Functional Somatic Syndromes" (ME/CFS/FM, etc.) As Serious As other Medical Conditions

Cort

Founder of Health Rising and Phoenix Rising
Staff member
"Functional limitations in FSS patients are common, and as severe as those in patients with MD when looking at QoL and work participation, emphasizing that FSS are serious health conditions."

You might not like the name - functional somatic syndrome - but the upshot of this HUGE 90,000 person study (who paid for this?) is that not only are "functional somatic syndromes" much more common than "medical diseases" but that they're just as functionally impairing and should be taken as seriously.
Psychosom Res. 2015 May 16. pii: S0022-3999(15)00439-0. doi: 10.1016/j.jpsychores.2015.05.004. [Epub ahead of print] Functional limitations in functional somatic syndromes and well-defined medical diseases. Results from the general population cohort LifeLines. Joustra ML1, Janssens KA2, Bültmann U3, Rosmalen JG1.
Abstract

Functional somatic syndromes (FSS), defined as physical syndromes without known underlying organic pathology, are sometimes regarded as less serious conditions than well-defined medical diseases (MD). The aims of this study were to evaluate functional limitations in FSS, and to compare the results to MD patients with the same core symptoms.
METHODS:

This study was performed in 89,585 participants (age: 44.4±12.4years, 58.5% female) of the general-population cohort LifeLines. Quality of Life (QoL) and work participation were examined as indicators of functional limitations. QoL was assessed with two summary scales of the RAND-36: the physical component summary (PCS) and the mental component summary (MCS). Work participation was assessed with a self-reported questionnaire. QoL and work participation were compared between FSS and MD patients, using Chi-squared tests and ANCOVA-analyses, adjusted for age, sex, educational level, and mental disorders.
RESULTS:

Of the participants, 11.0% (n=9861) reported a FSS, and 2.7% (n=2395) reported a MD. Total QoL, PCS and MCS were significantly lower in all separate FSS and MD compared to controls (P≤.001). Clinically relevant differences in QoL were found between chronic fatigue syndrome and multiple sclerosis patients, and between fibromyalgia syndrome and rheumatoid arthritis patients. Compared to controls, FSS and MD patients reported a comparably reduced working percentage, increased sick absence, early retirement due to health-related reasons, and disability percentage (P≤.001).
CONCLUSION:

Functional limitations in FSS patients are common, and as severe as those in patients with MD when looking at QoL and work participation, emphasizing that FSS are serious health conditions.
 

meisnotMUPS

Member
Cort, It is a really worrying development (although it has been going on since the beginning and is based on the ideas of the old Wessely-school fuctional somatic syndrome ideas), gaining ground. You can see that a lot of these MUS/MUPS articles are referencing old Wessely articles about FSS. Worth looking in to. Because functional somatic syndromes, are based on the invalidated/unproven biopscychosocial model. Patients with functional somatic syndromes (ME, IBS, Fibro, POTS and now LYME are considered MUS/FFS) are in need of CBT/GET in the eyes of these psychologists.

See for example: https://clinicaltrials.gov/ct2/show/study/NCT02426788?show_desc=Y#desc

and Chalders presentations about MUS/MUPS http://slideplayer.com/slide/7335352/

and just look at twitter #MUS2016, in UK also effort, like in the netherlands, to implement this im primary care.
https://www.nhg.org/sites/default/f...load/final_m102_solk_guideline_sk_mei13_0.pdf This is a medical MUS guideline in the netherlands, written by one of the Dutch Health Council memembers writing a report on ME, which lists "CFS" (table 5) as a undifferentiated somatoform disorder !

Rosmalen (from the article you cited) is also on the Dutch Health Council with task to write advisory report on ME! So is Knoop (who with Bleijenberg wrote the well known commenatry on the PaCE trial). Both are very close "PACE colleagues" as Tuller calls them. written many articles with White, Wessely even. Rosmalen is on the advisory board of the Journal of psychosomatic research. So are White and Wessely etc. This journal is the official journal of EAPM......see for their upcoming conference....http://eapm2016.com/sessions/
They were/are all part of Eurasmus (a group, including White, Creed! (DSM working group!), and Per Fink! the one holding Karina) but their site has been taken down.
Both Rosmalen and Knoop are involved in a 1.5 million Euro MUS/MUPS (medically unexplained symptoms) project funded by health care insurers, referring MUS patients (they consider ME to be MUS/MUPS, functional somatic symptoms, or even somatoform disorder) to mental health care institutions for CBT based on the biopsychosocial model, which they claim is "evicende based" and "effective"....it simply is not true!

this is why Cort, the Dutch started the petition https://petities.nl/petitions/me-is...sie-en-houd-u-aan-de-adviesopdracht?locale=en
 

San Diego

Well-Known Member
And so the re-branding begins. I suspect it won’t be the last.


