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Problems with International Consensus Criteria

Andrew

Senior Member
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2,513
Location
Los Angeles, USA
As Peterson and others have pointed out, the reason the International Consensus Criteria was not immediately operationalized is they were awaiting double-checking by Leonard Jason. According to an article by Cort Johnson, Jason has published his results and it doesn't look good.

Also interesting is Cort's article is a comment that the old Ramsay Definition is probably the best one so far. For those who don't know, Ramsay was one of the original definitions, way back before the CFS term even existed.

Now, that doesn't mean the ICC is garbage. It actually does some things better than most. But it needs to be refined.

http://www.cortjohnson.org/blog/201...oth-may-select-for-more-psychiatric-patients/

Also, if you are curious about Ramsey, read here: http://www.name-us.org/DefintionsPages/DefRamsay.htm
 

alex3619

Senior Member
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13,810
Location
Logan, Queensland, Australia
Ramsay has the requirement of sudden onset IIRC. So all slow-onset patients are excluded. Ramsay was defined to meet epidemics/cluster outbreaks, not sporadic cases. I meet all criteria of Ramsay except sudden onset.

It is good though that the ICC is being tested. We need to know exactly what we are dealing with in any definition.

One of the factors according to Cort's article is that there is over-representation of somatization disorders. I am yet to be convinced that any such disorders even exist. So are we talking somatization disorder, some other disorder, or atypical ME? Nobody knows.

So is the ICC really over-diagnosing somatization disorders? I doubt it. However I am sure that some will make use of this claim, particularly those who want to promote a psychogenic view of ME.
 

Ember

Senior Member
Messages
2,115
How are these findings different from the ones Jason presented almost a decade ago when comparing the CCC to Fukuda? The consequences that Cort describes don't seem to follow from the evidence. He notes, “Since Jason’s study focused on CFS patients its not clear that the ICC would also inadvertently bring in people with mood disorders who do not have ME/CFS (sic) but it’s at least theoretically possible.” Howerver, the ICC requires PENE for a diagnosis of ME.
 

Bob

Senior Member
Messages
16,455
Location
England (south coast)
Lenny Jason seems to be doing some seriously heavy-weight work on diagnosing CFS/ME.
There is some further interesting reading in the latest edition of ME Research UK's Breakthrough magazine.
It's not available online yet, but when it is, it will be placed here. (Spring 2013 edition.)

It says that the UK's University of Newcastle are going to compare the clinical diagnoses of patients from a previous Newcastle research project (diagnosed with Fukuda, CCC & "an ME definition") with diagnoses, of the same patients, derived from the DePaul Symptom Questionnaire (DSQ). ME Research UK is going to fund this comparison study.

The magazine article says:
"The DSQ is a standard questionnaire developed and refined by Prof. Leonard Jason and colleagues at De Paul University, Chicago. Prof. Jason has been in the forefront of research into the application of diagnostic criteria for ME and CFS for many years, and he devised the DSQ as a way of identifying core symptoms of ME and CFS in a structured manner, ensuring that symptoms are assessed in a consistent way across settings to aid in diagnosis.​
"Importantly, the DSQ comes in a format which scores symptoms and Short Form-36 data, and produces a 'diagnosis' based on several of the more common definitions of ME, CFS and ME/CFS. Prof. Jason has made his questionnaire available to other research groups across the world for the operational testing on existing ME/CFS cohorts.​
"Considering the importance of the ME Research UK cohort and its well-characterised nature, the results could throw valuable light on diagnostic categories and on the utility of the DSQ in practice. If the DSQ is found to be sufficiently sensitive, it could greatly assist patient diagnosis, saving time (as it can be completed in the patient's home and brought to the clinic for scoring) and improving confidence in the diagnosis."​

There is some more information about the Newcastle team's research, but I can't type it all out.

So it looks like Lenny Jason's DSQ could be an exceptionally useful tool for researchers, as they would only have to enter one set of input data per patient (actually the patients enter the information), and then the DSQ scoring system will automatically subset all the patients according to the various CFS/ME diagnostic criteria, providing researchers with a wealth of cohort information. If Jason has incorporated the ICC into it as well, then that would satisfy a lot of patients. If every research project were to use the DSQ (if it works well) then they would all be able to provide results set against each of the various diagnostic criteria.

From Cort's article, it looks like Jason might be working on a simple new ME diagnostic criteria, or maybe he is aiming to revise the Ramsay criteria. Along with what the CDC are doing (I haven't seen Unger's latest presentation at the FDA meeting yet), it seems that there is an enormous amount of very useful work going on in this area at the moment.

I think if Jason can come up with a standardised, operationalised, empirical research criteria, then it could also be invaluable, especially if a wide range of specialists endorsed it.
 

