Persistent fatigue induced by interferon-alpha: A novel, inflammation-based, proxy model of Chronic Fatigue Syndrome, 2018, Pariante et al

Sly Saint said:
Before all this hype, CP was maybe only a small blip on the radar.
But now we have to question why the SMC has promoted this study and CP so much.
The last time they did this was with Crawley and the LP study and Crawley has repeatedly claimed that CBT 'changes biology'.
It would be good to know CPs opinion on this if anyone gets the opportunity to ask him.
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Yeah..... so, I was at the CMRC meeting in November, and (and this is only my impression, not "fact"), Carmine probably knows people who are close to the SMC, so was in a position to get their attention, & therefore get publicity. In fact, those he has contact with probably wanted to get this published, for whatever reasons. So they called a press conference, so all the papers arrived. ==> coverage nationally.

I suspect (again, I do not know) that this was also the case with EC's Smile trial - it's who you know/ are connected with, that gets the SMC interested. & they then trumpet it with press conferences etc. Meanwhile, vast amounts of biomedical research goes unreported. .... the SMC simply do not appear interested.

My personal view, FWIW, is that the SMC has a hideous BPS bias, and is not fit for purpose to the point that it should be investigated. & maybe shut down - it's a registered charity, FFS! (I think!). This response earlier in the year was awful. http://www.sciencemediacentre.org/cfsme-the-illness-and-the-controversy/ Merry Christmas!
 
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phil_in_bristol said:
My personal view, FWIW, is that the SMC has a hideous BPS bias, and is not fit for purpose to the point that it should be investigated. & maybe shut down - it's a registered charity, FFS! (I think!).
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I understand Simon Wessely is one of the founders and directors of the SMC. I think that tells us all we need to know about their bias, and why CP got his research promoted.
 
Trish said:
I understand Simon Wessely is one of the founders and directors of the SMC. I think that tells us all we need to know about their bias, and why CP got his research promoted.
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It tells us how he got it promoted, but I'm not sure it completely tells us why.
So my question still stands, about CP, and Wesselys/SMC motives for promoting him and this particular research.
 
phil_in_bristol said:
Carmine probably knows people who are close to the SMC
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as pointed out he has ties to SW; they have also worked together.

I found a link to the info I alluded to in an earlier post:
"
Dr Carmine Pariante has received Funds for a member of staff and funds for
research.
Professor Pariante’s research on depression and inflammation is supported by:
the grants ‘Persistent Fatigue Induced by Interferon-alpha: A New Immunological Model
for Chronic Fatigue Syndrome' (MR/J002739/1) and ‘Immuno-psychiatry: a consortium
to test the opportunity for immunotherapeutics in psychiatry’ (MR/L014815/1; together
with GSK), from the Medical Research Council (UK); the National Institute for Health
Research (NIHR) Mental Health Biomedical Research Centre in Mental Health at South
London and Maudsley NHS Foundation Trust and King’s College London; by Johnson &
Johnson as part of a programme of research on depression and inflammation; and by a
Wellcome Trust-led consortium that also include Johnson & Johnson, GSK and Lundbeck."

https://www.rcpsych.ac.uk/pdf/CALC_GAPconfDOI for website 7 Oct.pdf
(2015)
 
Article published today not about this particular research paper but the area that Pariante is working on:
Researchers: Depression May Be a Physical Illness Linked to Inflammation
A growing body of research, including scientific papers and results from clinical trials, appears to be revealing a connection between treating inflammation and alleviating depression. In late July 2017, Stanford researchers revealed that they could create a diagnostic laboratory test for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), along with what may be a world-first treatment. This work confirmed and built on prior work connecting ME/CFS — a disease which is often associated with depression — and inflammation.
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http://www.mysterious-times.com/201...be-a-physical-illness-linked-to-inflammation/
 
phil_in_bristol said:
http://www.sciencemediacentre.org/cfsme-the-illness-and-the-controversy/
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Science Media Centre said:
The existing evidence for CBT and GET for CFS/ME, cited by the scientific community and underpinning NICE recommendations, consists of approximately a dozen randomised controlled trials and meta-analyses published in journals like The Lancet and PLoS, and three Cochrane reviews (generally considered the gold standard of medical evidence). Those who disagree with this body of evidence cite review articles and reanalyses of trial data published in low impact factor journals such as The Journal of Health Psychology and Fatigue: Biomedicine, Health & Behavior
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That's a logical fallacy known as "Argument from authority", they should judge papers based on their merit not which journal they were published in. As for meta-analyses, garbage in - garbage out.
 
DigitalDrifter said:
As for meta-analyses, garbage in - garbage out.
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I have used the phrase BIBO, Babble in, Babble out. As for the fallacy, this is a well recognised problem in academia and especially the media.

Their use of "gold standard" leaves a lot to be desired. Its one of those widely misused phrases. In m view it mostly means whatever is currently accepted as best practice. Gold standard can be very biased or inadequate. The Cochrane papers in question should probably be retracted. But who is going to do that?

For example, I have long argued the RCT is NOT the gold standard in medical trials. It can be a gold standard, if there are lots of caveats, like good study design, placebo controls, double blinding, and so on. That is it has extra things to control even more biases. That is a major point of study design ... to remove as many biases and confounds as possible. Even with all that the study can still be highly biased, as in the PACE trial. PACE was kind of an RCT (not exactly) but failed to even deal with the other things that are known biases.