All truth passes through three stages. First, it is ridiculed. Second, it is violently opposed. Third, it is accepted as being self-evident. ~ Arthur Schopenhauer, German philosopher (1788 – 1860)

It seems we’re coming out of phase 2 and knocking on the door of phase 3! Exciting times.
 

Snow Leopard

Active Member
Note that prevalence of mental disorders including anxiety was 26.4% - far from a majority and not that high really, when considering how hard it is to cope with ME or CFS.
 

Justin

Active Member
This is a way of government and health authoritys to cover up infectious, vaccine and toxic causes of illness.

This I see is a reason to cover plagues that have gotten out of control and find a way out of not paying for and study and developing treatment and drugs to fix the masses....

This name disgusts me and showcases just how debilitating these illnesses, biological illnesses are.

To add to this further it is way out for insurers and governments not to test people.

Dont get me startd MUS may be making its way to Canada as well.....not good...
 

Onslow

Active Member
Because functional somatic syndromes, are based on the invalidated/unproven biopscychosocial model.

I'm not sure what you mean by that. It has been very well established that psychological factors can cause fatigue, pain, immune dysfunction (Th1->Th2), mitochondrial suppression, changes in gut motility and absorption, autonomic nervous system and HPA axis dysfunction, etc. If you're not familiar with that, you might want to browse the literature. Certainly there are some biopsychosocial models that are built on shaky ground (e.g. theories about CFS being caused by abnormal illness beliefs or deconditioning). However that doesn't mean that all biopsychosocial models are invalidated. That's strawman logic.

Whether or not these factors are at play in any particular person's illness, or in some/many CFS patients is a difficult question to answer, as we don't have any definitive tests. However given that stress is a trigger for many CFS patients, and given that so many people have apparently recovered through therapies like the lightning process, it seems plausible that a certain number of CFS cases are functional.

I myself am agnostic as to the etiology of CFS. However I think it is very important to research this, so we know once and for all whether or not it's a factor in CFS. Unfortunately because there is so much antipathy towards anything in any way related to psychosomatic causation of CFS (including many of the leading researchers), I think it will be difficult to get a good answer to this question.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
Note that prevalence of mental disorders including anxiety was 26.4% - far from a majority and not that high really, when considering how hard it is to cope with ME or CFS.
Good point! Not that high at all really considering the incidence in other chronic illness

Many people with these illnesses become depressed. In fact, depression is one of the most common complications of chronic illness. It's estimated that up to one-third of people with a serious medical condition have symptoms of depression.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
I'm not sure what you mean by that. It has been very well established that psychological factors can cause fatigue, pain, immune dysfunction (Th1->Th2), mitochondrial suppression, changes in gut motility and absorption, autonomic nervous system and HPA axis dysfunction, etc. If you're not familiar with that, you might want to browse the literature. Certainly there are some biopsychosocial models that are built on shaky ground (e.g. theories about CFS being caused by abnormal illness beliefs or deconditioning). However that doesn't mean that all biopsychosocial models are invalidated. That's strawman logic.

Whether or not these factors are at play in any particular person's illness, or in some/many CFS patients is a difficult question to answer, as we don't have any definitive tests. However given that stress is a trigger for many CFS patients, and given that so many people have apparently recovered through therapies like the lightning process, it seems plausible that a certain number of CFS cases are functional.

I myself am agnostic as to the etiology of CFS. However I think it is very important to research this, so we know once and for all whether or not it's a factor in CFS. Unfortunately because there is so much antipathy towards anything in any way related to psychosomatic causation of CFS (including many of the leading researchers), I think it will be difficult to get a good answer to this question.
I don't know what it means that some cases of ME/CFS are functional but it's as clear as day to me that I became much, much, much more susceptible to stress after getting ME/CFS. I suppose that's at least partly due to having an illness that affects the two stress response systems in the body.

