How should biological researchers present their results about ME/CFS to the media - discussion thread.

[Robert 1973]

Of course emotional/mental states can impact ongoing disease processes,

I don’t think I would say that – a bit too close to saying that unhelpful thoughts can perpetuate the illness for my liking!

 

[Utsikt]

I think you say something like, Of course emotional/mental states can impact ongoing disease processes, but that's very different from claiming that they cause the disease in the first place.

That’s what Wyller is saying, that ME/CFS is a stress response that’s being perpetuated by thoughts and behaviours. Any trigger/cause will do in his model.

 

[Turtle]

I don't understand the anxiety gene being such a big thing. So what!!
Let all the other genes do the talking. BPS is worried, why should we. I stopped taking that crowd serious anyway.

The only thing they've ever done is claiming ME/CFS is psychological because the doctor's tests didn't show anything.
Maybe( most probably) the doctor did not order the right tests.

I had CPET just 40% VO2max, exercise intolerance, check, AT at 1 1/2 minute, metabolic problems, check.
Tilt table test, -25% CBF, OI, check. No NK-cell reactivity, CD4-CD8 numbers upside down, immuun problems, check.
High lipids, no high cholesterol, check.

And above all a proper assessment by a proper psychologist. No questionares, but DSM 3 and 4.
"No disorder was found that could cause or continue the complaints".

Nothing has been proven, many members say, o yah, I did as n=1

 

[Trish]

Perhaps one way to argue is to see if the anxiety related genes also turn up in the genetic predisposition for other physical diseases.

 

[Robert 1973]

'DecideME', exactly.

Sometimes autocorrect is genius. My favourite was when it changed Wessely to Weaselly

I’m also liking the new emoji range. I see @Trish has one for herself

 

[Kiristar]

I don’t think I would say that – a bit too close to saying that unhelpful thoughts can perpetuate the illness for my liking!

That fallout happens in any chronic illness but psychosocial perpetuating factors is part of their model and we need to get away from ME being treated as an exception in having that levied at it.

I wonder if drawing parallels with other non contested diseases where perceptions are different would be helpful here, at least in general media.
"Our findings demonstrates it's underpinnings are as biological as (Lupus or Cancer or MS ).." or whatever an appropriate comparator would be based on comparable genetic studies.

I also wonder if the narrative that
"historically many diseases have tended to be thought of as psychological until science advanced and biological causal factors were identified..." might be another avenue to close that line of attack down?
"...This was the case until surprisingly recently for Cancer, MS, and Stomach ulcers for example. Thanks to the DecodeME Study in the case of ME/CFS we now know where to look and what pathways are involved in its pathogenesis. It's also shown us .... " (returns to the key messages we wanted to get across all along) sort of thing?

 

[Kitty]

I think you say something like, Of course emotional/mental states can impact ongoing disease processes, but that's very different from claiming that they cause the disease in the first place.

For once I disagree—ha!

We should simply stick to the facts about the study. What a GWAS is, why they are done, what they can tell us. What we think this one might tell us, though of course it's going to take time to work through it.

There's no point getting into all the things it can't tell us, which I imagine includes the impacts on disease risk of environmental factors, emotional states, annual income, lifetime exposure to televised darts, and preference for dogs or cats.

 

[dave30th]

That’s what Wyller is saying, that ME/CFS is a stress response that’s being perpetuated by thoughts and behaviours. Any trigger/cause will do in his model.

Very different from what Wyller is saying, I think.

 

[Ravn]

I’ve only been able to read a minuscule number of posts in this thread. At the risk of repeating points already made I want to add my voice to those advocating for strategies involving deflect and return to own talking points rather than wasting time trying to defend any it’s not mental/psych position which is a fruitless debate at any rate

So I would steer away from talking about proof of biological illness vs (part) mental/psych altogether. Terms like biological can still be slipped in at the level of talking about pathological pathways and suchlike, just not at the top level of ‘this illness is biological and/or mental/psych’ where you immediately get into all sorts of tangled weeds

Some tactics that may be useful, depending on the specific question asked***

‘All in the head’ is not a useful scientific concept, every conscious experience is ultimately ‘in the head’. What this study looked at was...

Our study wasn’t designed to answer any mind vs body questions. What it does do is look for potential biological (molecular? biochemical?) pathways that may be broken and what we found was...

