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

Well done @JohnTheJack !

Very interesting to hear what Carmine Pariante had to say:
CP - “Yes. I think, that actually that experience, that personal experience that we just heard, links perfectly into the research there we’ve done, because we’ve been able to use a group of people that have a high risk of developing chronic fatigue syndrome, in this case, following an activation of the immune system through a medication that they take for a therapeutic purpose, which in reality is very similar to what happens to many patients at the time at which they have a strong viral infection. And what our research shows is that people who go on to develop chronic fatigue syndrome later on have a hyperactive immune system already even before encountering these immune challenges. So it is part of their, if you like, genetical personal make-up. And when they encounter the immune activation, let’s say for example a viral infection, I think as we just discussed, then their immune system will respond even more. And the uniqueness of our study is that we have been able to study people at this early stage of the illness, um, at a time where, you know, as we’ve just heard, symptoms can be confused just as part of the normal infection process and so these people would not normally be involved in research.”

Interviewer - “What will this mean in practice? Will there eventually be some kind of screening process?”

CP - “Well I think it is two-fold. I think first of all, and again as we’ve just heard, and I totally agree that chronic fatigue syndrome/M.E. should be considered as a multisystem disorder and many organs are involved. And we don’t know what does this increased immune activity early on does to the rest of the body – the brain, the muscles, the liver, other cells in the body – so, and, which then creates the fatigue and the post-exertional malaise, which remains long-lasting. So the first thing is to try to understand what is downstream of this increased activity of the immune system.”
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And good questioning from John:
JP – “I’d just like to ask the Professor to clarify something. We’re not certain that the people in this study do in fact have ME/chronic fatigue syndrome, are we, because they are not actually ME patients but people who had fatigue after interferon-alfa. Is that correct?”

CP – “Well, they have chronic fatigue, err, 6 months after stopping interferon-alfa. So the qualitative experience is very similar to the experience of patients with chronic fatigue, including the fact that they no longer have an immune activation by the time that they have this chronic fatigue.”

JP – “But there is not, for example, post-exertional malaise, and you can’t actually say for sure that these people have ME. But I do think it is interesting that someone is having an illness, and there is no obvious biomarker, and that perhaps could be seen as similar to those people with ME. Is that correct?”

CP – “Absolutely. And, you know, for us this is some kind of light in the fog – you know it’s a direction of travel for research – it is not a conclusive study .”

JP – “You could confirm that there are no psychosocial factors in who develops a chronic fatigue, is that correct?”

CP – “In this study, we found a clear distinct between, for example, depression or other aspect of mental disorders and the patient that developed chronic fatigue.”
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adambeyoncelowe said:
The Telegraph article (and its syndicated spin-offs) has a serious error. They say infections or emotional stress can trigger the illness, while the paper specifically refutes the latter.
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I’m not sure that’s correct. The paper shows no correlation between pre-illness psychosocial factors and persistent fatigue, but, as far as I understand, it does not specifically refute the notion that a similar immune response could be triggered by acute emotional stress. Participants were not predisposed to persistent fatigue due to psychosocial factors, but that does not rule out the possibility that a normal emotional response to a very stressful event could be a trigger for an immune response which leads to persistent fatigue in patients with predisposed immune systems.

I’m not saying that that is true. I’m just saying that, as far as I understand, such an idea is not specifically refuted by the paper.

However, it is certainly wrong for the report to claim that the study suggests that CFS can be triggered by an out-of-control immune system which overreacts to emotional distress. The study provides no evidence to support or refute this idea – as far as I can see.
 
Robert 1973 said:
I’m not sure that’s correct. The paper shows no correlation between pre-illness psychosocial factors and persistent fatigue, but, as far as I understand, it does not specifically refute the notion that a similar immune response could be triggered by acute emotional stress. Participants were not predisposed to persistent fatigue due to psychosocial factors, but that does not rule out the possibility that a normal emotional response to a very stressful event could be a trigger for an immune response which leads to persistent fatigue in patients with predisposed immune systems.

I’m not saying that that is true. I’m just saying that, as far as I understand, such an idea is not specifically refuted by the paper.

