A test of the adaptive network explanation of functional disorders using a machine learning analysis of symptoms, 2018, Melidis, Hyland et al

[Joel]

A test of the adaptive network explanation of functional disorders using a machine learning analysis of symptoms

Author Information:
Melidis C, Denham SL, Hyland ME.
University of Plymouth

Abstract
The classification and etiology of functional disorders is controversial. Evidence supports both psychological and biological (disease) models that show, respectively, that functional disorders should be classified as one (bodily distress syndrome) and many (e.g., irritable bowel syndrome (IBS), fibromyalgia syndrome (FMS), and chronic fatigue syndrome (CFS)). Two network models (symptom network and adaptive network) can explain the specificity and covariation of symptomatology, but only the adaptive network model can explain the covariation of the somatic symptoms of functional disorders. The adaptive network model is based on the premise that a network of biological mechanisms has emergent properties and can exhibit adaptation. The purpose of this study was to test the predictions that symptom similarity increases with pathology and that network connection strengths vary with pathology, as this would be consistent with the notion that functional disorder pathology arises from network adaptation. We conducted a symptom internet survey followed by machine learning analysis. Participants were 1751 people reporting IBS, FMS or CFS diagnosis who completed a 61-item symptom questionnaire. Eleven symptom clusters were identified. Differences in symptom clusters between IBS, FMS and CFS groups decreased as overall symptom frequency increased. The strength of outgoing connections between clusters varied as a function of symptom frequency and single versus multiple diagnoses. The findings suggest that the pathology of functional disorders involves an increase in the activity and causal connections between several symptom causing mechanisms. The data provide support for the proposal that the body is capable of complex adaptation and that functional disorders result when rules that normally improve adaptation create maladaptive change.

 

[Hoopoe]

The findings suggest that the pathology of functional disorders involves an increase in the activity and causal connections between several symptom causing mechanisms.

If you have a checklist with symptoms, the symptom profiles will tend to converge as number of checked symptoms increases. Since symptom clusters is just a different way to represent this data, you're obviously going to find this correlation.

The findings suggest that the pathology of functional disorders involves an increase in the activity and causal connections between several symptom causing mechanisms. The data provide support for the proposal that the body is capable of complex adaptation and that functional disorders result when rules that normally improve adaptation create maladaptive change.

You cannot draw this conclusion without a control group of people with nonfunctional illness. Maybe what they're seeing is exactly the same that is seen in conditions like multiple sclerosis.

Plus the concept of functional disorder as illness category is stupid: it misleads people into thinking there must be some common features shared by all illnesses in this category, when in reality all it means currently unexplained illness.

 

[Andy]

The findings suggest that the pathology of functional disorders involves an increase in the activity and causal connections between several symptom causing mechanisms.

I assume that this is psych-speak for "we've made up some conditions and this is the dubious reasoning for them". But equally, couldn't you say the same thing about a real/physical/insert appropriate description condition i.e. I have a cold at the moment. The pathology of my cold involves an increase in the activity and causal connections between several symptom causing mechanisms (i.e. the assorted ways my immune system reacts to the cold virus).

Oh, brainwave. Because it can be put that way, it theoretically adds weight to their argument that their made-up conditions exist, on the assumption that you accept that the symptom causing mechanisms that they claim to be able to identify actually exist.

 

[Dolphin]

A potential problem is people might not have all the diagnoses they should have. I was diagnosed first with IBS. I had ME/CFS at that stage but not the diagnosis. Also the definition of Fibromyalgia has widened with the 2010 criteria which don't require a tender point evaluation. A lot of doctors particularly it seems rheumatologists diagnose people with fibromyalgia even when they have CFS symptoms.

 

[Trish]

I agree, @Dolphin. I was diagnosed first with ME, I have also subsequently added diagnoses of fibromyalgia and IBS. Lots of us have overlapping conditions, or one condition with a wide range of symptoms. I can't see that this tells us anything about whether our condition is physical or 'functional' and whether it has a single or multiple causes.

I haven't accessed the full paper, but I've read the abstract 3 times and I really don't understand it. Too many words or concepts I'm not clear about.