I too wish we could get beyond the mind/body dichotomy. We recently had a post that they've now found a physical cause for bomb induced PTSD but they still treat it (probably not all that well admittedly) with mind/body techniques and drugs.
 

Onslow

Active Member
I don't know what it means that some cases of ME/CFS are functional but it's as clear as day to me that I became much, much, much more susceptible to stress after getting ME/CFS. I suppose that's at least partly due to having an illness that affects the two stress response systems in the body.

Well, that's one of the interesting (if you can call it that) aspects of stress. Chronic long-term stress (or exercise overtraining) basically causes the stress system to shut down, making it more difficult to handle stress. It's thought that this is a protection mechanism, which has evolved to conserve energy during threats that are beyond the organism's ability to cope (Fries, 2009). I suspect this is a factor in some/many cases of CFS.

I too wish we could get beyond the mind/body dichotomy. We recently had a post that they've now found a physical cause for bomb induced PTSD but they still treat it (probably not all that well admittedly) with mind/body techniques and drugs.

As I mentioned in a comment there, that probably only applies to a certain percentage of PTSD. Many/most PTSD patients have not been anywhere near a blast. However you're right that PTSD treatment isn't terribly effective. Although I don't really know too much about it, I suspect the best treatment would be a combination of psychotherapy (talking about the trauma) and lifestyle changes (e.g. social activity programmes). A large part of the problem seems to be that soldiers don't cope well being at home with nothing to do.
 

Snow Leopard

Active Member
I'm not sure what you mean by that. It has been very well established that psychological factors can cause fatigue, pain, immune dysfunction (Th1->Th2), mitochondrial suppression, changes in gut motility and absorption, autonomic nervous system and HPA axis dysfunction, etc.

Most of the stuff you mention, including the "Th2" stuff, mitochondrial suppression, "leaky gut", "HPA axis dysfunction" is itself mostly just speculation based on little to no evidence (regardless of underlying mental or physical medical condition).

Speculation about psychology leading to unproven, vaguely defined, speculative medical states... It's pretty flaky either way.

Well, that's one of the interesting (if you can call it that) aspects of stress. Chronic long-term stress (or exercise overtraining) basically causes the stress system to shut down, making it more difficult to handle stress. It's thought that this is a protection mechanism, which has evolved to conserve energy during threats that are beyond the organism's ability to cope (Fries, 2009). I suspect this is a factor in some/many cases of CFS.

"Stress". The word stress is a weasel-word, it means so many different things in different contexts. There is no specific or central "stress system" in the body and chronic long-term stress can mean many, many different things. The HPA-axis does many things not to do with perceived psychological stress (or physical overactivity), cortisol likewise its primary function has little to do with stress.

I don't know the reference you are referring to (Fries 2009), but I speculate that it is a narrative paper/speculative hypothesis.
 
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Onslow

Active Member
Most of the stuff you mention, including the "Th2" stuff, mitochondrial suppression, "leaky gut", "HPA axis dysfunction" is itself mostly just speculation based on little to no evidence (regardless of underlying mental or physical medical condition).

I'm not entirely sure what you mean here. Are you saying that "Th2" isn't proven? It's a fundamental part of immunology. Or do you mean that it isn't proven that psychological stress can shift the immune system from Th1 to Th2? Have a look at the wikipedia page for cortisol and you'll see that we know that cortisol shifts the immune system from Th1 to Th2. We also know that cortisol is released during psychological stress. Note that this isn't directly relevant to CFS, as most CFS patients aren't under stress.

There is no specific or central "stress system" in the body

Actually there is, and it has been definitely proven (or at last, as close as science can come to definitively proving anything). The HPA axis and sympathetic nervous system are "stress systems". There isn't really any doubt about this.

The HPA-axis does many things not to do with perceived psychological stress (or physical overactivity), cortisol likewise its primary function has little to do with stress.

