• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

Functional somatic syndromes may be either “polysyndromic” or “monosyndromic” - Peter Denton White

Messages
15,786
A BIG CASH PRIZE (well actually major kudos and a big virtual hug) to the first person who unearths the original scientific rationale for this notion that the greater the number of symptoms the more likely you are dealing with a 'functional somatic disorder' ***

The non-scientific rationale is that functional somatic disorder is defined as involving a variety of physical complaints without known cause. It's really just a definition. And the definition for CFS overlaps somewhat. So some non-scientists take this as proof that symptoms of CFS can be taken as evidence for having a psychosomatic disorder.

But to sum up the entirety of the BPS model for ME, and perhaps psychosomatic medicine as well, I present this quote:
Finally, it should be noted that our conclusions are primarily based on common sense, in the absence of a sound evidence base.
Huibers M, Wessely S. The act of diagnosis: pros and cons of labelling chronic fatigue syndrome. Psychological Medicine 2006: 36
 

PhoenixDown

Senior Member
Messages
455
Location
UK
Oh I expect they will argue with you Alex that FSSs are real diseases especially if the resultant research unearths evidence that they agree with. This 'mediating chemistry' you mention is to me the same thing as 'biomedical' evidence. And even if the categorisation of FSSs is considered to be mental; then if the treatment works - who cares
What about getting ideas in to people's heads that these patients are irrationally scared of exercise and that no damage comes to them from exercise? What about getting ideas in to people's heads that these patient's symptoms are generated by unhappyness, fulfilment, or deluded beliefs? That's why people care.

Yeah ok they might be fairly accused of trying to cram too many syndromes into too small a box - but if the research results in evidence and more effective treatment - again - who cares?
What effective treatment would that be? What about the down side of using these labels? Would changing the label prevent this research?

All this faffing around with names is what gets on my tits. And anyway, I thought the DSM thingy wasn't including CFS as a somatic condition? Pretty sure they weren't anyway.
What gets on my tits, are people who keep up this tired old charade of pretending labels can't harm the way we treat each other.
 

Simon

Senior Member
Messages
3,789
Location
Monmouth, UK
Building on sand (again)
It lookd to me like the two studies Peter White cites in his editorial and are either very or substantially flawed - which makes his intepretation of them rather irrelevant. There were 2 studies [quotes from Peter White's editorial]:

Study 1: Clustering of FSS
They recruited a sample of 368 members of “functional somatic syndrome patients' websites”, and asked them to fill in a questionnaire by the internet to elicit the presence of 47 somatic symptoms within the previous two weeks...

The samples were not clinically derived and we are not told how the patient websites were selected or what FSS they concerned. The data were all self-reported, so we cannot be sure that the patients did in fact have an FSS, since no clinical assessment was made. This was reinforced by the striking finding that 62% of the sample reported not having a current FSS at all.
So, they recrutied a bunch of people online and relied solely on self-report: most reported they didn't have a current FSS... "GAME OVER".
But, while I'm here: why didn't they also ask participants if they also had physical illnesses? Perhaps said FSS are actually misdiagnosed physical illnesses, and there may be a correlation with other physical illnesses. Such a question would, at least, provide some kind of reference point for the levels of additional FSS.

Study 2: Retrospective study of previous FSS in women with Interstitial Cystisis
.. a one year retrospective case control study of 312 women with a specific FSS, interstitial cystitis (irritable or painful bladder syndrome) (IC), matched by age, sex and locality with the same number of women without this condition recruited by random telephone calling [18]. They asked all subjects to recall whether their doctor had diagnosed any one of seven FSS in the year before they developed IC.

...One might argue with the inclusion of migraine, sicca syndrome and panic disorder as FSS,
This looks like a more substantial study, though again looked only at other presumed FSS and not at any correlation with other physical illnesses. From our prespective, it says nothing about CFS either.

Studies not done
Surely, when dealing with something as vague and ill-defined as FSS, what's needed are detailed studies trying to understand what is going on in any specific FSS, teasing out any sub-groups?