However, it is certainly wrong for the report to claim that the study suggests that CFS can be triggered by an out-of-control immune system which overreacts to emotional distress. The study provides no evidence to support or refute this idea – as far as I can see.
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That may be so. Thanks for the clarification.
 
adambeyoncelowe said:
To put it another way: this is useful because it shows that illness can persist despite the absence of obvious markers. It's a major nail in the coffin of the 'no abnormalities = no problem' narrative.
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We all know we are ill despite the absence of obvious biomarkers, as would anyone who had ever listened to us. We have known for decades. Nobody ever had any business putting about a "no abnormalities = no problem" narrative in the first place. And in fact they didn't, they said "no abnormalities = illness perpetuated by biopsychosocial factors following an initial assault on the system". This paper doesn't seem to contradict that, merely that they have identified an initial assault which can result in some participants still feeling "fatigued" six months later.

So what?

The BPS brigade can still argue about why the fatigue is perpetuated, or does this paper suggest a mechanism which disputes the BPS narrative?

What this paper does is position some of the very same BPS quacktards who have been abusing us for decades as saviour scientists, complete with completely over the top media coverage and overuse of words such as "new" and "first time" etc, which is basically an insult to all the biomedical research they have been ignoring or making sure hasn't been funded for the last X years. Having dumped BPS manure on the ME garden for so long, they now feel entitled to come up smelling of roses. Worth a try I suppose, and probably one step up from forcing mice to swim.

JohnTheJack said:
I'm on BBC Wales at 4:40 discussing illness and this paper. https://www.bbc.co.uk/programmes/b0079gdh/broadcasts/upcoming
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Fabulous, just fabulous.

JaimeS said:
The implication is that her arguments were from emotion rather than facts, or that women arguing in general should be thought of as emotional. I like your joke about all of Westminster being emotionally motivated, @TiredSam but I think we know what the author is implying here. Morally repugnant use of language.
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Yes, I thought that they just wanted to get the words "Carol Monaghan" and "emotional" in the same sentence, inviting the reader to think "she's hysterical", but considering how the sentence was constructed I didn't feel I could make such a bold claim. I'm pretty sure it's what was going on though, especially as it was immediately followed by the bare-faced lie:

Others defended the treatment.
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JohnTheJack said:
Interesting analysis of the study by @sTeamTraen

https://steamtraen.blogspot.com/2018/12/have-scientists-found-explanation-for.html
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Thanks. :)

Something that didn't make the post: I think there may be a small silver lining here for the ME/CFS patient community. To the extent that, in this study at least, the authors were prepared to entertain the idea that whatever is causing hepatitis C patients to still be fatigued six months after their treatment could be the same thing that is causing ME/CFS patients to be fatigued after many years (even if I don't think they have got remotely close to actually showing that), it suggests that these researchers are open to the idea of a physiological cause. The alternative would be to argue that the hepatitis C patients with persistent fatigue are also (starting to be) affected by whatever psychological factors purportedly cause or reinforce ME/CFS symptoms; however, no such suggestion was made in the article, and indeed in section 3.5 they note that there was no difference between the "persistent" and "resolved" fatigue groups on any of their psychological measures, some of which have been associated with ME/CFS in previous research.

Also, it seems to me (but as a non-patient I'm not the best placed to comment on this) that the message from the press coverage is "ME: It's not just in your head" (e.g., Mail Online here). As my blog suggests, I don't think this study actually tells us anything about that question, but it seems better than the Rod Liddle version ("It's all in your head, snowflakes").

I thought the senior author, Pariante, rather over-egged the pudding in the Radio Wales discussion. See here around 48:10: "What our research shows is that people who go on to develop CFS later on have a hyperactive immune system"... "We have been able to study people at this early stage of the illness". But nobody in the study actually developed CFS, as far as we know.
 
Having listened to the various parties give opinions I think I en dup with this conclusion:

1. That the research programme is an intelligent attempt to use interferon induced fatigue to inform general approaches to ME.
2. That the current set of results tell us little and probably nothing at all. The correlations found do not allow any sort of prediction that anything similar would apply in ME as such.
 
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