Agreed. Cortisol and the HPA axis do multiple things, including regulate digestion and the immune system, and energy regulation. If you want to give it an overall job title, probably "energy regulator" would be the best description. Psychological stress acts on the HPA axis in a similar way, because to the body they have similar energy requirements (fight or flight for psychological stress, or fighting an infection).

I don't know the reference you are referring to (Fries 2009)but I speculate that it is a narrative paper/speculative hypothesis.

Sorry, I meant Fries 2005 ("A new view on hypocortisolism"). Yes, it is a hypothesis, but is interesting nonetheless. It's just speculating on a *reason* for the hypocortisolism that is seen in chronic stress. The fact that chronic stress can result in hypocortisolism is supported by many reviews, so isn't really in much doubt.

I'm not sure why some CFS patients feel the need to bat at windmills and try to prove that stress doesn't have a physical effect on the body.
 

Snow Leopard

Active Member
I'm not entirely sure what you mean here. Are you saying that "Th2" isn't proven? It's a fundamental part of immunology. Or do you mean that it isn't proven that psychological stress can shift the immune system from Th1 to Th2? Have a look at the wikipedia page for cortisol and you'll see that we know that cortisol shifts the immune system from Th1 to Th2. We also know that cortisol is released during psychological stress. Note that this isn't directly relevant to CFS, as most CFS patients aren't under stress.

The Th1/Th2 model is just that. A convenient (but not completely accurate) model. There is no fundamental demarcation between t-helper cell subsets, t-helper cells of one subset can easily be induced (and often do in the body) to secrete the cytokines associated with the other subset, depending on the conditions... But there is more discussion in the literature Th3, Th17, Th9, I'm sure we'll add a few more to that list in the next 5-10 years. Clearly the Th1/Th2 model is not all there is.

Actually there is, and it has been definitely proven (or at last, as close as science can come to definitively proving anything). The HPA axis and sympathetic nervous system are "stress systems". There isn't really any doubt about this.

Many central aspects of the body "respond to stressors" so the HPA axis is not specific in that regard. It is just one part of the system. Conversely, the Hypothalamus and pituitary are involved in other bodily systems - that cannot be ignored to create a singular "HPA axis".
It is also a mistake to think of the HPA axis as a simple CRH/ACTH/cortisol feedback system - simple systems like that have been modelled and they don't match what happens in the body.

Sorry, I meant Fries 2005 ("A new view on hypocortisolism"). Yes, it is a hypothesis, but is interesting nonetheless. It's just speculating on a *reason* for the hypocortisolism that is seen in chronic stress. The fact that chronic stress can result in hypocortisolism is supported by many reviews, so isn't really in much doubt.

Mild Hypocortisol results can be induced in anyone simply with an alteration of sleep rhythm and taking blood samples at a specific time. You might call that a stressor, I'd call it a confounder of results. You see, studies that only measure cortisol and not a whole set of other biological parameters don't really tell us much at all about the state of the

I'm saying there is plenty of doubt about "chronic stress causing hypocortisolism" the findings are equivocal (why does chronic stress in most cases lead to normal or high cortisol levels?) and no one has unambiguously demonstrated how it occurs, nor any specific impacts.

I'm not sure why some CFS patients feel the need to bat at windmills and try to prove that stress doesn't have a physical effect on the body.

I'm not doubting that stressors (however you'd like to define them) have various effects on the body, including increasing the risk of many diseases. The question is what specific, testable effects this has and demonstrated models of how such can trigger or perpetuate specific* disease ("risk factor" is far too vague).

But I've read too many crap papers, making all sorts of unsupported claims and hypotheses to believe these ideas without good evidence - and I have spent far too much time looking to no avail, such that I am inclined to be sceptical until I see promising new in-depth experiments being done. Much of the evidence found so far is either isolated or nonspecific and requires far too many leaps of faith to put into a big picture. I'd like to see less hype and speculation and more science.

*If the model claims it can lead to many different diseases then the model is vague and probably worthless.
 

Onslow

Active Member
The Th1/Th2 model is just that. A convenient (but not completely accurate) model. There is no fundamental demarcation between t-helper cell subsets, t-helper cells of one subset can easily be induced (and often do in the body) to secrete the cytokines associated with the other subset, depending on the conditions... But there is more discussion in the literature Th3, Th17, Th9, I'm sure we'll add a few more to that list in the next 5-10 years. Clearly the Th1/Th2 model is not all there is.

