 'omics technology to understand subgroups of illnesses eg 15 different types of breast cancer and how this leads to tailored treatments. That's the kind of thing he's keen to see much more of in ME/CFS research.
     
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  15. alex3619

    alex3619 Senior Member

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    Yes, systems biology and the entire 'omics revolution is what I have been hoping for since about 2000 ... though I am kind of fuzzy on the exact year as I have trouble even remembering this morning.

    Even Fukuda was well aware subgroups were essential, and said so publicly. Its just that almost nobody else was paying attention until recently.
     
  16. user9876

    user9876 Senior Member

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    I worry about comments of speaking with a single voice we need lots of different voices and strong logical criticism of different theories. That is how science progresses, isn't it?

    The key is keeping criticism constructive and at the level of the ideas being presented.
     
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  17. Valentijn

    Valentijn Activity Level: 3

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    I think he's trying to be conciliatory toward the BPS crowd. While not much can be done about having the BPS fundamentalists involved, I'm strongly opposed to any of the rational members of the CMRC giving into BPS demands or compromising with reality in order to appease them.
     
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  18. Sasha

    Sasha Fine, thank you

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    If Prof. Holgate's summary was all we had to go on I'd be a lot more concerned about these nods to the BPS school than I am. Given @Jonathan Edwards's summary of the conference, however, I'm reassured that things are heading in the right direction.
     
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  19. Cheshire

    Cheshire Senior Member

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    Yes, I'd like it to be a kind of mirror response to their:


    "Don’t challenge the patient's delusional belief in a physical cause for his/her symptoms. But try to slowly drive them to face his/her psychological issues."


    That could be:


    "Don’t openly question the BPS delusional belief in a psychiatric cause for ME/CFS. But keep searching and try to understand what causes the disease till you've built a strong and irrefutable biomedical model and the BPS sand castle collapses."


    And by the way a huge thank you @Simon!
     
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  20. Sean

    Sean Senior Member

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    Unfortunately, human reality inevitably includes political considerations, and politics is the art of the possible, not of the ideal. It demands often grubby and distasteful compromise, but is necessary to achieve your goal, which in this case is to get more objective biology based research done.
     

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