I don’t think anybody still thinks ME/CFS is not real, that idea is long gone. The real game nowadays is finding effective treatments which are currently lacking and our study shows areas xyz are worth looking at [remember that even the most dedicated BPS/functional folks say ‘the symptoms are real’, at least publicly]

If genes related to neurons pop out, emphasise the word brain and avoid the word mind

If asked if neuron involvement means CBT or other mind therapies would help, explain the study can’t answer that question but that decades of patient experience show they don’t address the underlying issue even if for some individuals they may help them cope better with being ill. Return to the study findings and what further research should be done to find treatment capable of addressing the underlying problem/s

If findings overlap with those in the likes of depression or anxiety or similar, be prepared to explain that the existence of some shared pathways does not mean it’s the same illness; it would be good to have some examples of uncontested diseases that happen to share some pathways but are clearly different diseases (candidates?)

Could also express the hope that this study will increase research interest in those shared pathways and that it would be wonderful if the knowledge gained could help people with other conditions as a neat side effect

***If not asked, don’t bring it up yourself. This whole myth-busting urge of ‘It’s biological, it’s not all in the head/psych-something’ is understandable but it doesn’t work, it just reminds people of their prejudice and more often than not actually strengthens their prior beliefs, no matter how often you say not not not. And it eats up valuable media time. Instead flood the space with the actual findings and, importantly, ideas for further studies to create an impression of momentum (to hopefully lead to real momentum)

 

[dave30th]

don’t think I would say that – a bit too close to saying that unhelpful thoughts can perpetuate the illness for my liking!

I understand. But it's not the same as saying it's perpetuating the illness. If there were no impact or effect of mental states that arise generally in response to being sick, there would be no reason for anyone with any illness to seek supportive care in terms of counseling, psychotherapy, etc. But everyone agrees that can be indicatad. I see no way of dealing with this issue by ignoring this.

 

[dave30th]

For once I disagree—ha!

We should simply stick to the facts about the study. What a GWAS is, why they are done, what they can tell us. What we think this one might tell us, though of course it's going to take time to work through it.

There's no point getting into all the things it can't tell us, which I imagine includes the impacts on disease risk of environmental factors, emotional states, annual income, lifetime exposure to televised darts, and preference for dogs or cats.

But no one is making an argument about dogs and cats and so on. I agree you focus on what the study shows, but the way to deflect the stupidity is to acknowledge the obvious truth that people often need or want supportive care related to mental health factors while distinguishing those needs from causal factors.

 

[Sean]

My reading of CBT in particular is that it's built on the idea of anxiety about symptoms.

More like they think it is anxiety about non-symptoms, about misinterpreting normal somatic signals and sensations (e.g. DOMS).

Someone might have a chronic illness and be worried - we've seen the anxiety surveys that ask questions like 'do you keep worrying about the future?' 'are you worried about your health?'. There are many situations where being worried is the normal and healthy response; it is wrong to see that as a diagnosable disorder, but unfortunately that happens.

Exactly.

It is dishonest and underhanded in the extreme for the psychs to claim that being worried about a life-destroying change in health status, with no explanation or treatment let alone cure, with profound consequences for employment and financial and material status, that destroys social relationships and well being, and is highly stigmatised (ironically by psychs themselves), is somehow the cause of all that.

Real mystery why a person might be concerned about what is happening to their lives, and their future prospects for even mere survival in those circumstances. NOT!

I don't believe for second that psychs don't understand this. Understanding the role of such secondary compounding psychosocial factors is Basic Psych 101. Truth is they don't want to admit it, because then the question becomes why they have not only failed to account for all that, but have instead wilfully ignored it, conflated correlation with causation, and arbitrarily reversed the causal chain. And there is no good answer they can give to that which doesn't involve admitting serious guilt, apologising unreservedly, and withdrawing from any further involvement.

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re psycho-behavioural factors:

Behavioural changes, in the broadest sense of the word, can certainly be helpful in both managing many biological disease processes, and preventing some (e.g. the role of diet and exercise in many diseases, like hypertension and cancers).