Help!!!

@Jonathan Edwards, can you make sense of it?

 

[Jonathan Edwards]

@Jonathan Edwards, can you make sense of it?

I doubt there is much sense to be made.

I suspect what they are proving is that diagnoses are made by people who use adaptive learning and sometimes go maladaptive. Its a bit like psychosomatic research I suppose - all in the heads of the researchers. Symptoms fall into certain clusters because the people who decide what out as symptoms (doctors) like to cluster them.

 

[Indigophoton]

I pricked up my virtual ears at this paper, partly because I find systems stuff very interesting in general, and partly because the idea of dysregulation, whether immune, metabolic, endocrine/neurological and/or something else, being integral to ME as a potential prolonging factor of some sort is intriguing, not least because it might be fixable/reversible.

That is, some hit-and-run stressor like a virus, for example, knocks one or more of the body's set points away from normal, and for some reason the system stays off-kilter thereafter, even when the initial insult is gone. Other body systems domino-adapt to the new normal, causing the plethora of symptoms.

However, I am not a life scientist, so am prepared to stand corrected if this doesn't make sense (and if it does, I have no idea whether it is actually the case).

A bit of googling reveals that Michael Hyland, the third author on the paper, wrote a book on the subject in 2011 ('The Origins of Health and Disease), where CFS is one of his examples.

The fourth phenomenon for which there is no clear explanation is how some of the body’s control systems work. The body’s control systems consist of two kinds: those where the reference criterion or set point is fixed and those where the reference criterion or set point varies.

Those control systems with fixed reference criteria (called homeostatic control systems) are easy to understand. The genome specifies what the set point should be.

The control systems with varying reference criteria (called homeodynamic control systems) are not easy to understand. Something must be controlling the reference criteria. Something, for example, controls the level of inflammatory biochemicals in the body, increasing and decreasing these levels on the basis of external threat or relaxation.

In addition, for many diseases the reference criterion of a control loop is set at an incorrect level –for example, too much inflammation. There must be something that controls the body’s control systems.
This book sets out a theory that provides an explanation for all four of the above unexplained phenomena.

There is something that controls the body’s homeodynamic reference criteria and that simultaneously manages the many different and sometimes competing control systems. This something can become dysregulated and, when it becomes dysregulated, the dysregulation leads to medically unexplained symptoms and functional diseases as well as acting as a precursor to the diseases with known pathophysiology. Finally, this something is influenced by psychological inputs, and it is here that the ‘other part’of therapy has its effects.

(paragraphs added)

In the book he says,

Chronic fatigue syndrome (CFS) is another disease that poses a challenge for modern Western medicine and which, depending on the method of classification, affects between 0.3% and 1% of the population (Bates et al., 1993).

CFS involves extreme feelings of tiredness, malaise and a large and variable group of other symptoms. Although there are often disturbances in physiology, none of these disturbances is sufficiently consistent to define the disease, and in any case the disturbances are not sufficiently extreme to explain the debilitating levels of symptoms.

He does not appear to conflate CFS with MUS:

In addition to IBS and CFS, there is a group of patients who have a wide range of medically unexplained symptoms. Like CFS and IBS, patients with medically unexplained symptoms have no specific pathophysiology associated with their symptoms. Patients with medically unexplained symptoms comprise a surprisingly large group. Depending on the survey, between 15% and 30% of GP visits involve patients who cannot be given a diagnosis and therefore are labelled medically unexplained (Kirmayer, et al., 2004).

He goes on to say,

When the biomedical model is incapable of explaining a disease or symptoms, one possible response is to suggest that the philosophy of specific pathophysiology is correct but that scientists just need longer to get it right.

For example, it is possible to argue that once the genetics of IBS and CFS are properly understood and genetic treatments have been developed then these diseases will no longer pose the challenge they do today, and that medically unexplained symptoms will be explained by some pathology as yet unnoticed.

An alternative response is to suggest that the assumption of specific pathophysiology may not always be correct and that a new paradigm is needed. Given the above, it seems reasonable that any such new paradigm must not only include psychological factors, but more importantly must provide a rationale for how psychological factors and biochemistry are integrated. Simply reiterating the biopsychosocial model is unlikely to produce any great advance.

