By David Tuller, DrPH
In teaching courses on covering public health and medical issues, I have often highlighted how university press releases about studies can read like efforts at obfuscating problematic findings rather than providing an accurate account of research. A recent press release from King’s College London, about a high-profile study published by Lancet Psychiatry, is an excellent example of this problematic genre.
I plan to write more about the study–‘Cognitive behavioural therapy for adults with dissociative seizures (CODES): a pragmatic, multicentre, randomised controlled trial’–when I get a chance. This post focuses on some discrepancies between the KCL press release and the study itself.
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On June 3, Kings College London posted a press release touting a major study of cognitive behavioural therapy for the treatment of what have long been called psychogenic non-epileptic seizures (PNES) but are now sometimes referred to as dissociative seizures (DS). The press release bore the following headline: “Cognitive behavioural therapy reduces the impact of dissociative seizures.”
And here’s the first paragraph: “Scientists have found that adding cognitive behavioural therapy (CBT) to standardised medical care gives patients with dissociative seizures longer periods of seizure freedom, less bothersome seizures and a greater quality of life, in a study published in Lancet Psychiatry and by the Cognitive behavioural therapy for adults with dissociative seizures (CODES) study group funded by National Institute for Health Research (NIHR).”
The study was the largest of its kind, with 368 participants randomized to receive either standardized medical care, or standardized medical care combined with a form of CBT designed specifically for the disorder. The results were published by Lancet Psychiatry, a high-impact journal. The press release included comments from the investigators about the significance of the work, a common feature of such releases.
“We have delivered the first large-scale multi-centre and multi-professional trial investigating treatments for adults with dissociative seizures,” said Laura Goldstein, a professor of clinical neuropsychology at KCL’s Institute of Psychiatry, Psychology & Neuroscience. Trudie Chalder, a professor of CBT at the same KCL institute, declared that “we now have evidence for the effectiveness of dissociative seizure specific CBT combined with standardised medical care.”
But effectiveness for what, exactly? Professor Chalder’s statement did not elaborate. Readers of the press release could be forgiven for not realizing that the outcome selected as the primary endpoint by the investigators–the average number of seizures per month at 12 months after randomization–had null results. In other words, a course of CBT that included specific seizure reduction techniques and that Professor Chalder touted as an effective treatment had no impact on the reduction of the number of seizures–the study’s most important and significant finding.
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Psychogenic non-epileptic seizures, or dissociative seizures, are part of the larger category called functional neurological disorders (FNDs), which themselves are part of the even larger category called medically unexplained symptoms (MUS). All of these conditions and illnesses share the characteristic of having no identified pathophysiological cause. Experts differ sharply on whether the absence of currently known or identified pathophysiological causes means that no such pathophysiological causes exist.
In the UK, CBT is a favored intervention for all kinds of conditions placed in the MUS domain, including irritable bowel syndrome and what investigators often call chronic fatigue syndrome–despite the paucity of quality evidence to support this approach. The findings of the PACE trial, which purported to be the definitive examination of the effectiveness of CBT for chronic fatigue syndrome, have been convincingly rebutted, despite continued bleating from the study’s dwindling number of defenders.
Earlier this year, I documented that a web-based CBT program for IBS produced statistically significant but clinically insignificant reductions in symptom severity–yet is being deceptively marketed as an effective treatment for reducing symptom severity. And articles on the Opposing MEGA website have highlighted questions about some of the data underlying the UK’s MUS project, which involves presuming those diagnosed with these complex disorders require psychological treatment rather than specialist medical care.
(Northwestern University law professor Steven Lubet and I have recently published a commentary about MUS that advocates humility in making declarative statements about conditions of unknown etiology. That piece can be accessed here; unfortunately, it is behind a paywall. Professor Lubet has blogged about our paper and included short excerpts here.)
In the pilot study that formed the basis for the CODES trial, the investigators made clear they believe the absence of evidence that pathophysiological processes cause dissociative seizures is proof that pathophysiological processes do not play a role in causing dissociative seizures. Here’s how they explained the situation in the pilot study, published by Neurology in 2010:
“Psychogenic nonepileptic seizures (PNES) are paroxysmal episodes of behavior resembling epileptic seizures but lacking organic etiology. Most clinicians agree that in most cases the episodes are involuntary, arising through unconscious psychological mechanisms.”
