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

Well, maybe, but to be fair, he was interested in looking at cytokine levels etc. to see / prove that the immune system was overactive, in this case, apparently not just after the int-alpha, but also BEFORE the treatment. Which i personally find quite interesting - ie. if your immune system is overactive BEFORE you get the ME/post viral triggering infection, you're more likely to go on to develop ME/cfs or (in this case "chronic fatigue". ... (I'm sure my immune system was buzzing in the months leading up to my triggering infection in 1997). (Much calmer now!).

I really don't think Carmine is BPS - he's not a therapist, he's not into clinics etc, he's a researcher? , so he won't be remotely interested in CBT/ GEt? (no doubt people will pile in with study references saying he has!!!!). Also, Neil Harrison, is also a psychiatrist, but he's researching ME with brain imaging, he is trying to find clues in the study of the physical side of the brain.....

 

The odd thing is that someone posted a referee's report from Pariente in which he criticised a paper manuscript on the basis that CFS was 'known to have a BPS basis' and the paper disagreed so he insisted that the paper was changed. As I indicated in a previous pst I think he has to tell us what he really thinks.

 

It's not about whether someone is "good" or "bad" (or "BPS", sigh), he's somewhere in between. The problem is he has worked with some questionable people and has been permissive of poor quality methodology as a result - specifically using the Oxford criteria, and the Chalder Fatigue Scale in this study for example.

 

I'm sure most people are somewhere "in between", but as we know, this study wasn't about ME/cfs, so whichever criteria were used, it would never be kosha ME/CFS patients. Interesting at most, I'd say. But not deserving of the media blitz last (?) Monday..... IMO.

 

There were "CFS" (Oxford criteria) patients included in this study as a comparison group.

 

Unfortunately part of the BPS paradigm is also hiding one's true thoughts from patients in order to avoid conflict. If you have noticed, when they are pressed to take a position, they always use ambiguous language.

 

And they are very seldom challenged when interviewed. Speaking of which, did anyone hear Wessely and Prof Sami Timimi on the BBC Radio4 Today programme this morning, talking about ADHD? (starts at 1.46.30 here: https://www.bbc.co.uk/sounds/play/m0001phx)*

Listening to Timimi challenging Wessely about his views on diagnosis and the NICE guideline, I felt frustrated that they have never offered the same opportunity to anyone who disagrees with Wessely/Crawley's views on ME/CFS. I wonder if this may be a sign that the chimpanzees may be starting to turn on their leader (to borrow @Jonathan Edwards 's Dynasty analogy) or whether it is simply a reflection of the fact that doctors are allowed to be challenged on any subject apart from ME/CFS.

I note that Timimi has written a commentary in JHP on IAPT in which he states, "Mike Scott’s study provides data demonstrating that the national Improving Access to Psychological Therapies project is not leading to improved outcomes or value for money." (https://journals.sagepub.com/doi/pdf/10.1177/1359105318766139) I've not read the full commentary, or any of his other papers, but I wonder if he's familiar with ME/CFS issues.

Sorry, this is a bit off-topic. Please feel free to move to a new thread @Trish

 

Just listened to that..........SW got the last word as usual.

 

from last year see this post;
https://www.s4me.info/threads/jeremy-vine-bbc-radio2-discussions.2042/#post-72259
the program is now on Youtube and features Carmine Pariante

https://www.youtube.com/watch?v=YpjYmYPKZNE

(for background)
(also, I can't find the link but I think that some of the funding for this research was used to fund one of his other research projects)

bit more info:

 

Can a mind be inflamed, other than metaphorically? Presumably a brain, or parts of a brain, might be.

 

This is not actually how they present it. The BPS position is that:

1. Biomedical people are wrong to insist that all causes of illness are physical because this wrongly dissociates physical from mental.
2. This incorrect distinction is the mistaken view of Descartes - Cartesian dualism (which it is not).
3. The correct view is that the physical and the mental interact and that all illness depends on both types of causation. (This is actually Cartesian dualism or interactionism.) So it is the BPS pundits who are Cartesian. - they believe that there is a ghost in the machine and that the two interact.

Things are further complicated by the fact that 'Ghost in the Machine' is a reference to Gilbert Ryle's tirade against Descartes. But in fact Ryle, as he himself admits half way through the book, is arguing against a machine in the ghost. The ghost is the whole person and he denies that you can attribute mentality to anything inside the person, only to the person.

In other words everyone is talking complete bullshit here. But the key point is that the BPS crowd DENY that all causes are physical, although they never say what they are instead - because they have never stopped to think what they actually mean by this.