Many, many physical illnesses have a broad range of symptoms (eg pain, fatigue, concentration problems)- which is precisely why CFS is so hard to diagnose - as are many chronic illnesses.

Relying on questionnaires to look for similarities between presumed FSS, with little or no medical examination to verify the details strikes me as looking at the problem from the wrong end of the telescope. Contrast this with Ian Lipkin's approach of painstakingly assembling a large and carefully defined group of CFS patients and matched controls, then looking in detail at the pathophysiology. He might draw a blank, but from such robust work it will probably be possible to draw some robust conclusions. Which is a very different scenario to this kind of rather meaningless speculation about FSS.
 

Sean

Senior Member
Messages
7,378
Finally, it should be noted that our conclusions are primarily based on common sense, in the absence of a sound evidence base.

Then why are they so damn certain about their precious conclusions?

'Common sense' is nothing more than contemporary collective ignorance and prejudice.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Then why are they so damn certain about their precious conclusions?

'Common sense' is often nothing more than contemporary collective ignorance and prejudice.

"Common sense", to me, is a rhetorical device to appeal to general understanding. Its like someone is asking: is there anything obviously wrong with this? No. Then it must be right, that's common sense.

This is of course a well hidden fallacy.

Another other issue is an appeal to intuition, although this is mostly just restating my first point. Most of the brain and its functions is intuitive. The rational part of the brain is superimposed on that. When an appeal is made to common sense, I think its often an appeal to intuitive understanding. Its an attempt to bypass reason, either deliberately or just because they didn't use reason to form a better argument.

That intuitive understanding is subject to experience. When the public has had decades of information thrown at them on psychiatric illnesses, "all in your head" and other issues, and when the preponderance of media outlets in the UK (for UK audiences) is pro-psychogenic and portreying disability claimants as scavengers, then common sense is to believe psychogenic and other claims. Intuition is uncritical experience. Its not reason.

Bye, Alex
 

Firestormm

Senior Member
Messages
5,055
Location
Cornwall England
Studies not done
Surely, when dealing with something as vague and ill-defined as FSS, what's needed are detailed studies trying to understand what is going on in any specific FSS, teasing out any sub-groups?

Thanks Simon. Does not White's comment (shown again below) point to future study direction that will indeed 'tease out any sub-groups'?

The future now lies in increasing our understanding of FSS by moving beyond considering symptoms by themselves, and instead concentrating our attention on differentiating FSS sub-phenotypes.

We can do this by using already available biomarkers, such as: sleep–wake circadian rhythms, nocturnal sleep architecture, autonomic nervous system, hypothalamic–pituitary–adrenal axis, cytokine distributions, and central nervous system sensitisation, amongst others, in order to reveal the underlying pathophysiology specific to an individual FSS, and even the underlying endophenotypes [5], [6], [7].

Some links between pathophysiology and aetiology, such as childhood adversity, have already been described [4]. Future genomic studies should also inform both aetiological and pathophysiological pathways as well as the unexplained link with depressive and anxiety disorders [21].

Understanding the relevance of the pathophysiology and endophenotypes to both monosyndromic and polysyndromic functional somatic syndromes will then potentially inform treatments.

From a clinical point of view, assessment of symptom count [14], [22] and a history of both mood disorders and other functional somatic syndromes will inform prognosis and treatment [23].

To our patients' benefit, we have now moved the debate a long way from functional somatic syndromes being considered “all in the mind” [24].

12 November 2012 - From the OT publication: http://www.jpsychores.com/article/S0022-3999(12)00282-6/fulltext

I would suggest that - whilst it has taken an inordinate amount of time and effort and money - White and others might finally be getting this message of a need to move beyond collectively grouping clusters of symptoms and over-relying on determining what's what from a subjective point of view.

If for example, Newton's work and that of the other investigators who received funding from the MRC last year, reveal sub-groups based on physiological evidence, that indicate specific tests and future drug developments or refine the way in which current treatments are rather arbitrarily applied - then White and colleagues will indeed be in agreement (less likely to overly criticise).

To what extent the past reliance on the assessment of and grouping of common symptoms was necessary is obviously subject to much debate. But perhaps 'these people' are finally getting it and the future is more encouraging now?
 