Research shows that cortisol upregulates Il4, IL10 and IL13 (all Th2) and inhibits IL12, Ifn-gamma and TNF-alpha (all Th1). The model is just helpful for us to understand the system, but you can certainly delve into the details of the research.

Many central aspects of the body "respond to stressors" so the HPA axis is not specific in that regard. It is just one part of the system. Conversely, the Hypothalamus and pituitary are involved in other bodily systems - that cannot be ignored to create a singular "HPA axis".
It is also a mistake to think of the HPA axis as a simple CRH/ACTH/cortisol feedback system - simple systems like that have been modelled and they don't match what happens in the body.

Yes, of course. But just because we don't fully understand a system doesn't mean that it is useful for modelling certain aspects of it.


I'm saying there is plenty of doubt about "chronic stress causing hypocortisolism" the findings are equivocal (why does chronic stress in most cases lead to normal or high cortisol levels?) and no one has unambiguously demonstrated how it occurs, nor any specific impacts.

Actually, if you look at animal research, you can induce hypocortisolism with certain types of stressors, and we know some of the brain mechanisms responsible. You appear to be introducing a strawman and saying "because there is some crappy and/or conflicting science about stress, we should just throw our hands up and ignore it all".
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
A lot of this is beyond me but I would bet the autonomic nervous system is far more involved than the HPA axis in ME/CFS at least my ME/CFS and I'll bet its tied to the weird anxiety or jitteriness or difficulty settling down or wired and tired sensations or whatever you want to call them. Something whacked me physically/mentally at the same time...I don't mind saying that. I am not the same person as I was pre ME/CFS.

I don't believe for a second it was psychological, though...
 

Onslow

Active Member
A lot of this is beyond me but I would bet the autonomic nervous system is far more involved than the HPA axis in ME/CFS at least my ME/CFS and I'll bet its tied to the weird anxiety or jitteriness or difficulty settling down or wired and tired sensations or whatever you want to call them. Something whacked me physically/mentally at the same time...I don't mind saying that. I am not the same person as I was pre ME/CFS.

The ANS and HPA axis are linked. We know that acute stress activates both the HPA axis and sympathetic nervous system, and this happens for both physical exercise and psychological stress. That doesn't directly apply to CFS, because with CFS it seems that in CFS the HPA axis is suppressed, and the parasympathetic branch of the ANS is also suppressed. Normally stress increases sympathetic activation and that then suppresses the parasympathetic, but in CFS it seems as if the parasympathetic nervous system is abnormally low, and the sympathetic nervous system is activated as a consequence of that (i.e. the opposite of what happens during acute stress). i.e.:

STRESS: +HPA, +SNS -> -PNS
CFS: -HPA, -PNS -> +SNS

We know that the parasympathetic nervous system is activated after the stressor, after the HPA axis activation has reduced back to normal. So it's possible that in CFS the same mechanism that is causing reduced HPA axis activation is also causing reduced parasympathetic activity.

I don't believe for a second it was psychological, though...

Why do you say that? Both psychological and physical stress affect the HPA axis and ANS the same way, so I'm not sure why some people don't like the idea of psychological stress causing physical effects. (In fact, certain aspects of hypocortisolism have been shown in animal experiments to *only* apply to psychological stressors and not physical stressors).
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
The ANS and HPA axis are linked. We know that acute stress activates both the HPA axis and sympathetic nervous system, and this happens for both physical exercise and psychological stress. That doesn't directly apply to CFS, because with CFS it seems that in CFS the HPA axis is suppressed, and the parasympathetic branch of the ANS is also suppressed. Normally stress increases sympathetic activation and that then suppresses the parasympathetic, but in CFS it seems as if the parasympathetic nervous system is abnormally low, and the sympathetic nervous system is activated as a consequence of that (i.e. the opposite of what happens during acute stress). i.e.:

STRESS: +HPA, +SNS -> -PNS
CFS: -HPA, -PNS -> +SNS

We know that the parasympathetic nervous system is activated after the stressor, after the HPA axis activation has reduced back to normal. So it's possible that in CFS the same mechanism that is causing reduced HPA axis activation is also causing reduced parasympathetic activity.