The statement that these paroxysmal episodes have no organic etiology but are instead triggered by emotional and affective distress through undefined mechanisms is a hypothesis stated as if it were a conclusion. Given the investigators’ adoption of the psychogenic framework, they understandably wanted to assess whether an approach that helped patients restructure or reformulate beliefs and ideations could reduce the number of seizures.
In the pilot study, the investigators explicitly rejected the idea that other primary endpoints might be more suitable than seizure reduction–presumably after careful consideration of other possibilities. Here’s what they wrote:
“Our CBT approach is predicated on the assumption that PNES represent dissociative responses to arousal, occurring when the person is faced with fearful or intolerable circumstances. Our treatment model emphasizes seizure reduction techniques especially in the early treatment sessions. While the usefulness of seizure remission as an outcome measure has been questioned, seizures are the reason for patients’ referral for treatment.”
The statistical analysis plan, citing several other papers, noted that “seizure frequency has been used as an outcome measure in other studies of psychological interventions for DS.” And it explained in detail how power calculations for the trial were based on assumptions related to that specific measure. The statistical analysis plan included no details about how the secondary outcomes would be analyzed–presumably because the investigators considered these outcomes to be of only secondary importance.
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In the pilot study, with 66 participants, the primary outcome was seizure frequency, at the end of treatment and at a follow-up assessment six months after the end of treatment. In the CBT group, a reported benefit at the end of treatment was no longer statistically significant by six-month follow-up. At follow-up, results for one of several secondary outcomes “tended to” indicate benefit from the CBT. These modest results were apparently enough to secure funding from a major UK agency for a full-scale trial. Not surprisingly, the full-scale trial seems to have produced similarly unimpressive findings.
In CODES, the primary outcome was the average number of seizures per month at 12 months post-randomization. That number fell in both arms of the study–great!–but CBT provided no benefit, with no statistically significant differences between the two trial groups. Let’s say that again: The outcome that the investigators had spent at least a decade promoting as the critical measure of treatment success had null results. The therapy did not work as billed, leading to questions about the therapy’s theoretical underpinnings.
Of more than a dozen secondary outcomes measured, nine showed statistically significant improvement, although how clinically significant these changes were is another question. Moreover, the number of secondary outcomes showing statistically significant improvements dropped to five by the more conservative analytic strategy preferred by many experts in study design and statistics. (More on these outcomes in another post.)
As written, the press release represented a valiant effort to obscure the bad news. The headline and first paragraphs did not mention the null results for the primary outcome. In a cumbersome sentence tucked into the bottom half of the release, these null results were referenced in passing–at which point the sentence immediately switched gears to focus on the purported “better functioning” demonstrated by other measures. The status of all these other measures as secondary outcomes was not mentioned.
Here’s what the release stated:
“While overall there appeared to be a reduction in how often people in both groups of the study were having dissociative seizures at the end of the trial, with no clear difference between the groups, the group who had received our package of dissociative seizure-specific CBT were reporting better functioning across a range of everyday situations.”
Readers can judge for themselves whether they or anyone would understand from that sentence, and from the rest of the press release, that seizure reduction was the predesignated primary outcome—per both the trial protocol and the statistical analysis plan. It goes without saying that press releases about major studies should make it clear whether the primary outcome of interest reported positive or null results and whether reported benefits are from primary or secondary outcomes.
It also goes without saying that investigators should review press material about their work before it is distributed. If the primary and secondary results are not transparently communicated as primary and secondary results, investigators should request changes to ensure this sort of clarity. That does not appear to have happened in this case.
Comments
23 responses to “A King’s College London Press Release Hides the Bad News”
Having watched on for several years to witness the difficulties real researchers have accessing funding for authentic research – it so irritates me to see funding go to this kind of degrading and dodgy …I’m not calling it research – it’s a means to an end, a money grab! Infuriating,
“We have delivered the first large-scale multi-centre and multi-professional trial investigating treatments for adults with dissociative seizures”
This is starting to make me think of patent trolling. Except worse. They fabricate the need for a useless intervention, in part by inventing a fictitious problem category (which includes real problems but they are simply reframed differently and overlap various things, like CFS or FND), run a series of experiments leading to a quasi-serious looking experiment/”trial” that may or may not be relevant to the health problem in question, then celebrate the fact that it is the first of its kind, therefore the only game in town. It doesn’t even matter what’s in it, nobody actually cares, it’s the only thing around. If you don’t like it just run your own multi-million trial showing otherwise (actual answer from Michael Sharpe).