I've only read a little via the free kindle sample, so don't know what Hyland's detailed ideas about CFS actually are.

In the part of the intro available for free, which is well-written and interesting, he sounds pretty sane, eg, acknowledging that, in effect, bedside manner is responsible for 90% of the benefits of psychological therapies, and noting that scientists are not always open-minded:

The following is a quotation from the Venetian physician Parisano. It is included here in part because it provides an example of how scientists do not see (or hear) things that are inconsistent with their underlying theories. Harvey [who suggested that the heart pumps blood around the body] was criticised by Parisano, who believed in the philosophy of Hippocratic medicine.

"We have no problem to admit that, if the horse swallows water, we can perceive a movement and we can hear a sound. But that a pulse should arise in the breast that can be heard, when the blood is transported from the veins to the arteries, this we certainly can’t perceive and we do not believe that this will ever happen, except Harvey lends us his hearing aid. But above all, we do not admit such a transport of the blood …If blood is transported from the veins of the lung …into the branches of the arteries, how could a pulse be felt in the breast, how a sound? I am completely innocent of such subtle speculations. Above all, Harvey has it that a pulse should arise from the movement of the blood from the heart into the aorta –no matter from which ventricle. He also claims that this movement produces a pulse, and, moreover, a sound: that sound, however, we deaf people cannot hear, and there is no one in Venice who can. If he can in London, we wish him all the best. But we are writing in Venice"

 

[Indigophoton]

PS @Valentijn, thought you'd particularly like this quote from the book,

The term ‘explanatory fiction’ was introduced by B.F. Skinner (Skinner, 1971) as a criticism of theoretical terms in psychology. Explanatory fictions are explanations that appear, to the unwary, to explain but in reality do nothing of the sort. An explanatory fiction is a theoretical term – or some other type of theoretical argument – that purports to explain something but is really just a redescription in fancy language of that which is to be explained.

ETA correction.

 

[Marco]

I doubt there is much sense to be made.

I suspect what they are proving is that diagnoses are made by people who use adaptive learning and sometimes go maladaptive. Its a bit like psychosomatic research I suppose - all in the heads of the researchers. Symptoms fall into certain clusters because the people who decide what out as symptoms (doctors) like to cluster them.

My first reaction to this was - so multiple overlapping symptoms make differential diagnosis difficult. Whoopee!

I think we're both being unfair.

One of the authors (last listed - I assume it's his baby) proposes that rather than being due to false illness beliefs, 'functional' illnesses can be explained by 'emergent' network interaction between biological systems.

I'd like to see some explanation of this explanation but I can at least see where he's coming from and it isn't from the BPS camp :

https://www.researchgate.net/profile/Michael_Hyland4

 

[Indigophoton]

Very helpful @Marco, as he has a comment on that page in answer to a question:

Robert is correct in identifying the group of physicians and scientists who believe that CFS is psychosomatic. More specifically, they believe that CFS is due to illness cognitions with the implication that all you need to to is stop thinking you are ill. Of course, this explanation is still technically organic as minds don't occur without bodies. The difficulty some of us have who discount this mechanism (I have recovered from CFS) is showing that the psychosomatic explanation is wrong. I have just resubmitted a paper to that effect - based on my theory that CFS is a network problem. Specifically, the theory proposes that disease mechanisms are almost entirely causally unconnected whereas there is another sort of mechanism that is strongly causally connected, and so exhibist the emergent properties of a complex system. We have been able to publish the idea as a narrative for patients - but using a simplified description - but my aim is to show that the network of biological mechanisms is the correct explanation. The difficulty is getting this idea past referees - psychologists don't like it because it is non-psychological and biologists don't like it because it deals with emergent properties of a biological system, rather than finding 'the little bit' that happens to be wrong. The paper I have just resubmitted (and not to a high prestige journal) shows that data are consistent with the network but not the psychosomatic mechanism. I am attaching the narrative paper which gives a flavour of the work we are doing.