PACE also used invalid statistical analysis, which at least PD White was aware of, in calculation of normal in SF36PF data. Deliberate use of invalid methods to bias the result is .... ?

ETA Corrected the spelling of BIBO, thanks to @MeSci pointing it out.
 
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I have search alert on Google, this paper by Pariante et al just keeps on coming up! :mad:

Here's the latest...

Strongest Evidence Yet Links Chronic Fatigue Syndrome And an Overactive Immune System

According to a study by researchers at King’s College, London, when a certain individual’s immune system is attacked by an infection it may cause long-lasting fatigue when that immune system over-reacts and that fatigue may continue long after the infection is eradicated.
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There’s hope though with the rise in research efforts in the last few years. And while it seems difficult to pinpoint the exact part the immune systems have in the development of CFS, the newest findings are showing that an overactive immune system may be the culprit.

Researches (sic) turned to people with an illness of Hepatitis C (HCV). 55 patients were treated with a drug called interferon alpha which is a common treatment for HCV and which causes the immune system to go into overdrive. It’s also known to cause acute fatigue similar to CFS which can last for many months after treatment.
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“In conclusion, findings from this study support the hypothesis that abnormal immune mechanisms are important in CFS, but only early in the course of the illness, around the time of the trigger, rather than when the syndrome is established,” the authors conclude.

“A better understanding of the biology underlying the development of CFS is needed to help patients suffering with this debilitating condition,” says co-author Carmine Pariante, an expert in biological psychiatry at King’s College.
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Looks like some nice PR for the new year. I can't really fathom why this website would care about the subject to begin with.
But all praise to Kings College. Kings College rocks. They will be our saviours. Either that or I've been deeply into the kool-aid punch.

On a different note. I'm inclined to think it possible that over the long term the body may mount multiple 'abnormal' immune assaults before going back to functioning that would not show anything.
 
“In conclusion, findings from this study support the hypothesis that abnormal immune mechanisms are important in CFS, but only early in the course of the illness, around the time of the trigger, rather than when the syndrome is established,” the authors conclude.
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my emphasis

ahhh now i see why there was all the SMC hype & spin - so they can use this study to appear to add weight to their hypothesis that it starts off with an organic problem but is them perpetuated by the cycle of abnormal beliefs>misinterpretation of normal bodily sensation>too much rest >deconditioning & so on.

If they can appear to show that the condition is caused by an overactive immune system at the beginning & show that the abnormality goes away, then hey presto that will be the next thing that shows up in patient treatment guides
"at the outset of your illness there was a problem with your immune system, but it has been proven that this problem no longer exists so you can be reassured that any uptick in fatigue (-the catastrophic collapse in cognitive & bodily functioning) after exercise is completely normal (all in your imagination)"

No wonder they over promoted it to such a ludicrous degree. They now have something to use to "prove" that the organic onset abnormality is no longer operating & any ongoing problems are a result of our own thoughts/behaviour.

In addition of course they can tell people in the early stages that mindfullness/CBT etc can 'calm' that overactive immune response if any of it is still in play.

Wow no wonder they love him, Pariante is now the darling of the BPS world, he has done a study which can be spun to appear to 'prove' their original hypothesis in organic terms. Never mind that the study was done on people who may or may not have anything whatsoever to do with us.

said in soothing tones .... "see now dear little patients & naughty little activists, we never said that there wasn't anything physically wrong, there was something wrong, you got a bug & your stress levels/anxiety about it caused your immune systems to overreact. But it's not happening any more, there there now, just do the work & you'll be in 'recovery'."
 
We are being drawn into the hype.
It is not about ME.
It is not new news.
That' s what should be being highlighted. It' s about fatigue in a specific circumstance.

The 2 important points that could be worth promoting is that
Fatigue can persist without a biomarker
There is no psychological illness slant

Other than that i would caution against the rise of " proxy" . Paediatrics already have CDF ( chronic disabling fatigue) as a defined proxy for CFS ( and ME) , and nobody is batting much of an eyelid about it.

I would also suggest as we enter into the NICE guideline period, that patient committee members/ representatives are able to provide more details on studies than is given in abstracts. Abstracts are a publicity device and are spun as such.
 
Amw66 said:
Fatigue can persist without a biomarker
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I would modify this to "Fatigue can exist even without a known biomarker." Its only a matter of time, in my view, before it will become "Fatigue can exist with these biomarkers ...".
Amw66 said:
Abstracts are a publicity device and are spun as such.
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Abstracts are to tell you if a paper is potentially relevant and worth reading. Any study that uses just abstracts is junk science at best, and I am being generous writing that.
 
alex3619 said:
I would modify this to "Fatigue can exist even without a known biomarker." Its only a matter of time, in my view, before it will become "Fatigue can exist with these biomarkers ...".

Abstracts are to tell you if a paper is apotentially relevant and worth reading. Any study that uses just abstracts is junk science at best, and I am being generous writing that.
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Yes, i would agree with these points.
My understanding is that the relevant research literature for NICE review is being selected via abstracts only.

From some recent papers, the limitations can only be judged by reading the full paper, as it is there that the gaps in data/ bias/ consideration of outliers and ambiguities are found. This is concerning to me.

Happy to be corrected if i have picked this up wrongly.
 
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