It’s done with exaggerated celebration over its efficacy, which is what people will remember since nobody really checks whether any of it works, just that it claims to. It gains credibility simply by existing, discouraging serious research, which will not progress since there is not much need for it anymore. The problem isn’t solved but the complaints are. Whenever a new complaint occurs, it goes into the hidey hole of “take this or leave”, a choice between a useless thing and an even less useful one. But the patient is gone, and that’s what matters. The box is ticked. The patient now lives in it, trapped but unable to complain about it. They can do the treatment, what more could they want? Vexatious bastards.
I don’t know if you’ve read the 3-body problem by Cixin Liu, highly recommended. Long story short it involves an attempt at stifling the scientific progress of a civilization by making fundamental physics research impossible. Basically a regression machine to make scientific progress impossible past a certain point. This is doing the same thing to the areas of medicine that are still unsolved. Unwittingly, by sheer foolishness and hubris, which is even worse. Even though those problems are already recorded well enough to count, since they involve sick people, which is what medicine is supposed to be about. Or so I thought. WTF is this?
I’m starting to get the feeling that there are far fewer (if indeed anyone other than your group is) investigators checking out pseudo-scientific crap claims than there are making them, and the people (I’m not going to dignify them by calling them scientists) who put up these papers do not expect to get caught.
What would have happened without you? More sick people even more traumatized by this thievery.
Spin, spin and even more spin. When will this stop? They seem to be masters of spin – an ultracentrifuge of their own spin, I’d say, that cleanly separates out bad scientists. Is this what they teach their students? What exactly did they learn from Hans Eysenck?
Kings and TC are just like ‘wack a mole’!…….
You knock one out only to see it pop up somewhere else…….
i) It becomes clearer with every paper that is published that The Lancet and BMJ publications can now be considered bywords for incompetent, clique-driven gobbledegook designed only to promote the careers of those involved at the expense of patients. Richard Vallee’s observations seem pretty much on the money.
ii) Enough with the silly acronyms. Is there a DSM entry for pseudo-scientists who relentlessly use pathetic acronyms as decoration for their junk science? It’s just a case of polishing a ****!
“Kings and TC are just like ‘wack a mole’!…….” ; or maybe more like whack an opossum in this case … we need an animal study with ‘possums to see what they go torpid under stress? It’s appalling to see how much rubbish is now found under the cover of ‘science’, especially since Covid-19 has hit, and quacks have come out from the woodwork, propelled by political and financial motives as well as their own nuttiness and fanatical ideology.
This has been growing for years, however, as the empire collapses, climate change shows its effects, the wars ‘regime changes’ fail, and both the real and financialized economies tank.
It’s might seem that ‘dissociative seizures’ has moved from just individual afflictions to society as a whole (Paul Levy’s ‘malignant egophrenia’?) . Carl Jung would laugh.
Well the bad science works on both sides of the Pond. This is what Sir Simon Wessely had to say about Ron Davis’ needle stick to discover the response to immune cells in CFS patients under stress: https://www.telegraph.co.uk/science/2019/04/29/test-chronic-fatigue-syndrome-may-picking-symptoms-not-condition/
However some experts in Britain warned the test may be picking up symptoms of fatigue or anxiety rather than the disease itself, and could not be used as proof the condition is real.
Prof John Martin, Professor of Cardiovascular Medicine, University College London (UCL), said: “If a test is to have meaning it has to be able to be applied to a population of patients who can be defined clinically.
“The patients described had a variety of symptoms that could have arisen from a variety of causes.
“Further the authors do not relate the cellular finding in the test to a possible cause of the disease. CFS/ME is probably not a disease but a syndrome.
“The authors should consider whether their test is related to an effect of symptoms and not related to the cause.”
Prof Sir Simon Wessely, President of the Royal Society of Medicine, said: “There have been many previous attempts to find a specific biomarker for CFS. The problem is not differentiating patients with CFS from healthy controls. The issue is can any biomarker distinguish CFS patients from those with other fatiguing illnesses?
“And second, is it measuring the cause, and not the consequence, of illness? This study does not provide any evidence that either has finally been achieved.”
The Stanford team has also been using their test to see if drugs can dampen down the electrical response of cells under stress. They have already discovered that one medication in common use does, and hope to start clinical trials soon.