Why do you say that? Both psychological and physical stress affect the HPA axis and ANS the same way, so I'm not sure why some people don't like the idea of psychological stress causing physical effects. (In fact, certain aspects of hypocortisolism have been shown in animal experiments to *only* apply to psychological stressors and not physical stressors).
To make it clear - there was no reason to think that psychological issues triggered my ME/CFS because I was doing really well psychologically at the time. I had found my niche, I was in love with what I doing, I was in great shape physically, I was doing great in school - I was a high point really.

I think one reason that a lot of people don't like the idea of psychological stress contributing to ME/CFS is that it doesn't seem to lead to an answer; at least in our case it it seems to lead to CBT and GET...

I get what you're saying though. I have read that both psychological and physical stress have very similar effects on the body. In fact I remember Andrew Miller writing that researchers were sure that they were going to see big differences but they didn't...So its probably a wash...

Afterwards its a very different story - now my system over- reacts to both physical and psychological stressors; it just can't seem to settle down either way...
 

Onslow

Active Member
To make it clear - there was no reason to think that psychological issues triggered my ME/CFS because I was doing really well psychologically at the time. I had found my niche, I was in love with what I doing, I was in great shape physically, I was doing great in school - I was a high point really.

I think one reason that a lot of people don't like the idea of psychological stress contributing to ME/CFS is that it doesn't seem to lead to an answer; at least in our case it it seems to lead to CBT and GET...

I get what you're saying though. I have read that both psychological and physical stress have very similar effects on the body. In fact I remember Andrew Miller writing that researchers were sure that they were going to see big differences but they didn't...So its probably a wash...

Afterwards its a very different story - now my system over- reacts to both physical and psychological stressors; it just can't seem to settle down either way...

Ok, you're saying that in your case you don't think psychological factors triggered your illness, which seems a fair assumption. However there do seem to be quite a lot of CFS patients whose illness was triggered by psychological stress such as rape, or after job stress, or long-term sleep deprivation.

I agree that CBT and GET are sometimes delivered with dubious theories, such as deconditioning or abnormal illness beliefs - neither of which make sense or have any evidence. However there was a recent study showing that CBT was much more effective in the Netherlands than in the UK, so perhaps the Netherlands were using a different flavour of CBT. If CFS is caused by the brain shutting down the body's energy supply after chronic stress then CBT and GET are both plausible treatments, but probably not if they are based on deconditioning and illness beliefs.

Fred Friedberg did a case study showing that GET helped a patient by replacing stressful work activities with non-stressful activities. There was no difference in actual physical activity, it was just the type of activity that was important. We know that exercise causes relapses in patients, and it also helps people to recover, which appears to be a paradox until you look at the type of activities that people are doing.
 

Snow Leopard

Active Member
Ok, you're saying that in your case you don't think psychological factors triggered your illness, which seems a fair assumption. However there do seem to be quite a lot of CFS patients whose illness was triggered by psychological stress

How? While such factors may well be risk factors, they are neither necessary, nor sufficient to trigger or maintain the illness. I've looked hard for such mechanisms in the literature for years and haven't seen anything I'd consider convincing. Hence I'm not so excited about discussing such associations - unless we have a strong understanding of how they increase the risk that could give clues as to understanding the underlying factors of the illness.

I agree that CBT and GET are sometimes delivered with dubious theories, such as deconditioning or abnormal illness beliefs - neither of which make sense or have any evidence. However there was a recent study showing that CBT was much more effective in the Netherlands than in the UK, so perhaps the Netherlands were using a different flavour of CBT.

The study provides no such evidence of efficacy, as no objective measures of functioning were measured and such studies cannot be blinded. The study shows that subjective short term questionnaire answering behaviour was different in NL vs UK patients - and therapist effects, cultural biases etc could explain that just as much as subtly different methodologies.

Fred Friedberg did a case study showing that GET helped a patient by replacing stressful work activities with non-stressful activities. There was no difference in actual physical activity, it was just the type of activity that was important. We know that exercise causes relapses in patients, and it also helps people to recover, which appears to be a paradox until you look at the type of activities that people are doing.

