Science at the UK CMRC Conference, 1-2 Sept 2014

Bob

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I thought he'd given up because of the flaw. Did the lab run the tests again at no charge?
Yes, he was adamant that the lab run the tests again for free, because they'd messed up. And I should imagine that it's quite hard to argue with Dr Lipkin about stuff like that!

I'm trying to remember the initial conclusion before they discovered the error.
I can't remember any details, but I got the feeling that the results really were utterly irrelevant because of the collection flaw.
 

Scarecrow

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Esther Crawley Summary of the Panel Discussion presentation

The University of Bristol have been following a birth cohort from the early 90s.

This CFS/ME study is looking at the prevalence of the illness in children at 13, 16 and 17 and is examining the relationship to certain 'risk factors'. Which factors are causal and which are not? At 13 there was an equal sex ratio but at 16 and 17, CFS/ME was much more common in girls than boys. The graph was up too briefly to see the ratio.

[In 'Last Leg' fashion but no joking, is it wrong to say that I rather like this study? But on the other hand there seemed to be an awful lot of 'risk factors' so I'm thinking it's quite likely they'll find a relationship to something.]
 

greeneagledown

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Another reason I think Lipkin could be referring to the RNA sequencing study is that he already hinted at an important finding in his interview with Mindy Kitei back in May, in which he said, "A paper coming out in the not to distant future about which I’m very encouraged has to do with RNA profiling host response." He went on to note that they were still analyzing the results at that point in time. http://www.cfscentral.com/2014/05/candid-conversation-with-dr-ian-lipkin.html
 

Snowdrop

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Yes, well, refrigerator mothers and autism didn't pan out for the psycho/babble community so try, try again.

Since she was giving a presentation could she not have included preliminary findings ie what conclusions they were drawing from this shared with the public.
 

Scarecrow

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Carmine Pariante Summary of the Panel Discussion Presentation

Using Hep C patients treated with Interferon-alpha as a model for CFS.

Why do some people, when challenged by an infection, develop acute fatigue, while others don't. Further, why do some of those who develop fatigue later recover and other do not?

Interferon-alpha stimulates inflammation. 90% of Hep C patients treated develop fatigue. 50-60% of these return to normal when treatment stops. 40-50% remain fatigued. The fatigue outcome seems to be independent of whether or not the virus is cleared.
 

Simon

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Summary of the UK CMRC Conference, Day Two (Tues Sep 2)
Tweets by Sonya Chowdhury [SC], Action for ME [AfME] notes by @Scarecrow, thanks all.

Plenary Session 2: MRC funded CFS/ME research

Chair: Stephen Holgate
[not many tweets - perhaps the researchers didn't want preliminary results disclosed]

Stuart Watson (for Julia Newton): Understanding the pathogenesis of autonomic dysfunction in chronic fatigue syndrome and its relationship with cognitive impairment- An Update

Fai Ng: Biological fingerprints of fatigue
Fai Ng discussing fatigue fingerprints in Sjogren patients and insight for #mecfs
Fai Ng Summary of Panel Discussion presentation

Studying fatigue in Sjogrens syndrome
  • about 30% of Sjogrens patients don't have fatigue at all
  • anti TNF treatments in Sjogrens (and in RA) completely clear fatigue in a subgroup of patients
  • in some patients, fatigue remains even after inflammatory symptoms are treated
Carmine Pariante: Inflammation & fatigue: is it different from depression?

Sue Wilson (for David Nutt): Sleep & chronic fatigue
Summary of Panel Discussion presentation.

This was a 'psychopharmacology' sleep study. The treatment artificially increases deep sleep.

From what I could gather it only involved patients. They were required to come into the centre for two separate weeks. On one occasion the treatment was administered and on the other, the placebo.

The affect on function was measured. I think that subjective and objective measures were used.

Anne McArdle: Mitochondrial function & cytokine production in skeletal muscle of patients with CFS
SC said:
Prof Anne McArdle outlining mitochondria function and cytokine production research. Double blinded sample analysis

- importance of mitochondria in preserving muscle function. Systemic measures of inflammation and muscle biopsies approach
Esther Crawley: The epidemiology of CFS/ME in children
Esther Crawley Summary of the Panel Discussion presentation

The University of Bristol have been following a birth cohort from the early 90s.

This CFS/ME study is looking at the prevalence of the illness in children at 13, 16 and 17 and is examining the relationship to certain 'risk factors'. Which factors are causal and which are not? At 13 there was an equal sex ratio but at 16 and 17, CFS/ME was much more common in girls than boys. The graph was up too briefly to see the ratio.