Thanks for the link, John, and rather belated thanks to Professor Wessely for drawing attention to the definition issue. Clearly having a very clear and narrow definition does matter if the next few decades aren’t to be wasted…..and not least so that certain people can’t denounce any interesting findings on the grounds that ‘CFS’ patients are indistinguishable from others who have fatigue.
I am reminded of WC Fields kicking the coffee machine whilst saying “come on Ethel get excited”. Recent reports in the media say women have immune systems the are more robust and more complicated than men. 20thC research scientists used a male model (women being too complicated). They devised treatments to stimulate our immune systems that let viruses into our bodies. This is like giving men (prostate cancer) a seat in the lifeboat which women (CFS/ME/IBS/Fibro) and children (autism) are left in steerage. Women are then carted off to Bedlam for mental health issues when every cell in their bodies is malfunctioning.
CT and John: I read John’s comment, arriving at the same conclusion CT made: we need the tightest possible clinical definition to make findings meaningful. Clearly the Wesselyite ‘Oxford Criteria’ were designed to muddy the waters and create such a broad definition, bringing in many with psychiatric maladies and actually sifting *out* anyone who might have neurological signs or symptoms, that nothing meaningful can be extracted from the body of research using that set of criteria. The IOM observed the same and that harms could result from using the Oxford criteria. Having said that many patients despair of the SEID nonsense that the IOM then decided to proffer. Yes it’s possible to find people with ME using SEID but it’s also possible to draw in any man and his dog at the same time. It’s like fishing with such a huge and holey net that the subsequent catch is almost indistinguishable from the sea from which it was drawn.
Sadly the OMF seem a little contrary with how they assess their patient cohorts… although their severely ill cohort, one might assume by virtue of the degree of disease presentation, is likely nearer the truth than some. Other papers such as this https://www.omf.ngo/wp-content/uploads/2016/08/Naviaux-PNAS-CFS-Metabolomics-2016.pdf throw so many ingredients into the mix that the cohort might well resemble a minestrone. In order not to be accused by members of the BPS of the very muddle the BPS like to themselves manufacture, it behoves researchers to be very clear about the population they ascribe their findings to. I’m surprised that a body like the OMF with the calibre of scientists it has accrued can’t be more rudimentary on this point.
Many long-timer, severely ill patients as well as those who have given enough thought to the existing literature and the prevailing politics around this disease, and whose need for speedy resolution of the disease is, for many, truly existential, realise that there is only one sensible set of criteria to reasonably sift out a cohort of authentic ME patients (not ME/CFS or CFS/ME or CFS or CF or any other variable). That is the ICC criteria and has been endorsed by over seven and a half thousand people: https://www.change.org/p/the-us-department-of-health-and-human-services-cdc-adopt-the-distinct-disease-myalgic-encephalomyelitis-me-as-defined-by-icc-now
Here is another great resource providing information about the way in which ME has been defined over the years including a useful ‘quickie’ questionnaire which might help those who aren’t sure about their diagnosis & which allows them to see whether or not they might fit ICC (and we as patients must remember that a negative result is as important as a positive one). If people don’t see that they fit the ICC criteria but have been told they have ME then they should be interrogating other pathways to trying to understand why they are ill. Accepting a diagnosis like ME without question might well be the equivalent of preventing one from securing a different diagnosis, maybe even one with very good options for care and amelioration of symptoms. https://www.meadvocacy.org/resources
Question: How IRONIC is it, that CFS shares almost identical symptomatology to hypothyroidism? Did CFS “disease” say “hey, i want to confuse everyone by making a new disease called CFS and I am going to make the symtoms shadow hypothyroidism”. ;))
Seems like the British medical profession has looked into almost every area of medicine to try and find out what causes CFS.
http://www.simonwessely.com/index.php/cfs-personal-story/
http://www.simonwessely.com/index.php/misunderstandings-misperceptions-2/
They have found low diurnal cortisol which hydrocortisone worked well on but say it is not something that can be used long term. They also found some immune function abnormalities but it was not sufficient for a biomarker and did not affect outcomes. They admit to altered endocrine response.
please see simonwessely.com for the research he has done into CFS at King’s
https://www.nationalelfservice.net/other-health-conditions/chronic-fatigue-syndrome/the-pace-trial-for-chronic-fatigue-syndrome-choppy-seas-but-a-prosperous-voyage/
I did what you said, Martin, and look what I found – see above.
