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Extended network learning error: A new way of conceptualising chronic fatigue syndrome (2007)

JaimeS

JaimeS

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Silicon Valley, CA
Very surprised this isn't anywhere on the forums. It's a strange little piece, from 2007.

Extended network learning error: A new way of conceptualising chronic fatigue syndrome
Michael E. Hyland a a Department of Psychology , University of Plymouth , UK Published online: 19 Dec 2007.

Thc cause of chronic fatigue syndrome (CFS) is controversiaI: psychological. hypothalamic and immune mechanisms have been proposed as well as the possibility of some form of interaction between these mechanisms. Patients' own conceptual models vary and sometimes adversely affect self-management. This paper suggests an interactional way of conceptualising CFS using developments in complexity theory (networks, parallel processing or connectionism). I propose that the neurological, immune and endocrine systems are part of a single, self-regulatory, extended brain-body network. Furthermore, that CFS is caused by self-organisational change in this extended network created by normally adaptive error-sensitive learning rules that malfunction when physiological and psychological challenges coincide. This psychoneuroimmunoendocrinological model shows how previously proposed mechanisms could interact to cause CFS, explains the heterogeneity of the presentation of the disease, and provides a conceptual model that may be acceptable to patients but is, also consistent with effective self-management .

__________________________________

Reads like proto-BPS. This is probably what the BPS model of CFS was before it was boiled down to its essence.

You can access the article here after jumping through a few hoops: http://docslide.net/download/link/e...-a-new-way-of-conceptualising-chronic-fatigue
 
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JaimeS

JaimeS

Senior Member
Messages
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Location
Silicon Valley, CA
Yes, well.

My thanks to Jon Ayres, John Challenor, Lars Hanson, George
Lewith, and Simon Wessely for commenting on earlier drafts
Click to expand...

However, if you can stand to wade through the nonsense, it's worth reading through. It's a much better attempt to link psychology to physiology than the BPS school has tried since; now it's all hand-wavey "the mind is powerful" vagueness. I think this paper is as close as we will get to an earnest accounting of BPS.

In short, if you are interested at all in the nature of the theory, or if you want to learn how to argue against it and not a strawman stand-in for it, then I'd say give this a read.
 
Woolie

Woolie

Senior Member
Messages
3,263
Ooh, this one's right in my area of specialty.

Quick summary: Bullshit rises to a new level!! Yes, its a BPS model carefully hidden in a lot of jargon.

Basic logic: people have proposed that MECFS is psychological, because they had no evidence of any other causation. Then people have proposed other things like the HPA axis stuff. And some studies have detected elevated levels of cytokines in PwMEs. Here, we will morph together all these questionable theories into the mother of all BS theories and use a lot of words we don't fully understand.

The basic idea (without the network BS) is this:

1. The initial onset trigger for CFS (infection or whatever) sets off a reaction, part of which is the production of cytokines.

2. Then - via cortical learning systems - we learn to adapt to the "lifestyle challenges" presented by this new situation in a negative way. Part of this adaptation includes increased arousal, and increased production of cortisol (yes, increased, not decreased), and "repeated activation" of these systems leads to "hypervigilance and anxiety". In neurotics, this system is enhanced.

3. The learning mechanisms described in 2. can be "interrupted" by activity that interferes with the "fatigue related signal". e.g., the person exercises despite the fatigue. That resets mechanism 2, leading to knock-on changes in cortisol levels, etc.

So its BPS bullshit.

This is not how you use connectionist models at all. Those models are supposed to be an antidote to this kind of general arm waving, because you are supposed to present a computer simulation of your model, demonstrating that the effects you say it possesses it really does posses. And don't get me started on the way they confuse brain function/bodily systems levels of description and psychological levels of description (learning and cognition). Here, the paper reads like a "what not to do" manual.

Can't believe it got published.

I note that is was written in 2000, so is quite old.
 
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Woolie

Woolie

Senior Member
Messages
3,263
PS. Its pretty much a BPS model, but I guess there are some differences. The "learning" is not presumed to be accessible to conscious awareness. That is, there's fear avoidance but you might not know that its the fear making you avoid. So CBT might not work. You would need a direct intervention like GET to "break" the learned "pattern".
 