[In 'Last Leg' fashion but no joking, is it wrong to say that I rather like this study? But on the other hand there seemed to be an awful lot of 'risk factors' so I'm thinking it's quite likely they'll find a relationship to something.]
Peter White: PACE: A trial & tribulations

Q&A session


Plenary Session 3: Infection
Chair: Paul Little

Andrew Lloyd: Acute infection & post-0infective fatigue as a model for CFS
SC said:
Prof Lloyd explaining his Dubbo Infection Outcomes Study and what this might mean for #MECFS

Prof Lloyd outlining genetic determinants of severity and duration #mecfs UK Research collaborative conference
from Andrew Lloyd's summary of this presentation for patient's yesterday:
They looked at the mechanisms underlying the disease process and post infective fatigue. The beauty of their study is that it starts on day one of the illness, and examines the acute phase and recovery. [In other words, they're not presented with a post infective fatigued patient and left wondering what's happened before they got into that state.]

I don't think that this was anything other than a very short summary of the Dubbo study, although I don't remember EBV, Ross River Fever or Q Fever being specifically mentioned.

Ian Lipkin: Microbiology & immunology of CFS/ME & other challenging disorders
SC said:
Prof Lipkin introducing his presentation having travelled despite breaking his ankle on Saturday!

- sharing zoonotic work. Building a picture to inform #mecfs work. @actionforme seminar tomorrow [WEDS] with Prof Lipkin [this will be filmed, for those who can't make it]

-Prof Lipkin sharing results from his (hopefully) soon to be published #mecfs cytokine study.

-Prof Lipkin can't yet share details of #mecfs something "really hot". Exciting news!

"It’s critical that we stay the course.." [from another tweet]

Lunch, and more posters

Plenary Session 4: Pain, paediatric CFS & epidemiology
Chair: Esther Crawley

Maria Fitzgerald: Understanding pain mechanism in children & adolescents

Jon Tobias: The epidemiology of adolescent CFS and Chronic Widespread Pain

Roberto Neuvo: Recovery and persistence from CFS/ME in adolescents


Taking collaboration forward: next steps
SC said:
Prof Holgate summing up CMRC Conference for # MECFS research. "Attention must be paid to prioritising topics for raising funds."

"We must penetrate the medical/scientific hierarchy to increase the profile of #MECFS and put patients at the centre."

"We can't go backwards. We must be outward looking to develop international collaborations.
End of conference summary
SC"[B]]Final word from Prof Hugh Perry: this has to be a shared journey. Patients said:
The buzzing UK CFS/M.E. Research Collaborative Conference has now drawn to a close - look out for our full report on the event!
 
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Scarecrow

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Yes, well, refrigerator mothers and autism didn't pan out for the psycho/babble community so try, try again.

Since she was giving a presentation could she not have included preliminary findings ie what conclusions they were drawing from this shared with the public.
Not without a lynching, perhaps? I wonder if she shared it with other researchers today?

By the way, the 'risk factors' were up and down so quickly, I couldn't take in what they were. We can only hope some sort of infection was one of them.
 

Sasha

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Outstanding, @Simon - thanks for putting all that together.

Very impressed, incidentally, that Dr. Lipkin broke his ankle on Saturday and yet still flew over to the UK (presumably the very next day). Really wish I knew what this hot new finding was!
 

Sasha

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Prof. Edwards is back from the conference and said on another thread:

Looking forward to hearing more about that.
Er, yes, touch of brain fog tonight collapsing after a nice curry and beer back home. I have got notes of key points and will try to get them down here over the next day or two. Maybe the most important thing is that there was a really clear consensus about the methodological issues that get discussed here on PR. Everyone is up to speed on patient subgroup issues, problems with looking for mediators in the wrong place and getting false negative results etc etc. Homing in on local events in the brain and probably microglia looks the way a lot of people are thinking. Interferons continue to look interesting.

I am pretty sure that Lipkin's hot news is something we have not heard of before at all. It may take a while to come through. It is not the cytokine stuff we have seen but it does come from Mady Hornig, I think.

And although we must, as Sasha said, keep this to the science I was very encouraged by the political atmosphere. this was overwhelmingly a conference about neuroimmunology. The word biopsychosocial was used precisely twice and the second time for the purpose of saying that the word was completely meaningless and unhelpful. It was clear that almost everyone present was in strong agreement. The word suggested to replace it is just 'biological'.

Interestingly, apart from the Lipkin/Hornig lab and the Newton lab the science this week was all different from that at IiME. The two meetings complemented each other for me very nicely. We have now had a really broad exposition of the best science at UK meetings this year and new collaborations are sprouting like weeds. It all looks very exciting to me.
 

Scarecrow

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I'm back for the Q&A summary. Once again, I have to apologise. I'm so bad at this. I haven't noted down everything, just what was of particular interest to me. @Leopardtail was to have been at the patient session as well as @Jonathan Edwards, so hopefully any omissions and errors will be attended to.