That is flawed logic. Avoidance is not a solution that leads to improvement in capacity - it's just that proper pacing is preventative for people getting worse. If the person's underlying health had improved, then they would be able to do the 'stressful' or more physically demanding work (which they no doubt could easily do before the illness) without problem.

Actually, if you look at animal research, you can induce hypocortisolism with certain types of stressors, and we know some of the brain mechanisms responsible. You appear to be introducing a strawman and saying "because there is some crappy and/or conflicting science about stress, we should just throw our hands up and ignore it all".

The problem is the science isn't very good. The lack of specificity of the findings and the fact that it is usually just cortisol, or at best one or two other things measured at the same time (GR expression needs to be measured at a minimum) means we don't learn very much about the mechanisms involved from such experiments.
 
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Onslow

Active Member
How? While such factors may well be risk factors, they are neither necessary, nor sufficient to trigger or maintain the illness.

Two possibilities:

[1] When the brain gets into the hypocortisolism state, it is difficult to break out of.
[2] Psychological factors from the illness itself.

I've looked hard for such mechanisms in the literature for years and haven't seen anything I'd consider convincing.

I guess it depends what you determine "convincing". You sound like a hard person to convince (and I'm not going to try).

The study provides no such evidence of efficacy, as no objective measures of functioning were measured and such studies cannot be blinded. The study shows that subjective short term questionnaire answering behaviour was different in NL vs UK patients - and therapist effects, cultural biases etc could explain that just as much as subtly different methodologies.

It seems unlikely that "questionnaire answering behaviour" could cause an extremely high effect size of 1.74, but if that's what you want to believe...

The problem is there are no objective measures of functioning. CFS patients have normal fitness (unless deconditioned, but that is not fundamental to the illness). Moderately affected patients have normal step counts. Severely affected patients obviously have lower step counts, but they typically aren't included in these studies.


That is flawed logic. Avoidance is not a solution that leads to improvement in capacity - it's just that proper pacing is preventative for people getting worse. If the person's underlying health had improved, then they would be able to do the 'stressful' or more physically demanding work (which they no doubt could easily do before the illness) without problem.

The point is that there was no difference in how physically demanding the activities were. The "treatment" involved doing activities that were just as physically demanding as the work that was avoided. It was the mental stress of the work (he didn't want to do it) that appeared to make the difference. Avoidance of stresses like this certainly is a valid strategy, although this particular strategy obviously this only applies to moderately affected patients who are still working.
 

Snow Leopard

Active Member
Two possibilities:

[1] When the brain gets into the hypocortisolism state, it is difficult to break out of.
[2] Psychological factors from the illness itself.

Which are mediated (biologically) how? (rhetorical question)

It seems unlikely that "questionnaire answering behaviour" could cause an extremely high effect size of 1.74, but if that's what you want to believe...

I'm surprised that anyone cares about effect sizes when there is no control. As Neuroskeptic said when specifically asked about this: generally that's meaningless. That's why you need a control. Within-group D = natural improvement + regression to the mean + placebo effect + real effect. Real effect is generally only a small % of the within group effect, only a placebo controlled study can reveal that.

The problem is there are no objective measures of functioning. CFS patients have normal fitness (unless deconditioned, but that is not fundamental to the illness). Moderately affected patients have normal step counts. Severely affected patients obviously have lower step counts, but they typically aren't included in these studies.

The key is to use a combination of objective measures, including fitness testing, actigraphy, neuropsychological testing and to set composite measures of improvement (eg if step count is normal, then improvement on that is not required). Jonathan Edwards had some stuff to say about how outcome measures could be improved (and how composite measures are sometimes used in other trials for other medical conditions - even when it means the end result seems less impressive). But actigraphy is more than step count and the patterns (eg day to day variation and intensity of exercise are much more revealing than total step count).



The point is that there was no difference in how physically demanding the activities were. The "treatment" involved doing activities that were just as physically demanding as the work that was avoided. It was the mental stress of the work (he didn't want to do it) that appeared to make the difference. Avoidance of stresses like this certainly is a valid strategy, although this particular strategy obviously this only applies to moderately affected patients who are still working.

So when doing less psychologically demanding activities, we answer differently on questionnaires. That's great, but it doesn't mean that person's physical health has improved.
 

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