‘orrible, ‘orrible – it has sent me running straight back to Kent Heckenlively and Judy Mikovits
As far as I know, ME is only caused by an Enterovirus. I said this to a Dr years ago and he said the literature did not support that view. He was a virologist as well. But certainly Dr Byron Hyde’s view of ME seems to be the best fit I can see, The question is what does one do about a viral attack on the CNS once it has happened?
That is interesting because I had a coxsackie virus over 20 years ago caught at a Centre Parks holiday – water borne? and my daughter got henera schienlein purpora virus at the same time. My osteo/medical herbalist and all-round wise woman said to take care because coxsackie was one of the viruses linked to CFS but I was pretty nonchalant in my 40’s but in my early 60’s several viruses reared up when my health collapsed (including a minor display of shingles (I had chickenpox as a child).
It wouldn’t take 20 years to get ME/CFS after a coxackie infection I would not think. Nothing Hyde said has been actually proven. I asked a doc here in the UK about it as I already said and he said that is not what has happened. Different doctor different viewpoint. LOL.
These things have all been researched in ME/CFS by Simon Wessely.
We set up the first proper epidemiological studies in this country.
As part of that, we were able to show that the label “Yuppie Flu” was a misnomer. In fact the illness was commoner in those lower down the socio economic ladder, not higher. Most of those in lower socio economic levels didn’t use words like ME or CFS to describe their condition, and many of them were not being seen in hospital clinics, which is why the “yuppie flu” label had been used, but it was wrong.
At the start I did think that this might be a form of what we called atypical depression, and early work suggested that there were definitive overlaps with depression. But we showed that about half of those with CFS at the Square weren’t depressed anyway. And then once I moved down to King’s, we did a series of neuro endocrine studies, in which one of the first findings was that there was a different neuro endocrine profile in CFS to that in classic depression. The same neurotransmitter systems seemed to be involved, but in a different way.
That led to a long series of neuro endocrine studies, largely led by my then lecturer, and now Professor, Tony Cleare. The work showed that the hypothalamic pituitary axis functioned differently in CFS to how it does in well people – with a particular pattern of low diurnal cortisol. This finding is now I think the single most replicated biological abnormality in CFS
That in turn led to one of our first randomised controlled trials – of low dose hydrocortisone. It worked, confirming that low cortisol was playing a role, but sadly its not a treatment that one can use over the medium or long term.
We looked at how infection is related to CFS – an obvious thing to do since so many patients told us that their condition had started with a virus, and one of the other labels for the illness at the time was postviral fatigue syndrome. We did a big study in primary care, in which we followed up over a thousand people who presented to their GP with an infection, and then the next person in the surgery who didn’t. This study failed to show that common viruses such as influenza were triggering CFS. But at the same time, looking at more severe infections, we showed that viral meningitis definitely did. Meanwhile our colleague Peter White at Barts produced the definitive study that linked the Epstein Barr virus, the virus that causes glandular fever, to CFS. We went on to replicate that, and look at what predicted early symptoms versus late symptoms after confirmed EBV.
Back then, another big theory around was that CFS was due to hyperventilation. We linked up with our chest physicians, and showed that it wasn’t.
Sufferers didn’t just have physical fatigue and fatigability, they had mental fatigue and fatigability as well. So we did a neuropsychological study, using something called the CANTAB battery of neuropsychological testing, and showed that although most cognitive function was normal, patients did have problems with selective attention. CFS wasn’t dementia (as some were saying) but there was a higher level cognitive impairment.
We teamed up with our local immunologists. We found evidence of an increase in a particular subset of cytokine producing immune cells, confirming a mild immune activation, although we were not sure of the cause. It is possible still that this is a reflection of either sleep deprivation or the low levels of circulating cortisol hormone that we had earlier demonstrated. Its a pity that this still isn’t really sorted. At the same time we showed that immune dysfunction didn’t relate to clinical outcomes.
Which takes us to prognosis – in a much cited paper we showed that the prognosis of patients attending specialist clinics was rather poor, especially if they weren’t treated (as they usually weren’t) but we also found evidence that the situation was more optimistic for the less severe cases seen in primary care, and also children.
We did a lot of biological studies – you can see from the paper list on the website. We published on vitamin levels, the autonomic nervous system, HLA antigens and other genetics papers, growth hormone, why you need to test for celiac disease, anti nuclear antibodies, neuro imaging, DHEA and others. No, we didn’t find the elusive biomarker, but it was not for want of trying.