Pacing, for example, is a behavioural management response to the underlying primary disease process, and which may well also help reduce long-term consequences. (Pacing, incidentally, being something that patients discovered and adopted themselves – against considerable resistance and hostility from the psychs – thus proving that we are not against such approaches, where suitable.)

Psychotherapy may well be useful to some (not all) to help deal with the secondary emotional distress that comes with such circumstances.

Problem starts when that gets uncritically conflated with psycho-pathology being the primary cause (i.e. psychosomatic), which it does all the time.

 

[SNT Gatchaman]

Pacing, for example, is a behavioural management response to the underlying primary disease process, and which may well also help reduce long-term consequences. (Pacing, incidentally, being something that patients discovered and adopted themselves – against considerable resistance and hostility from the psychs – thus proving that we are not against such approaches, where suitable.)

Imagine sending children with tetralogy of Fallot, who quite distinctively learn to squat as a compensation, off to psychobehavioural re-education.

First observed by Helen Taussig. From Medscape —

A characteristic fashion in which older children with tetralogy of Fallot increase pulmonary blood flow is to squat. Squatting is a compensatory mechanism, of diagnostic significance, and highly typical of infants with tetralogy of Fallot. Squatting increases peripheral vascular resistance and thus decreases the magnitude of the right-to-left shunt across the ventricular septal defect.

Children with the tetralogy of Fallot soon discover the symptomatic relief obtained by squatting after exercise. Indeed, the trick is probably usually learnt in infancy when they adopt a knee-chest posture. Helen Taussig' was the first to give a full description of the phenomenon of squatting, and it is particularly interesting that, in speculating about the mechanism of relief given to patients in this way, she quoted the words of a 10-year-old patient," It cuts off the circulation to my legs and increases the circulation to my lungs."

Since that time there has been considerable controversy about the exact way in which squatting affects the circulation in these patients. W. F. Hamilton and his colleagues2 emphasized the importance of the rise in systemic vascular resistance that occurs during squatting, claiming that this would increase the relative flow into the pulmonary artery. They also stated, without clear evidence, that squatting increased the systemic venous return, and subsequently other authors5 have argued on similar lines. Nevertheless, L. Brotmacher,8 using plethysmography and oximetry, concluded that squatting actually decreased the venous return from the legs, though he was unable to measure venous flow directly.

Recently W. G. Guntheroth and his colleagues have measured directly the flow in the inferior vena cava in patients with Fallot's tetralogy. They have confirmed Brotmacher's conclusion about diminished venous return during squatting, and have also shown that there is a sustained decrease in flow in the inferior vena cava in the knee-chest position adopted during squatting after exercise. This is accompanied by a rise in systemic arterial pressure and a rise in arterial oxygen saturation, which had fallen to low levels during exercise. Guntheroth and his co-workers point out that these phenomena may be understood by considering what has been happening during the exercise immediately preceding squatting. A large oxygen debt has built up, the muscle vascular beds are dilated and remain so after exercise, and there is increased extraction of the available oxygen locally, so that oxygen saturation of the venous blood is further reduced. Since in Fallot's tetralogy some of the venous return to the right heart passes directly into the aorta, any reduction in the venous oxygen saturation leads directly to a reduction of the arterial saturation as well. The vasodilatation in the exercised limbs lowers the total systemic vascular resistance, and hence there is also a fall in blood pressure.

Squatting helps to counteract these effects in two main ways. Firstly, by diminishing the blood flow to the legs it helps to maintain the peripheral vascular resistance, and hence more of the cardiac output is directed into the lungs. Secondly, by allowing the oxygen debt after exercise to be paid off over a longer period it corrects the precipitous fall in arterial oxygen saturation that has accompanied exercise. Helen Taussig's patient was right.

 

[Obermann]

Another important point that has been raised in many contributions here: In empirical sciences, it is impossible—or at least very difficult—to prove a negative. Even if we could identify processes that are relevant to the pathology of ME/CFS, one can always argue that there are other, unknown psychological factors that cause these processes. There are still researchers who claim that psychosocial factors influence which carriers of Helicobacter pylori develop ulcers. The burden of proof is on the person making the claim. We should avoid claims that it has been proven that psychological factors do not play a role in ME/CFS. By doing so, we accept that the burden of disproving psychological factors is on us. Instead, we should point out that there is no evidence of causal psychological factors, no validated biopsychosocial illness model, and no evidence based psychological or psychiatric treatment for ME/CFS.