 

[Valentijn]

Hyland is a psychologist who had moderate ME/CFS for 2 years, and both factors seem to be strongly influencing his beliefs about ME/CFS. While he has enough first-hand knowledge to reject the psychosomatic paradigm, he still sees the disease in a very psychosocial framework. The result seems to be a central sensitization theory - eg, all of the hardware is in good shape, but something in your brain or adrenal system ("network") is giving the wrong signals.

He also explicitly attributes the disease to lifestyle, probably based on his personal experience rather than any scientific evidence:

Professor Hyland: The cause of CFS is a lifestyle that has created error in the network. Often, this CFS-causing lifestyle involves a combination of immune challenge (e.g., infection) and either stress or over-activity. This particular combination confuses the network. So, the treatment involves correcting the network error, and conventional treatments (that treat specific error) are unlikely to work.

"Relearning how to listen to your body's signals" sounds an awful lot like learning to ignore symptoms and interpret them differently:

The main message is that we should listen to our bodies and rest when we get ill - and not go into work, as I and many other people tend to do. If you keep ignoring your body's signals, then your body will change its signaling system - and create the kind of dysregulation that is CFS. Once CFS has occurred, the body's messages are all mixed up so you can't rely on them entirely. That is the difficult thing with CFS. You have to relearn how to listen to your body's signals when some of those signals are wrong.

Fortunately the key to recovery is to emulate him and avoid stress, toxins, caffeine, alcohol, etc, and get exactly the right amount of exercise (despite being "very disinclined" due to the disease), because a car battery won't recharge itself if you don't drive it

 

[Trish]

Sounds like one of the lucky few who recovered relatively quickly by pacing and luck.

Assuming whatever one is doing at the time of recovery is the cause of the recovery is not good science. Nor is extrapolating from one's own experience to assume it applies to everyone else, and building a theory on the basis of those false assumptions.

I still don't really get what he's on about.

 

[lansbergen]

because a car battery won't recharge itself if you don't drive it

And he thinks the accu will recharge when the dynamo does not work?

 

[Jonathan Edwards]

I think we're both being unfair.

Maybe, I certainly agree I may have been a bit quick to respond. But on further deliberation I am not sure I end up with a very different view.

Highland says amongst other things:

This paper presents the idea that diseases can be explained and treated with biological theories, mental illness with psychological theories,

I do not buy that. Mental illness is not explained by psychological theories. Schizophrenia is not, severe depression is not, mania is not, obsessive compulsive disorder is not. None of them are explained at all, except perhaps by the finding of genetic predispositions and the use of psychotropic drugs like LSD. Explaining mental illness with psychological theories is the realm of Freud, which hopefully we have long since abandoned.

My take is that we take a biological systems dynamic approach for ALL illnesses. (And I guess maybe I think he is wrong about the causation of the 'diseases' too - they involve complex systems dynamics too, not just simple causes.)

But having worked with complex systems dynamics I have found words like 'emergence' completely unhelpful. Positive feedback loops are important and easy to understand. Co-operative interactions ditto, and so on. The problem with 'emergence' is that it really means 'not predicted' and that is no use to science because scientific theories are all about prediction and testing. So rather than saying there is emergence one needs to work out the dynamic rules. For immunology and for brains that can take years but I don't think you need any special expertise in artificial intelligence. You just need the sort of common sense that a vacuum cleaner designer might make use of.

 

[Marco]

I can't access the full paper but I pretty much agree on most points.

Where I might diverge is on the issue of 'emergent behaviour' in respect of complex system dynamics and our ability to understand them. On one hand I can accept that 'emergent' is a handy cop-out that avoids the mental effort required to understand and predict. On the other I struggle to accept that it's possible to fully understand to the point of being able to predict complex interactions between multiple systems involving feedback loops; adaption etc etc.

 

[Valentijn]

The classification and etiology of functional disorders is controversial.

They're starting off with the unfounded assumption that there is a class of functional disorders at all.

. Evidence supports both psychological and biological (disease) models that show, respectively, that functional disorders should be classified as one (bodily distress syndrome) and many (e.g., irritable bowel syndrome (IBS), fibromyalgia syndrome (FMS), and chronic fatigue syndrome (CFS)).