And we did psychological studies as well. We published papers showing differences between CFS and depression, but also in a long series of work spanning many years established that previous depression increases your risk of developing CFS later in life, or after you are exposed to an infection, something confirmed in several studies now. We looked at personality – linked to the “yuppie flu” stereotype was a perception that sufferers tended to be perfectionistic, hard driving people. We found that once you controlled for the effect of chronic illness, there was no such thing as a “CFS prone personality”. We also showed that our patients were not anti psychiatry, which was in contrast to some of those who were writing about this on the internet.
Whilst at Queen Square I had met up with Trudie Chalder, then working as a behavioural nurse therapist on the same ward. It was the start of a 20 year collaboration that is still going strong. We talked a lot about CFS, and why everyone seemed to think that nothing could be done. So in 1989 we wrote a paper advancing a theory, which was that cognitive and behavioural factors might help explain not why patients got ill in the first place, but why they weren’t getting better. And from that we developed a specific intervention for CFS, adapting something known as cognitive behaviour therapy, which was already achieving considerable success in the pain world. So we first of all simply tried treating 50 patients at Queen Square, with good results (1991), and perhaps most interestingly, with improvements that could still be detected some years later.
Then in 1991 I got a consultant/senior lecturer post at King’s College Hospital. I set up what was one of the first NHS only services exclusively devoted to CFS patients – still going strong today, with Trudie, now Professor Chalder, in charge. We got a grant to do what was needed, which was an randomised controlled trial (RCT) of CBT, comparing it with the same number of sessions of relaxation therapy. CBT performed well. At the same time Mike Sharpe at Oxford, now Professor Sharpe, had independently developed a cognitively behavioural approach to treatment and carried out a trial that had similarly positive results. We both published our results in 1997.
A lot of work followed that. During that decade we showed that you could even get good results in the most severely disabled patients (either in wheel chairs or bed bound) using the same principles, although it was never possible to do an RCT. Trudie opened a clinic for families with children with CFS, and developed a new way of delivering family oriented CBT, which has been the most successful intervention of all. We tried new ways of outreach, such as telephone CBT, and even now Trudie is leading on a study delivering home based treatment to adolescents who are too sick to even get to the clinic.
CT and John: I read John’s comment, arriving at the same conclusion CT made: we need the tightest possible clinical definition to make findings meaningful. Clearly the Wesselyite ‘Oxford Criteria’ were designed to muddy the waters and create such a broad definition, bringing in many with psychiatric maladies and actually sifting *out* anyone who might have neurological signs or symptoms, that nothing meaningful can be extracted from the body of research using that set of criteria. The IOM observed the same and that harms could result from using the Oxford criteria. Having said that many patients despair of the SEID nonsense that the IOM then decided to proffer. Yes it’s possible to find people with ME using SEID but it’s also possible to draw in any man and his dog at the same time. It’s like fishing with such a huge and holey net that the subsequent catch is almost indistinguishable from the sea from which it was drawn.
Sadly the OMF seem a little contrary with how they assess their patient cohorts… although their severely ill cohort, one might assume by virtue of the degree of disease presentation, is likely nearer the truth than some. Other papers such as this (https://www.omf.ngo/wp-content/uploads/2016/08/Naviaux-PNAS-CFS-Metabolomics-2016.pdf) throw so many ingredients into the mix that the cohort might well resemble a minestrone. In order not to be accused by members of the BPS of the very muddle the BPS like to themselves manufacture, it behoves researchers to be very clear about the population they ascribe their findings to. I’m surprised that a body like the OMF with the calibre of scientists it has accrued can’t be more rudimentary on this point.
Many long-timer, severely ill patients as well as those who have given enough thought to the existing literature and the prevailing politics around this disease, and whose need for speedy resolution of the disease is, for many, truly existential, realise that there is only one sensible set of criteria to reasonably sift out a cohort of authentic ME patients (not ME/CFS or CFS/ME or CFS or CF or any other variable). That is the ICC criteria and has been endorsed by over seven and a half thousand people: (https://www.change.org/p/the-us-department-of-health-and-human-services-cdc-adopt-the-distinct-disease-myalgic-encephalomyelitis-me-as-defined-by-icc-now)
Here is another great resource providing information about the way in which ME has been defined over the years including a useful ‘quickie’ questionnaire which might help those who aren’t sure about their diagnosis & which allows them to see whether or not they might fit ICC (and we as patients must remember that a negative result is as important as a positive one). If people don’t see that they fit the ICC criteria but have been told they have ME then they should be interrogating other pathways to trying to understand why they are ill. Accepting a diagnosis like ME without question might well be the equivalent of preventing one from securing a different diagnosis, maybe even one with very good options for care and amelioration of symptoms. (https://www.meadvocacy.org/resources)
[I had problems posting this thus the links have been adulterated a little and you’ll need to copy and paste without the ‘-link’ added at the end of each.]
