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

The link is at the side of the article. Click on the blue picture.
Acknowledging that it is a replication of the press release, not that the press release exists.

My attempted point is that a blog, typically, represents some original content by the blogger. Now, given that we have identified that at least the opening two paragraphs of the MEA's 'blog' is just straight duplication of part of the press release from King's College, until advised otherwise, I will assume that all the rest of the text of the 'blog' which has the same typesetting as the first two paragraphs is from the same press release - which, to my mind, doesn't make it a blog, just a copy-and-paste attempt by the MEA to drive more traffic to their website.
 
Blog from the ME Association, can't say I'm particularly impressed with the part that I've bolded below.

https://www.meassociation.org.uk/20...-overactive-immune-response-17-december-2018/

Just to be clear. The words are taken from King's College's website. I added links to all the main headlines and BBC Today Programme. Quotes from Dr Shepherd carried in The Telegraph. And the tweet from Simon McGrath. On our social media I have carried all the reports individually. This was an attempt to have a summary for the website.

Edit: I have now added a title to the blog making it even clearer to everyone where the words come from. Hope that is satisfactory.
 
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This study is not bad, but crap design as far as CFS and PF criteria used, along with the use of poor quality metrics such as the Chalder Fatigue questionnaire limit the generalisablity of what otherwise would have been a good quality study.

There is also an assumption that it was the interferon-alpha intervention that was the primary cause of the persistent fatigue, rather than being a bad-luck consequence of the underlying chronic infection they are attempting to treat.
 
Not been able to read all the comments, no doubt others have said what I'm going to say, but I'll say it anyway.

This isn't a study of CFS. If you go to a CFS clinic with fatigue and tell them you've had/got Hep C then you won't be diagnosed with CFS. It literally means you don't have CFS because you have an explaination for your fatigue. Fatigue is common, you get it in dozens of diseases.

The study may have value if the fatigue in post treatment Hep C is the same mechanism as in CFS but I doubt there is any evidence to suggest that's the case.

Do these post treatment Hep C patients get PEM? If they do then it may be interesting, but if they don't then it may be of no value at all to us. Bet the study doesn't even ask the question, even though it's really obvious.

Finally, because of who this study comes from I can't trust the results because their other studies have been so badly flawed.
 
Given some of the comments here I thought this might be of interest:

It has already been noted that fatigue is a very common feature in interferon therapy. Patients on interferon who suffer from this fatigue find that it is exacerbated by physical exercise. Some patients have to stop working, particularly those whose occupations have a largely physical component, while the majority report that their social functioning is impaired. Despite the agreement on the occurrence of fatigue as a side effect of interferon therapy, there is difficulty in comparing this with that occurring in PVFS because "fatigue" is largely undefined in interferon studies. For example the distinction is rarely made between mental and physical fatigue.

Interferon in viral illness and ME. E McDonald and A Mann. Post viral Fatigue Syndrome (ME) 1991 eds Mowbray and Jenkins

it is interesting that the authors were from the Institute of Psychiatry. In those days the CFQ had probably not got a firm hold and greater judgment on such matters was possible.
 
Second, why do some people have overactive immune systems? Well, because of personality type, stress or trauma, of course.
As @Simon M points out, the researchers "measured psychosocial factors including childhood trauma before the interferon-alpha treatment started. And these factors did not predict subsequent fatigue."

Previously, psychosocial researchers have used weak evidence, such as that of pre-illness child trauma, as evidence that their psychosocial model was correct. It’s harder to argue that some people develop/maintain CFS after infection because of psychosocial issues (compared with those that don’t develop the illness) when there is no difference in psychosocial factors before the infection (Or immune activation). Why did these people who got CFS suddenly have psychosocial problems after an infection??

I think people are being too nitpicking. I agree with Simon. The basic study here is useful in documenting the fact that a known immunological stimulus can cause a long term and severe illness characterised by fatigue. That may not be the same as CFS or ME but it shows that you do not need to postulate any psychological factors in the causation of an illness at least similar to ME in some respects. A small step but an important one.

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.

I mostly agree with what Simon, Jonathan and Adam say above but I'm not sure that it necessarily contradicts the CBT model of CFS. The model suggests that it is patients' unhelpful beliefs, rather than any underlying abnormal pathology, which perpetuate the illness. These unhelpful beliefs are often assumed to be caused by pre-illness psychosocial factors but is there any reason why they could not be argued to be a consequence of what Sharpe refers to as "an abnormal or excessive immune response"?

Is there anything in the Pariante study which directly refutes the notion that those whose immune systems predispose them to having an abnormal or excessive immune response to interferon-alpha are more likely to develop unhelpful beliefs as a consequence of the severity of the symptoms caused by the immune response - just as the probability of suffering from psychological problems after being involved in a road accident may be directly proportional the scale of the accident?

As much as I'd like to, I can't see anything in the paper which necessarily contradicts Wessely's idea that an illness like ME/CFS can be triggered by a virus (or some other event which causes an immune response) but is then perpetuated by unhelpful beliefs - and this seems to be what Sharpe is still desperately clinging on to.

Presumably, the next stage will be to test whether CBT/GET can help reverse persistent fatigue (PF) and/or prevent it if it is given to those whose immune systems suggest they may be susceptible to developing PF following interferon treatment. And I have a sneaky feeling I know what the results may be! Perhaps this is why the SMC are hyping it so much.

Ironically, the best evidence we have that unhelpful beliefs do not perpetuate ME/CFS is the PACE trial, because it suggests that changing the way that patients think about their symptoms has no effect on levels of activity/disability. When one combines that with the evidence from Pariante, that pre-illness psychosocial factors are not predictive of persistent fatigue following interferon treatment, it makes the BPS ideas about ME/CFS look about useful as a creationist view of the universe.

[edit - typo]
 
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Soooo.... just to play a little bit of devil's advocate, I welcome the study. Yes, there are some issues regarding criteria for judging symptoms and the history of the group involved - but hearing/seeing the Today Programme and the Guardian write something about ME/CFS that implies a cause beyond unhelpful beliefs and doesn't focus on how all ME patients are just psychotics is a small but welcome shift.

Also (the devil's advocate bit), given that we have a PR problem as a patient group, I do sometimes think seeing tens of negative comments under science reporters' tweets on this topic may represent a bit of an own goal.
 
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