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

I note he says an overactive immune response is implicated in the cause of CFS. That could leave the BPS with their deconditioning etc as perpetuating it if they interpret 'cause' as a transient trigger. I'm sure the likes of Chalder and Moss Morris in their therapy department at Kings will plough on with CBT regardless.
 
We should remember that the research they are doing isn't on patients with ME but those treated with interferon alpha they are then trying to draw an analogy and I suspect have not done any work to validate if the analogy stands or is valid.
 
Sarah Knapton's Telegraph coverage is on yahoo news, again, didn't much of a reason why they'd be hyping these results like this: https://uk.news.yahoo.com/chronic-fatigue-syndrome-may-triggered-000100009.html

edit: This piece does start with:

"Chronic Fatigue Syndrome may be triggered by an out-of-control immune system which overreacts to an illness or emotional stress, a new study suggests."

I didn't see anything in the study to suggest that emotional stress triggers an out-of-control immune system, and it seems that wasn't tested.
 
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Just saw Kindlon tweeted the abstract to: http://sro.sussex.ac.uk/80506/

Looks like it is the results we already knew about, which still leaves the puzzle of why they decided to push media coverage of this.

Maybe this is laying the groundwork for Wessely going to the House of Lords, or a PACE pushback? Then hacks will be able to quote someone like Pariante as a representative of the 'other' side, and have him praise Wessely or say PACE is unfairly attacked?

Can't really think why this study would be getting promoted like this by the SMC & co.
 
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Independent coverage with some quotes from Pariante:

https://www.independent.co.uk/news/...us-infection-diagnosis-gp-kings-a8684111.html

“The model that we propose is that these people have an ongoing primed immune system,” professor Carmine Pariante, senior researcher at the King’s Institute of Psychiatry, Psychology & Neuroscience, told The Independent.

“That could be either because of a genetic predisposition or because they’ve been exposed to infections early on in their life.”

“So their immune system becomes more hyperactive, and when the trigger comes – in this case interferon-alpha but it may be an acute infection – that causes an even higher response which puts them on a trajectory for chronic fatigue syndrome.”

“Although screening tests are a long way off, our results are the first step in identifying those at risk and catching the illness in its crucial early stages.”
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The articles framing of *challenges CFS is 'all in the mind'* isn't useful imo.
 
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It does seem that the press coverage is over hyping the study and I worry that quotes I saw from Charles Shepherd come across as over positive about the authors' interpretations of their results. It is good that the press are taking seriously a biomedical study of ME and it does suggest that the British establishment is shifting. [Added - As long as, as others say above, this is not an attempt by the BPS crew to come up with a biomedical onset model that does not undermine subsequent CBT/GET.]

I have read the article through a couple of times, but as always struggle with understanding new terms, however the authors do seem to have taken at face value bad advice from the BPS crew about what ME is. My first thoughts are:

Profoundly disappointing that their 'CFS' patients were recruited on the basis of the discredited Oxford criteria, and the authors don't seem to demonstrate in the text that they understand the distinction between the symptom of 'chronic fatigue' and the condition ME/CFS or 'chronic fatigue syndrome'.

Though they refer to cognitive disturbances, they make no mention of the core ME/CFS symptom of post exertional malaise that is not required by the Oxford criteria.

Because they focus only on the symptom of fatigue it is not clear how much of a meaningful proxy model their HCV group might actually be, and because they use the Oxford criteria we have no idea how many of their CFS group actually have ME/CFS or rather just the symptom of chronic fatigue arising from other causes.

(That is not to mention also concerns about how useful the Chalder scale is.)

Further they suggest that the resultant chronic fatigue is related to a predisposed immune system but I do not see how that can relate this to ME as their hepatitis C group have already an active infection before they are exposed to the trigger of the drug treatment, also making this a dubious proxy model for at least the ME subgroup where the active infection is the primary trigger.

[Added - My feeling so far is that though the authors raise some potentially interesting ideas, they can not conclude much meaningful about ME at present and we are left with no clear idea if their proxy model of 'CFS' has any real relevance or not to actual ME/CFS.]
 
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I just had a quick skim of the paper, mainly looking for references to Moss-Morris' shit post-infection work (I couldn't see any).

Here were a couple of bits I thought could be of interest:

Interestingly, however, levels of the KYN/TRP ratio and 3-HK were lower in CFS patients than controls, while the tryptophan levels were similar to controls. This lower KYN/TRP ratio in CFS (and the lack of association with PF) is somewhat in opposition to a study of somatization which observed higher levels of the KYN/TRP ratio (Maes et al., 2011). This evidence points again to a different biological underpinning of primarily psychiatric syndromes, such as depression and somatization, as opposed to CFS. This notion is further supported by the lack of an association, in our study, between PF and any of the classic, stress-related risk factors for psychiatric disorders. Targeting the kynurenine pathway, through antidepressants or nutritional interventions, may thus not be a relevant therapeutic strategy in CFS (Borsini et al., 2017).
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I hadn't heard of that somatization study.

Of note, our approach to categorise fatigue as ‘resolved’ (returned to the same level or lower than baseline), and ‘persistent’ (higher than baseline) may also attract some criticism given that this could mean that even a 1-point change on the CFQ can determine the classification. However, we believe this to be justified in order for us to focus on change in the individual in response to the trigger, where baseline fatigue is acknowledged, and in the context of additional changes in fatigue during IFN-α.
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Finally, due to the sample size there was no correction for multiple comparisons; however, we aimed to limit the number of statistical comparisons by pre-selecting the cytokines to measure at the different stages of the study.
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I agree with others saying that this work is of some interest, but things like the above make it seem really odd that this is getting the sort of media coverage that it is in relation to ME/CFS. This is such early work with just 18 patients who were classed as having developed persistent fatigue.

Also, the fact that IFN-α now seems to have been superseded by treatments with less bad side effects means that we'll probably never see a larger replication of this study. If studies like this had been done twenty years ago, instead of wasting time of poorly designed 'pragmatic' assessments of Wessely's treatments, I'm sure we'd be in a better place today, but given where we are now I'm not sure that this will make much of a difference to patients, and the media hype around it is odd and smells to me of the SMC.
 
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