 

[Jonathan Edwards]

"historically many diseases have tended to be thought of as psychological until science advanced and biological causal factors were identified..."

Except that that is largely a myth. There may have been psychologisers throughout history but there were all sorts of other theories.

I think there may be mileage in comparing ME/CFS to MS and lupus because it may turn out that they are remarkably similar in their causation. It also may make people rethink the assumption that just because there is no damage the process should be self-remitting and temporary.

 

[Jonathan Edwards]

there would be no reason for anyone with any illness to seek supportive care in terms of counseling, psychotherapy, etc. But everyone agrees that can be indicated.

I don't. Where is your evidence, David? I am pretty sure that the evidence for all psychotherapy is as bad as PACE. Why concede this?

There is a big difference between wanting support and having someone to keep your spirits up while ill and psychotherapy.

If you concede that emotional states 'impact disease process' you are conceding the BPS position. It is another form of unjustified theorising. What are 'emotional states'? What is their mode of causation, and is it beyond nerves firing? Nobody has any scientific understanding of this that allows useful theorisation.

 

[Simon M]

I feel like Robert’s statement actually avoids their arguments and just encourages us to move one from the old ways. It’s how a politician would answer by focusing on their point.

It has been tried before, without success The BPS advantage is that most scientists, doctors (and people) instinctively accept the BPS view, the mind can be responsible for anything we can't explain (kind of like witchcraft in medieval times).

How would the presence of anxiety-related genes be evidence that thoughts are be involved in causing or maintaining the disease?

Because BPS has, at least, been clear that what perpetuates the disease (as opposed to triggering an illness) is excessive focusing on symptoms, which is easily cast as anxiety. For graded exercise (debunked in many ways, yet still offered as a treatment), Petr White has said it treats CFS "as you would a phobia", by gradually increasing the dose of the feared thing. That's why, if I were them, I would expect to see a link to anxiety-related genes, Of course, if nothing shows, I'm sure they won't mention it. But the absence of a strong genetic anxiety signal would be tricky for them to explain.]
]

You only need replication for definitive proof of absence. The suggested argument is that there is no evidence for presence. If there are no BPS-related genes (whatever that may be) in DecodeME, there would not be any evidence for the BPS view.

Yes, if no gene peaks, no evidence. But if there are sub-threshold peaks (and there are normally plenty of those in a GWAS) then replication is needed to support a claim of no evidence. Theoretically. Though if there are plenty of bio peaks that are significant, and no anxiety peaks, their case is weak. It depends on what DecodeME finds.

I would love to see a definitive answer from DecodeME. And hopefully we will get one. ut we've known from the off that a study of this size will struggle to deliver definitive results (as it would for any disease with relatively low heritability). I'm just saying that to be well prepared, we need to consider a wide range of possibilities.

For future reference, here is a recent study on genes and anxiety:

https://www.s4me.info/threads/gene-discovery-and-biological-insights-into-anxiety-disorders-from-a-large-scale-multi-ancestry-genome-wide-association-study-2025-friligkou-et-al.44724/

Thanks.

 

[Braganca]

I wish that ME researchers would just never mention “this proves it’s not all in the head” or anything regarding the BPS model. Every paper gets framed as “now we can prove it is a real disease” instead of just talking about the findings. The press therefore keep bringing up this negative stereotype of ME that perhaps otherwise would have been left in the past. Ignore, don’t address, move on assuming everyone knows it’s a non-psychological disease.

 

[Robert 1973]

I wish that ME researchers would just never mention “this proves it’s not all in the head” or anything regarding the BPS model. Every paper gets framed as “now we can prove it is a real disease” instead of just talking about the findings. The press therefore keep bringing up this negative stereotype of ME that perhaps otherwise would have been left in the past. Ignore, don’t address, move on assuming everyone knows it’s a non-psychological disease.

Yes.

Rule 1: Don’t bring it up.

Rule 2: Rehearse how to respond if/when others bring it up.

 

[Kitty]

Every paper gets framed as “now we can prove it is a real disease” instead of just talking about the findings.

This is exactly what I've been trying to argue.

We need to forget about it in our own messaging. If it gets thrown at us by others, we treat it with the disdain it deserves.