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

The radio 4 continues the mystery notion. This isn’t a complete mystery with this one chink of light now from our MRC and psychiatry saviours. The patient is actually quite good thankfully, although a short Time case usually preferred by the media . I don’t really accept CP as an ME expert, , I can see why he’s a SMC favoured CFS spokesman form what he said, PEM vs fatigue wasn’t conveyed at all.

 

I am not sure interferon alpha was available in 1988 but it may have been some time around then.

 

I agree that that bit of analysis is complete guff.

 

In 1987 a fellow member of our ME support group had been treated with interferon. I think he was part of a study but it was long ago. It had not helped him.

We are not being too nitpicking. This study says nothing at all about ME as the cardinal symptom of PEM was not looked for. It may say something about fatigue, but I did not experience fatigue for decades after I developed ME (i still have very little actual fatigue).

I have fatiguability with no warning. Some days I could walk miles, other days I could go a few steps. I never knew what would happen and the stop was sudden and complete.

Now something was broken inside me when I took the originating virus. It may be because of immune problems I do not know and this study does nothing to answer it. While it may be useful to counteract that we have a psychological problem talking and actually listening to patients for a few minutes could tell them that.

This study and press hype is another example of the same group of researchers making up an illness and saying it is what we have. because they invented it they can claim whatever they like about the causes and perpetuating factors. It is designed to benefit the researchers not to help patients.

 

Possibly 25 years. I have a memory of lying in bed reading the AfME newsletter and reading about this mysterious but proper-sounding stuff, interferon-alpha. Although that sounds too precise to be a genuine memory and one that my brain hasn't helpfully just this minute supplied...

 

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.

The study also expressly says (I know I'm repeating myself, but this is important):

 

Smith et al (1988)(Smith, Tyrell, Coyle and Higgins. Effects of interferon alpha on performance in man; a preliminary report . Psychopharmacology 96 414-416) injected normal volunteers with alpha interferon and those receiving 1.5Mu of interferon developed symptoms which closely resembled influenza. They also showed identical changes in performance to those shown by people with influenza, with some function being impaired but others remaining intact. Furthermore, after effects of interferon challenge were observed even though the symptoms had disappeared .

Cognitive Changes in Myalgic encephalomyelitis. Andrew Smith in Post viral fatigue syndrome (ME) 1991 eds Jenkins and Mowbray.

Edited to include date and italics

 

Thank you Adam, that is really all I was wanting to say.

 

I think I would have found this an interesting study if they presented it as a study of persisting fatigue that can be relevant for conditions like ME/CFS.

As Simon pointed out, persisting fatigue was not associated with psychosocial factors (history of depression, stressful life event, early life trauma etc.) but with immune factors like IL-6 and IL-10. The interesting thing is that the between group differences in cytokines were only visible in the beginning of the IFN-α treatment, even though the fatigue persisted for months afterwards. So if these patients were to go to a fatigue clinic, doctors would not be able to find differences in these immune markers. This study however showed that there were differences at the early stage, a time point that doctors normally can’t see.

The results very much contradict everything Wessely and Sharpe have been saying about patients with chronic fatigue. I guess psychosocial factors were only measured at baseline, but there would have to be some pretty dramatic psychological change for their cognitive behavioral model to be of any relevance to these patients. I think White Buchwald, Jason and the Dubbo studies previously found similar results (psychosocial factors are irrelevant) in patients with postinfectious CFS, so their model seems to have been proven wrong by the data.


I agree that it’s dubious to see persisting fatigue in this study as a proxy for ME/CFS. For one, on the Chalder fatigue scale, they showed much less fatigue (17) than patients selected by the oxford criteria (26).


There was an interesting finding regarding the kynurenine to tryptophan (KYN/TRP) ratio, which was lower in the (Oxford criteria) 54 CFS patients compared to controls. A Maes study previously found KYN/ TRP ratio to be higher in patients with depression and somatization. The oxford criteria can be misleading but maybe it’s a good idea as Anton Mayer did, to get Periante interested into researching this into more depth, with reference to Phairs metabolic trap hypothesis?

https://twitter.com/user/status/1074598606890520576

 

Yes, those headlines are 20 years past their use-by date.

 

Pariante on radio on mental versus physical wasn’t helpful. Whilst psychiatric illness might have biological underpinnings it presents primarily as issues with mood and behaviour, physical illnesses primarily present with physical symptoms. Whilst dementia might sit in both courts arthritis is a physical illness not a mental one, so is MS , why is it with ME that suddenly all boundaries and classification is unacceptable when most pwME do not have major MH presentation.

 

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/

 

I find the key to understanding the debate is that although it looks like it's about classification of illness, it actually seems to be primarily about who gets the right (or burden) of treating patients with the illness in question. When viewed in this way, the debate begins making sense.

 

Agreed. They should directly indicate that they're reposting a press release from elsewhere. @Russell Fleming, maybe worth checking?

 

So their 'blog' is just a replication of the press release but without acknowledging that?

 

I interpreted this as a quote from the authors, rather than the view of the MEA, though that was not made clear making it read like a ringing endorsement of this study. I would have been much happier if they had made it clear that it was a quote and rather gave a cautious response given the problems with interpreting the study and the ludicrous over hype by the UK media.

 

I have not finished the paper, but let me say some things nice about it at my point of reading. It potentially shows that the intensity of the response is associated with later chronic fatigue. That is basically it. In ME research its best a footnote, and in CFS research it might be a whole sentence. For fatigue research, and only fatigue research, involving these pathways, it might be good.

Now its suggested from the Dubbo studies that intensity of the pathogen response is the best predictor of later chronic fatigue. So there might be something there. Its a long way to go from that to a model of ME ... a very very long way. Its a long way to go from there to even potential treatments, net alone deliverable, approved treatments.