Someone asked a question about definitions, referenced the CCC and noted that brain fog was a major problem for him rather than fatigue. (I think that in part this was provoked by so many of the panel having an interest in 'fatigue' and 'chronic fatigue' rather than 'chronic fatigue syndrome' or M.E.)
  • Ian Lipkin was very quick to respond that it was really important to note that the patient group had more weight by sticking together. (In his own Panel Discussion presentation, he'd stressed the importance of different cohorts and that there were subsets in many diseases, eg cancer). Replying to the patient's question he used the phrase "lump but parse".
  • Robert Dantzer, in response specifically to the fatigue element of the question acknowledged that yes, they were studying 'fatigue' but that fatigue was usually associated with other symptoms such as brain fog.
Another question led to a terminology discussion.
  • Either Stephen Holgate or one of the panel pointed out that MS is likely to include as many as 30 different diseases but they are all referred to as Multiple Sclerosis.
A further question related to patient cohorts and severity of illness
  • Stephen Holgate (whose background is in asthma) said that there were six distinct subsets of asthma and that severity is a false classification. All six groups include mild, moderate and severe.
  • I think that it was the same question that led to a comment from Stuart Watson about stratification for research purposes. In the Newcastle studies, they've found that stratification has created differences in results, for example excluding patients with co-morbid psychiatric disorders, also jaw pain.
Sorry this is such a skewed report. In part, it's because making sense of a diverse patient group in research was my main theme for the conference and when I was making my notes, I wasn't expecting to have to relay so much of it here. But also, as I said in an earlier post, it's because it was genuinely the biggest topic at the conference and one which both patients and reseachers seem to have thoroughly embraced.
 

Sasha

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I have got notes of key points and will try to get them down here over the next day or two.
Thanks! That would be great.

Maybe the most important thing is that there was a really clear consensus about the methodological issues that get discussed here on PR.
I was interested to see the focus on engagement with patients, particularly the session on patient participation in the research process. Were similar suggestions coming out of that as the ones that come up here? Any new and interesting ideas?

this was overwhelmingly a conference about neuroimmunology.
So perhaps we're back full circle to ME (defined by WHO as a neurological disease) with immunological knobs on. Interesting to hear that the focus was that tight - I've seen ME referred to as a neuro-endocrine-immune disorder, among other things. So many systems are involved. Does that focus imply to you that certain systems are emerging as causative or do you think the neuroimmunological focus was just a function of which researchers happened to be there?

The word biopsychosocial was used precisely twice and the second time for the purpose of saying that the word was completely meaningless and unhelpful. It was clear that almost everyone present was in strong agreement. The word suggested to replace it is just 'biological'.
Outstanding!

Interestingly, apart from the Lipkin/Hornig lab and the Newton lab the science this week was all different from that at IiME. The two meetings complemented each other for me very nicely. We have now had a really broad exposition of the best science at UK meetings this year and new collaborations are sprouting like weeds. It all looks very exciting to me.
Very positive - could hardly have hoped for more. I think that some researchers were invited because they've got an interest in some of our symptoms (pain, fatigue) in the context of other diseases in the hope that there might be some productive commonalities and as a way of bringing new expertise into the field. Do you think that aspect worked well? Did they already seem up to speed on the issues?
 

NK17

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@Scarecrow you've done a marvelous job, your preliminary reporting is quite clear, considering our brain fog and the complexities of ME, which is finally resurfacing as a serious, debilitating, neuro-immune illness.

Thank you for taking up this task.

A big thank you to our extraordinary doctor @Jonathan Edwards, can't wait to hear more from both of you.
 

Scarecrow

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Did they raise there the question of money - It seems that more and more researchers are interested in ME but will they get money for ME research? we know that it´s always problematic.
There were some mention of crowd funding and also of raising the profile of ME/CFS to attract funding but, no, nothing concrete at the patient sessions.

It has to be a good sign that the Medical Research Council funded the conference.
 

Sean

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The word biopsychosocial was used precisely twice and the second time for the purpose of saying that the word was completely meaningless and unhelpful. It was clear that almost everyone present was in strong agreement.
:)

Possibly the single most important thing to come out of the reporting so far. Seriously. We really need that basic paradigm shift, above all else. Everything will flow from that, and indications increasingly are that this long overdue shift is underway.

Much thanks to all those who have been reporting back to us. :thumbsup: :hug:
 
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It's Esther Crawley. She'll find some way to accuse mothers of being neurotic and/or depressed, and somehow causing CFS in their children as a result.
Did Dr Crawley explain the science that leads to 'fatigue' clinics declaring children whose symptoms are completely unchanged as recovered from myalgic encephalomyelitis, then rediagnosing them with persistent refusal syndrome? The scientific research that has gone into that must be startling.