 

I've not managed to read much of this thread am in a bad patch atm, so this may well have been extensively discussed & i got no strength to go through it, apologies if im bringing up 'old news'. But i just needed to say that the whole SMC media spin on this is beyond bizarre. what on earth is going on? It freaks me out that there is clearly a purpose to the mega promotion & spin on what is, after all a pretty minor study.... and what IS that purpose? I feel very unnerved.

 

Some interesting posts above regarding the definitions we use when we're talking mental/physical/psychological. FWIW (and if this is too far off-topic I apologise to the mods in advance ), I think there is a million miles between the proposition that ME/CFS is primarily caused by an interaction between the immune system and the brain, and the proposition that it's just a false belief. I think that holds even if one believes that some psychological factors may weaken the blood-brain barrier [1] and predispose a person to neuroinflammation [2], and even if one separately believes that a subset of other illnesses traditionally seen as psychological (i.e. depression) may be caused by neuroinflammatory processes [3]. For me personally, I am very wary of statements that 'it's in the blood not in the head' that have been made at some ME/CFS conferences - neither is proved and the jury is out, but some ME/CFS symptoms (for me, it's the intolerance of sudden loud noises and some loss of language comprehension skills when I'm crashing) that would make me lean brain over blood, though with the caveat that I am of course guessing.

Therefore I try and distinguish between researchers looking at whether 'it's in your head' due to the immune system giving the brain/CNS a kicking and those who view it as 'in your head' because they think it's just the patient overfocusing on themselves or having got used to being in a cared-for-by-others role [4]. It's the latter who are likely to push potentially harmful treatments (you can't harm somebody if they're not really ill), who have put their thumbs on the scale when said treatments have failed to work, and then tried to gaslight anybody pointing this out. In short, there's a massive difference between the work of the PACE team and that of Jarred Younger. Pariente strikes me as being on that continuum closer to the Jarred Younger end.[5]



[1] Though that seems to be controversial and subject to contradictory results. Indeed, google 'stress + blood brain barrier' and the first two results are a study showing stress increasing blood brain barrier permeability in mice and the second showing that stress doesn't increase BBB permeability in mice...
[2] I'm using 'neuroinflammation' here as a shorthand for any kind of negative immune system/brain interaction; I recognise that @Jonathan Edwards is probably nashing his teeth here at this misuse, as it's not proper inflammation
[3] Again, an area that seems to be of real interest right now but that is controversial. I know that the publication of The Inflamed Mind caused some tooing-and-froing in the letters pages as to how much was established fact and how much was still speculative.
[4] The proponents of this model seem much more reticent to push false illness belief openly these days. But it still informs their view: I cannot believe you'd test something like the Lightning Process on children if you thought they were suffering from a genuine inflammatory illness.
[5] Yes, I'm using footnotes and I realise this makes me a dreadful pseud Please trust me when I say this post was even more rambling than it is now before I put them in...

 

IMO C Pariente is playing both sides in an effort to seem reasonable to those of us who know the psychosocial for what it is (flatly wrong). Ambiguity and being disingenuous is not an acceptable way to engage with people.

And I don't find it necessary to bend over backwards to give anyone the benefit of the doubt. We most certainly have never been extended that courtesy. The psychosocial view is one of endless machinations.

If you cut through all the waffle it supports a view of CP asa person who supports the psychosocial view.

Though I suspect he is in a position to change sides quietly when the time comes.

 

@Jonathan Edwards . Is there much research on fatigue mechanisms in other illness? Are fatigue conferences ever held to share ideas across specialities?

 

There has been interest in fatigue in rheumatic disease for twenty years or so. Fatigue in rheumatoid is fairly clearly due to cytokines - TNF and such. Fatigue in lupus is probably not due to cytokines but nobody has written much on the alternatives (effects of autoantibodies on DNA transcription for instance). Special interest groups discuss fatigue but I have not heard of whole conferences on fatigue.

A while back Julia Newton was pushing the idea that all fatigue was essentially the same and probably due to something like poor perfusion. I think we know that cannot be the case (not in RA or 'flu' for instance). The Newcastle group seem to have gone quiet on ME recently - not sure why. Cara Tomas has published on mitochondria but that is another angle. There was supposed to be a trial of rituximab in fatigue in primary biliary cirrhosis but I never heard any results and I am not sure it would tell us more than the result in RA (i.e. that when fatigue is due indirectly to antibodies rituximab helps).

 

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.