CT and John: I read John’s comment, arriving at the same conclusion CT made: we need the tightest possible clinical definition to make findings meaningful. Clearly the Wesselyite ‘Oxford Criteria’ were designed to muddy the waters and create such a broad definition, bringing in many with psychiatric maladies and actually sifting *out* anyone who might have neurological signs or symptoms, that nothing meaningful can be extracted from the body of research using that set of criteria. The IOM observed the same and that harms could result from using the Oxford criteria. Having said that many patients despair of the SEID nonsense that the IOM then decided to proffer. Yes it’s possible to find people with ME using SEID but it’s also possible to draw in any man and his dog at the same time. It’s like fishing with such a huge and holey net that the subsequent catch is almost indistinguishable from the sea from which it was drawn.
Sadly the OMF seem a little contrary with how they assess their patient cohorts… although their severely ill cohort, one might assume by virtue of the degree of disease presentation, is likely nearer the truth than some. Other papers such as this https://www.omf.ngo/wp-content/uploads/2016/08/Naviaux-PNAS-CFS-Metabolomics-2016.pdf-link throw so many ingredients into the mix that the cohort might well resemble a minestrone. In order not to be accused by members of the BPS of the very muddle the BPS like to themselves manufacture, it behoves researchers to be very clear about the population they ascribe their findings to. I’m surprised that a body like the OMF with the calibre of scientists it has accrued can’t be more rudimentary on this point.
Many long-timer, severely ill patients as well as those who have given enough thought to the existing literature and the prevailing politics around this disease, and whose need for speedy resolution of the disease is, for many, truly existential, realise that there is only one sensible set of criteria to reasonably sift out a cohort of authentic ME patients (not ME/CFS or CFS/ME or CFS or CF or any other variable). That is the ICC criteria and has been endorsed by over seven and a half thousand people: https://www.change.org/p/the-us-department-of-health-and-human-services-cdc-adopt-the-distinct-disease-myalgic-encephalomyelitis-me-as-defined-by-icc-now-link
Here is another great resource providing information about the way in which ME has been defined over the years including a useful ‘quickie’ questionnaire which might help those who aren’t sure about their diagnosis & which allows them to see whether or not they might fit ICC (and we as patients must remember that a negative result is as important as a positive one). If people don’t see that they fit the ICC criteria but have been told they have ME then they should be interrogating other pathways to trying to understand why they are ill. Accepting a diagnosis like ME without question might well be the equivalent of preventing one from securing a different diagnosis, maybe even one with very good options for care and amelioration of symptoms. https://www.meadvocacy.org/resources-link
Lady Shambles. I agree. In fact you got me thinking what ME/CFS is or could be!
I started thinking about this and came to the conclusion it might be an illness of “luckiness.” You know why? Because some people are severely ill and some are just mildly affected. IMO also, ME/CFS is a kind of stress illness and a ” I need to sleep” illness. When you sleep, your body is not in a state of stress and this allows it to recover and try to get back to homeostasis. Today I read a PhD about the Royal Free Hospital ME epidemic and the CSFs were mostly normal or negative for things like poliomyelitis and Glandular Fever. https://ora.ox.ac.uk/objects/uuid:809b4dd1-e52c-469a-9c97-966039da0b82
I did not read all of it as it was too long and boring but I got the idea he was trying to say that they could not find anything majorly wrong with the patients from an evidence point of view. But they still had all the symptoms right? So, the only thing I can come up with since I do not believe in Mass Hysteria, is that it is an illness caused by biological stress. The only thing I don’t understand is how so many people can get ill at the same time.
Wessely on distortion in science -http://www.simonwessely.com/index.php/cfs-personal-story/ , but isn’t this distortion -https://opposingmega.wordpress.com/2020/05/01/untangling-the-mus-web/ that’s documented in the article that David links to above? Who will hold Wessely and his colleagues to account?