Symptom perceptions, illness beliefs and coping in chronic fatigue syndrome, 2009, Moss-Morris

What is even stranger is that on PubMed the Journal of Mental Health is listed but this article does not exist under Moss-Morris - just some others.

 

Maybe the article has been officially withdrawn since it does not appear on PubMed?

 

Full text here

 

It might not look so good now, since NICE have recommended against basing treatment on this approach, having spent two years reviewing all the evidence.

 

Google Scholar says it has been cited 82 times!
https://scholar.google.no/scholar?q...+syndrome&hl=no&as_sdt=0&as_vis=1&oi=scholart

 

CFS patients also tend to be hypervigilant to symptom information and to maximize the extent of their symptoms and the consequences of experiencing symptoms.

And yet Michael Sharpe insists that everything a patient says about their symptoms is reliable evidence for their state of health. And the trials rely on that assumption.

Yes, we were here before, a very long time ago now.

 

ME should not be defined this loosely as it catches a too heterogeneous group of patients which produces junk research.

 

Yes, I'm aware of it. IIRC that drug suppresses the sympathetic response, but in ME/CFS the problem seems more likely to be hypoactive parasympathetic / HPA axis. The benzos work on a completely different way altogether from either.

It does. The point I was making is that a physical symptom doesn't indicate an organic cause.

 

What do you base that claim on?

 

Here is a review of perpetuating factors, which are mostly cognitive:

https://www.sciencedirect.com/science/article/abs/pii/S0022399910000632

 

The study you just posted showing that reducing sympathetic activation doesn't help patients, and the studies showing hypoactivation of the HPA axis and lower HRV (especially after intense exercise...see the study published today by Ruijgt et al.).

 

Do you have a link? Is it this?
https://www.s4me.info/threads/weara...onal-malaise-in-long-covid-2025-ruijgt.43236/

 

That narrative review does not in any way say that perpetuating factors are cognitive. It says that they may be, based on what is essentially a collection of opinions and interpretations of data from psychosomatic researchers and their studies.

 

Already has been for the last 30 years. It even continues to this day, with exploratory studies that never build on anything. Just pilot study after pilot study.

You are missing decades of history here, arguing for things to happen that have already been done to death.

All of this has already been done, most of it 10x at least. This is no different than arguing for vaccines causing autism and demanding it be studied again, again. It already has, and it's always done the same way: take any random correlation and argue for it. Like 'stress' hormone, which is not a thing. It's been argued to be highly significant, but studies are all over the place, some showing higher, some showing lower.

This has all been done. All of it poorly. This is why we have no patience for what has only become sea-lioning.

 

We can check those things, but in reality it's no more useful than the old polygraph. Polygraphs were for a long time asserted to be reliable, because some needle moved. They aren't. Not in the slightest. There are multiple explanations for all of those things, which is exactly the reasoning used to assert that there is nothing wrong with us.

 

Something that can explain anything, explains nothing.

This idea of any and all symptoms is the point where medicine abandoned science and went all in on superstitious mumbo jumbo. It simply replaced the old divine explanations for everything, shifting the authority inward, to a profession that was barely getting started, and turning it into a traditional belief system.

 

It's not like arguing that vaccines cause autism, as that is not based on any evidence. I'm not sure what you mean that "stress hormone is not a thing". Adrenaline and cortisol are the two main stress hormones. It is actually a thing, but not a biomarker in ME/CFS. What does seem to be somewhat consistently found is hypoactivation of the HPA axis, although the difficulty is that it's not possible to measure that directly in humans. Here is a review:

https://pubmed.ncbi.nlm.nih.gov/24959566/

 

Yes. It's just a preprint for now (I thought it was just published properly today, but it's just a healthrising article). They do a literature review into parasympathetic suppression in patients:

"Patients with long COVID have lower HRV values at rest in the time-domain [8,19] or during sleep in the frequency domain [8], suggestive of parasympathetic inhibition and autonomic dysfunction. However, some studies even report higher HRV in the time-domain in long COVID patients [20,21]. A recent literature overview confirmed a lower HRV in patients with long COVID, although methodological quality was poor and measurements were very short and not related to specific daily life activities or sleep [22]. These findings suggest autonomic dysfunction, characterised by diminished parasympathetic activity, which may be a key feature in long COVID patients [8,19], but how HRV is related to the pathophysiology of ppost-exertional malaise in long COVID is currently unknown. Indeed, HRV in patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) remained lower shortly after exercise, while HRV increased in healthy controls [23]."

 

I’m not an expert, but I’m pretty sure those hormones affect and are affected by plenty of other things than ‘stress’. So by themself, they mean pretty much nothing.