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trishrhymes

trishrhymes

Senior Member
Messages
2,158
tl;dr What follows is a rant about pseudo-science. Please don't waste scarce energy reading...

Not relevant to anything really, just wanted to get it off my chest. Probably the result of spending the last few days trying to respond to the 'muppets' fiasco.

Thanks @Woolie for your expert reading and summary. Saved me the bother of wading through a pile of crap!

Have these idiots not heard of the basic logic required here:

If A implies B, then not-B implies not-A.
In this case - if their theory is correct (A), then exercise leads to cure (B)
but exercise makes people worse (not-B) implies the theory is wrong (not-A).

I do find it amazing that a psychologist, probably with precious little understanding of physiology and, from what you say, no understanding of complexity theory should put together a pile of unsubstantiated speculation, wrap it up in lots of jargon from fields they are not specialist in, and get it published.

But then that's maybe why it got past peer review and the editor. They were probably reluctant to say they didn't understand the babble, and passed it because it confirmed their prejudices. The classic way of spoofing reviewers. Choose a field with strong 'beliefs' and write to flatter the editor's bias, fill it with jargon nobody in that field is familiar with, and hope not to get caught out.

I've seen it done by someone I know, with the best of intentions. An engineering student, stepped sideways into ergonomics, read a few psychology articles, came up with an idea connecting all three fields in an undergraduate project, got a job as a university researcher on the strength of it, and got a paper published and presented to a conference. I could see it was speculation, probably correct in common sense terms, but it wasn't evidence based science. I think he knew that too, because he declined to do a PhD on the subject and become an academic. I was very relieved when he moved on into other work where he genuinely knows what he's doing and is very useful.

I came across an even worse example of this on a free online University introductory course something to do with using science to analyse literature. It was utter bunkum, but the university were obviously impressed enough to give him a senior post on the strength of it. I guess the other English staff were hoodwinked by the jargon and pseudo-science.

I'm sure the woolly pseudo-sciences that call themselves social sciences (psychology, economics, sociology, political science etc) there must be an awful lot of this sort of bluffing and picking up ideas from other fields and misusing them. Far too many otherwise reasonably intelligent well meaning people are drawn in to doing PhD's in these fields using concepts they don't really understand, and replacing thought with jargon.

And don't get me started on the misuse of statistics...

I think I have a bad case of pseudo-indigestion.

I need a large dose of David Tuller and Jonathan Edwards to quell my queasy stomach.
 
alex3619

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
I have not read the paper and I am not sure I want to. The idea that ME might be a stable dynamic state is not new. I recall debating this circa 2000 to 2005. Its easy to see why when you realize that ME involves problems in all the command and control systems ... neurological, hormonal, metabolic and immunological systems. The issue is finding the evidence and doing some credible testable modelling. This most definitely has to be confirmed with testing of patients.
 
Snow Leopard

Snow Leopard

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South Australia
There are so many non-evidence based statements in this paper, I don't really know where to start, but well, this is the one that makes me want to sharpen my pitchfork:

A second implication of the ENLE theory of CFS is that a mall deterioration in fatigue caused by exercise may actually be therapeutic -because deterioration may be a necessary consequence of nudging the system off a local minimum. Some patients are reluctant to exercise because they experience deterioration. Of course, the possibility of beneficial deterioration makes it difficult to determine an optimum pattern of exercise and rest, because it would be difficult for patients to distinguish small and potentially beneficial deteriorations from more substantial and harmful deteriorations caused by over-exercise. Nevertheless, the possibility that 'you need to get worse in order to get better' - interestingly, a feature shared with homeopathy' - may encourage patients to exercise who are reluctant to do so.
Click to expand...

Over 15 years later, this claim is still contrary to the evidence - no studies have demonstrated empirically that patients can increase their activity levels, either during CBT/GET or at followup. GET also results in higher level of adverse effects than other therapies. The idea that patients must be willing to risk harm for reward is not only unfounded, but dangerous.
 
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