Messages
15,786
I would suggest that - whilst it has taken an inordinate amount of time and effort and money - White and others might finally be getting this message of a need to move beyond collectively grouping clusters of symptoms and over-relying on determining what's what from a subjective point of view.

And while that is certainly possible, past experience shows that psych groups conducting biological CFS research generally either take steps to make sure few ME patients are included, or they attribute biological abnormalities to psychiatric or behavioral factors.

I think the odds are quite low that any BPS researcher will do a 180 and contradict their sweeping statements of somatization and behavioral problems. Too much ego involved, especially since their previous generalizations had no evidence base, but were based on their assumptions about us. They'll look like nasty idiots if/when those assumptions are disproven.
 

taniaaust1

Senior Member
Messages
13,054
Location
Sth Australia
While trying to find a forum White may of recruited from for his study.. I noticed CFS being mentioned as a functional stomatic syndrome in the first thread I looked at

I dont know if anyone feels like doing some advocacy..but I feel that some is needed at the following site (thou the post is a month old) in the following thread as an old scientific publication has been put up which says

The term functional somatic syndrome has been applied to several related syndromes characterized more by symptoms, suffering, and disability than by consistently demonstrable tissue abnormality. These syndromes include multiple chemical sensitivity, the sick building syndrome, repetition stress injury, the side effects of silicone breast implants, the Gulf War syndrome, chronic whiplash, the chronic fatigue syndrome, the irritable bowel syndrome, and fibromyalgia. Patients with functional somatic syndromes have explicit and highly elaborated self-diagnoses, and their symptoms are often refractory to reassurance, explanation, and standard treatment of symptoms
and goes on to say
Thus, the more convinced patients with functional
somatic syndromes are that their symptoms
are serious and pathologic, the more intense, prolonged, and disabling the symptoms become.

http://www.tmshelp.com/forum/topic.asp?TOPIC_ID=7863
Hopefully someone has enough energy to sign up there and post on that thread that CFS isnt at all known as a functional somatic syndrome at all and the author of that study was wrong. Also in the replies there one has posted​
I might add that as a medical layman with no first hand experience I strongly suspect that CFS, FM, and other seemingly mass hysterical conditions are psychogenic but the case has not been made.
Maybe someone feels like pming him about what abnormal tests they now have due to our suspected "psychogenic" condition etc. Does psychogenic conditions give low blood pressure to most of a certain patient group?​
If we targeted such sites to do ME/CFS advocacy too.. I wonder how many would suddenly realise that they actually do have CFS? I know many can go into denial at having a very real illness..my sister has done that. I bet there is some people at those sites.. helping some to think their illness whether CFS or another.. is just functional somatic syndrome..​
 
Messages
15,786
I dont know if anyone feels like doing some advocacy..but I feel that some is needed at the following site (thou the post is a month old) in the following thread as an old scientific publication has been put up which says

I doubt it would do much good. They believe that they have psychosomatic pain, and if they're on that forum then they probably believe anything with unknown etiological cause is psychosomatic. It's also highly unlikely that a challenge to their belief system would be allowed to remain - the description of the site explicitly states that
TMS is a defensive reaction of the mind to prevent expression of repressed rage and anxiety and that the pain is created when blood flow to the tissues is restricted by the autonomic nervous system.

Anything challenging that would likely be deleted.


 

SilverbladeTE

Senior Member
Messages
3,043
Location
Somewhere near Glasgow, Scotland
yes, blame the victim what a lovely age old story that is being used still: women deserve to be raped for showing flesh, immigrants deserve driven out for stealing jobs...ME patients make themselves ill by thinking they are ill and not accepting our Godly powers of Bullshit Vodoo psychiatry Uber-Telepathy That Can Make them Right, Turn Them Straight and away from their Queer Ungodliness of Non-Acceptance! Praise be to Freud!
*bunch of psychs sprinkle the Holy Incense of bovine merde and rattle the collection tin* :rolleyes:
yadda yadda...small minded, evil,
SCUMBAGS!