I haven't seen any evidence supporting the psychological model of one broad syndrome, ever. Just some hacks playing at imagining grand theories to support their distorted perceptions and desired outcomes.

Two network models (symptom network and adaptive network) can explain the specificity and covariation of symptomatology, but only the adaptive network model can explain the covariation of the somatic symptoms of functional disorders.

For anyone baffled by the terminology, just ignore the "network" bit - they're ultimately talking about symptoms being static things versus things which interact with each other. The body is an inherently adaptive system where many parts constantly interact and change as a result, so labeling symptoms of any disease as being an adaptive network is simply stating the obvious.

The purpose of this study was to test the predictions that symptom similarity increases with pathology and that network connection strengths vary with pathology, as this would be consistent with the notion that functional disorder pathology arises from network adaptation.

How do they establish increasing pathology? It's also making quite a leap to assume that network adaptation causes disease, rather than resulting from a disease. There's no apparent way to prove such a thing, so I very much doubt that they have. And since network adaptation is the default state of the human body, if it caused disease then disease would be the default state of being for everyone

We conducted a symptom internet survey followed by machine learning analysis.

A survey on the internet ... how scientific This means diagnosis was not a rigorous process and completely unverified, which is a pretty essential problem in research.

Differences in symptom clusters between IBS, FMS and CFS groups decreased as overall symptom frequency increased.

Symptom clusters are an artificial construct, and likely to be heavily influenced by the diagnostic criteria themselves. And if criteria are used which focus on vague symptoms, then of course there will be a lot of overlap. However, I doubt that more specific symptoms such as properly defined PEM, GI bleeding, or tender points (versus tender everywhere) have much overlap unless there is a valid co-diagnosis.

The findings suggest that the pathology of functional disorders involves an increase in the activity and causal connections between several symptom causing mechanisms.

Again, they're stating the obvious - every disease causes symptoms, typically multiple symptoms which are accordingly related to each other by virtue of being caused by the same disease.

The data provide support for the proposal that the body is capable of complex adaptation and that functional disorders result when rules that normally improve adaptation create maladaptive change.

So instead of our brain malfunctioning by unreasonably thinking we're sick, they're saying that our body generates fake signals to make the reasonable brain think that we're sick. The end result is the same - you are misinterpreting your symptoms. The difference here from typical psychosocial bullshit is that there's some actual biology involved, in generating the false signals. But the solution is likely the same as given by Hyland previously - learn to reinterpret the signals, probably with some psychological help

 

[Joel]

My two pence worth is that people come up with these convoluted theories because as complex as they may appear to be, it is always much easier to come up with something like this which doesn't require any good evidence (you literately just make something up that sounds plausible,and likely convince yourself and some others that's it's right along the way as a result) than it is to do genuinely useful experiments which find something, because useful experiments usually find nothing, it's very hard to do good science which actually finds something useful, but it's still more useful to do a proper sound experiment that rules something out than this. This stuff here is much much easier. It's also almost certainly wrong, not just because there's a lack of evidence for it but because it's a unnecessarily complex and that means something, probably a lot, is going to be horribly wrong. What a waste of effort. My primary objection to this though is that there is no evidence, I'm willing to go wherever the evidence leads, but this research just takes us on an imaginary journey in the car, our eyes closed, imagining the scenery going by, but car isn't moving, the engine isn't even on. What's the point?

 

[Sean]

I have not read the paper but I am guessing that one unstated and/or untested assumption is that the symptom groupings are stable over time.

 

[Woolie]

If you have a checklist with symptoms, the symptom profiles will tend to converge as number of checked symptoms increases. Since symptom clusters is just a different way to represent this data, you're obviously going to find this correlation.

You cannot draw this conclusion without a control group of people with nonfunctional illness. Maybe what they're seeing is exactly the same that is seen in conditions like multiple sclerosis.

Plus the concept of functional disorder as illness category is stupid: it misleads people into thinking there must be some common features shared by all illnesses in this category, when in reality all it means currently unexplained illness.

Nice points, @strategist!