Candygram for Mr White, Wessely et al!
http://www.sophiaandme.org.uk/legal/l1.jpg
 

Simon

Senior Member
Messages
3,789
Location
Monmouth, UK
Thanks Simon. Does not White's comment (shown again below) point to future study direction that will indeed 'tease out any sub-groups'?
...
I would suggest that - whilst it has taken an inordinate amount of time and effort and money - White and others might finally be getting this message of a need to move beyond collectively grouping clusters of symptoms and over-relying on determining what's what from a subjective point of view.

If for example, Newton's work and that of the other investigators who received funding from the MRC last year, reveal sub-groups based on physiological evidence, that indicate specific tests and future drug developments or refine the way in which current treatments are rather arbitrarily applied - then White and colleagues will indeed be in agreement (less likely to overly criticise).

To what extent the past reliance on the assessment of and grouping of common symptoms was necessary is obviously subject to much debate. But perhaps 'these people' are finally getting it and the future is more encouraging now?
I wish this were true, but have my doubts.

It's worth noting that tracking down biomarkers in ANY disease in incredibly challenging and to date no one has managed it in CFS. The work done by psychiatrists to date has been small-scale and unconvinving. For instance, lower levels of urinary cortisol have been found in a couple of studies but a another paper by the same authors again found lower free urinary cortisol levels, but noted this wasn't corroborated by correspondingly lower levels of cortisol metabolites.There was no follow-up of this lack of corroboration. And no studies have even tried to show if the changes are specific to CFS or just general markers of ill-health.

So if you are going to track down pathophysiological changes specific to CFS - a huge challenge - then I think it's really helpful to have researchers whose heart is in itand who have a strong track record in biomedical research. But I'd be delighted to be proved wrong on this.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
I am reasonably sure CFS and possibly even ME will have no diagnostic biomarkers. This is because they are probably not one illness. I strongly suspect we will get diagnostic biomarker subgroups. In this sense if Peter White is serious then its the right way to go. I just doubt that psychiatrists are the best to investigate biomarkers, just as they have failed to meet gold standard research requirements in exercise physiology for a decade now.
 

Simon

Senior Member
Messages
3,789
Location
Monmouth, UK
One thou has been found (or maybe even two) .. thing is that research was ignored thou it can distinguish ME/CFS people from healthies.
Have any been independently validated? Only ones I'm aware of have been small studies and crucially set the key healthy/CFS thresholds post-hoc, after sight of the data and to maximise effectiveness for their particular sample. And that doesn't make a biomarker. Closest I'm aware of is reduced NK cell cytotoxicity in CFS patients vs healthy controls, but this was only a bioabnormality, with substantial overlap between patients and controls.
 

Firestormm

Senior Member
Messages
5,055
Location
Cornwall England
And while that is certainly possible, past experience shows that psych groups conducting biological CFS research generally either take steps to make sure few ME patients are included, or they attribute biological abnormalities to psychiatric or behavioral factors.

I think the odds are quite low that any BPS researcher will do a 180 and contradict their sweeping statements of somatization and behavioral problems. Too much ego involved, especially since their previous generalizations had no evidence base, but were based on their assumptions about us. They'll look like nasty idiots if/when those assumptions are disproven.

I am not going to disagree with you here Val, but I will say that in my own (and others') experience, ME or CFS has traditionally been treated largely through the administration of one (or as in my case several) antidepressants (and of course the CBT and GET and Activity Management and symptomatic treatments).

If 'these psychiatrists' through their own endeavours to sub-categorise and explore biological abnormalities can at the very very least improve upon the general meme of 'got ME have a general anti-depressant' then that would be progress. That said I am of course aware that anti-depressants generally possess far more properties that being an aide to depression.

My point I suppose - in this thread - is this. If you regard recent reported comments from the notable few psychiatrists etc. attracted to our condition as being even slightly reflective of 'change' then I think as we see more evidence produced of these biological reasons for our symptoms and/or (long shot) overall condition - these notables will back them.

Even if you (not you personally) are not 100% in agreement with the MRC funding allocations for example, you must surely acknowledge a change in direction and that this funding (in whole or in part) could result in the support of more than one biological cause for more than one symptom. We may even see specific targeted treatment of the pharmacological variety resulting from these studies.

Throw MRC initiatives together with all the private research taking place around the globe - and - dare I say it? Yes I think I will: The future has never looked more positive. And like Ampligen I would be more than willing to eat my shorts should this not prove to be so.*

(*I bet against the approval from the committee and so my shorts are still intact - though this is unfortunate of course for those who were hoping the company's evidence would prove convincing. Still there's always the February meeting and even then of course the case is not closed.).
 
Messages
15,786
If 'these psychiatrists' through their own endeavours to sub-categorise and explore biological abnormalities can at the very very least improve upon the general meme of 'got ME have a general anti-depressant' then that would be progress. That said I am of course aware that anti-depressants generally possess far more properties that being an aide to depression.

Sure. Let's take a look at a very recent Wessely study to see how it usually goes when psychs conduct biomedical research. The following excerpts are from Roberts ADL, Charler M, Papadopoulos AS, Wessely S, Chalder T, Cleare AJ. Does hypocortisolism predict a poor response to Cognitive Behavioural Therapy in Chronic Fatigue Syndrome? Psychological Medicine 2010: 40:515-522 :
. . . 39% of patients responded to CBT after 6 months of treatment. Lower 24-h UFC output was
associated with a poorer response to CBT. . . .
We found a significant negative correlation between 24-h UFC and WSAS scores, suggesting that lower cortisol was associated with higher levels of disability.
Low cortisol is of clinical relevance in CFS, as it is associated with a poorer response to CBT.
We suggest that the additional effects of lowered cortisol make CBT either less effective or more difficult to implement in these patients. This might imply that such patients require a longer duration of therapy, or perhaps a modified version of therapy.
In conclusion, this study suggests that HPA axis changes (reduced cortisol levels and a flattened diurnal release of cortisol) are of clinical relevance in CFS because they are associated with a poorer response to CBT. . . . This might imply that such patients require a longer duration of therapy, or perhaps a modified version of therapy, or alternative treatments alongside CBT to obtain maximum benefit.
They do not question the "pop an antidepressant and have some CBT" theory. If CBT doesn't work and there's a correlation with a physiological characteristic, they find a way to tie it in with their pre-existing theory. The accuracy of the theory is never challenged, nor its general applicability.

I don't see that ever changing. To be perfectly honest, I think there could be 100% incontrovertible proof of solely physiological causation and perpetuation of all ME/CFS symptoms, and they'd still find a way to conclude CBT is an essential part of the cure.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
There were comments to that effect Valentijn in White's Biopsychosocial Medicine with respect to peptic ulcers. While they are associated with Helicobacter pylori, apparently, something must still sustain the damage. It seems that back in, what?, 2005 or so, they still did not accept H. pylori as the sole cause. There must always be cofactors. Indeed there are additional issues, as I blogged about on this topic, and some of them are social factors which influence risk of pathogen spread, but this does not alter causation.
 

Dolphin

Senior Member
Messages
17,567
I am reasonably sure CFS and possibly even ME will have no diagnostic biomarkers. This is because they are probably not one illness. I strongly suspect we will get diagnostic biomarker subgroups. In this sense if Peter White is serious then its the right way to go. I just doubt that psychiatrists are the best to investigate biomarkers, just as they have failed to meet gold standard research requirements in exercise physiology for a decade now.
I don't think Peter White is that serious about properly subgrouping in CFS. His attitude is one treatment for all with CFS (graded exercise therapy). Subgrouping in my mind should be more meaningful. An example of his subgrouping was to have obese and non-obese CFS patients - not proper subgrouping of CFS.

He has argued against FSS. But I think that's at least partly but possibly mainly because he doesn't want to have to deal with other symptoms. For example, in the Barts service submission (where he's based and it looked like he wrote it - he certainly would have had to approve it), they argued that bowel symptoms weren't part of ME. Similarly fatigue has to be the main symptom to see him (some people have more pain).