Bob

Senior Member
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16,455
Location
England (south coast)
How are these findings different from the ones Jason presented almost a decade ago when comparing the CCC to Fukuda? The consequences that Cort describes don't seem to follow from the evidence. He notes, “Since Jason’s study focused on CFS patients its not clear that the ICC would also inadvertently bring in people with mood disorders who do not have ME/CFS (sic) but it’s at least theoretically possible.” Howerver, the ICC requires PENE for a diagnosis of ME.

It looks like Cort was simply speculating there. Cort is not a scientist, and so he might not get everything 100% entirely correct when writing about the science. But I did read recently (I can't remember where, as usual) that CFS/ME is not unique with regards to post-exertional malaise. But I'm not aware of any other diseases/illness have delayed PEM, as a symptom. I certainly don't think that there are any psychiatric illnesses that have PEM as a symptom.

Anyway, we should watch out for further information about Lenny Jason's work.
 

Bob

Senior Member
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16,455
Location
England (south coast)
Thinking about Cort's article further. As PENE is required for an ICC diagnosis, whereas it is not required for a Fukuda diagnosis, and neurological problems are required with the ICC, whereas they are not with Fukuda, I wonder if it is a surprise that there is a much higher level of mood problems for patients diagnosed with the ICC. I mean, if there is a higher level of neurological problems, is it a surprise that there are accompanying mood problems?

I need to see Lenny's research to understand it properly.

Of course, we now ought to be starting to look towards incorporating biomarkers into new diagnostic criteria, and not just symptoms. I was quite surprised to hear that Unger has said the CDC has now started to look at biomarkers for the CDC's diagnostic criteria project.
 

Simon

Senior Member
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3,789
Location
Monmouth, UK
As Peterson and others have pointed out, the reason the International Consensus Criteria was not immediately operationalized is they were awaiting double-checking by Leonard Jason.
I didn't realise that, and it's encouraging (the ICC did seem to be handed down as a tablet of stone). So does that mean Jason's work is backed or endorsed by the ICC? Would be interesting to have a comment from them, or at least from Carruthers.
 

Ember

Senior Member
Messages
2,115
Dr. Jason's results would seem more significant to me had he been less set on achieving them. He spoke at the IACFS/ME Conference in September, 2011 after Dr. Carruthers presented the ICC. Cort tweeted from his presentation: “suggests using more symptoms (eg ICC) runs the danger of bringing in people with pscyh diagnoses (#Jasoneg Holmes criteria)” ... “#Jason – lots of symptoms are what doomed Holmes criteria. Jason's ME criteria had 4 parameters and require acute onset.”

I'll be interested to read the full paper in light of Dr. Jason's competing interests. He designed the DSQ, by the way, to operationalize the CCC. Dr. Unger has relied heavily on the NIH PROMIS questionnaires in her research, but she also included questions from the DSQ. She seems to have come up pretty much empty-handed using questionnaires, but she reports: “Interestingly the sensitivity to noise and the alcohol intolerance were the factors that showed the most difference across combination. And some of these measures such as unsteady on feet, dizziness or painting (sic), part of the autonomic measures shows a very uneven distribution across the patients.”

Judging from the Ramsay definition's description of neurological symptoms in ME, emotional lability often comes with the territory: “Neurological disturbance, especially cognitive, autonomic and sensory functions, often accompanied by marked emotional lability and sleep reversal.”

The criterial feature of the ICC, of course, is PENE: a pathological inability to produce sufficient energy on demand with prominent symptoms primarily in the neuroimmune regions. Here Dr. Cheney's recent description of his patients rings true:
There are a lot of diseases that have chronic fatigue. In fact, most chronic illnesses have an element of chronic fatigue. But often in those diseases, people push through it. My patients will do minimal effort, like just walking across the room. Or they'll fix dinner and they'll have stood too long, and they're wiped out for days just doing this minimal effort. And I don't know of another disease that looks quite like that, but which also demonstrates severe cognitive derangement and abnormal neurological findings and has some of the other features that I've been talking about (Paul Cheney Seminar – Q&A at 16:55).
 

Bob

Senior Member
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16,455
Location
England (south coast)

Wessely won't miss a trick. If Jason has anything to say against the ICC, Wessely & co will use it to their advantage.

So, does Wessely's Tweet link to the paper that Cort's article discusses?
I wondered what research he was referring to.
Maybe I'm a bit slow to catch on, but I couldn't see any links to the research in Cort's article.

I'll have a look at Jason's paper, now I know what we are talking about!
http://www.questia.com/library/1G1-322563471/contrasting-case-definitions-the-me-international
 

Bob

Senior Member
Messages
16,455
Location
England (south coast)
Judging from the Ramsay definition's description of neurological symptoms in ME, emotional lability often comes with the territory: “Neurological disturbance, especially cognitive, autonomic and sensory functions, often accompanied by marked emotional lability and sleep reversal.”

That's a good point, Ember. I remember reading about emotional lability being a feature of ME, and I related to it, especially in my early days of illness. I think one visit to my doctor, during the early days, is the only time that I've ever cried in public as an adult. But I was never certain if emotional lability was a neurological symptom of the illness, or simply a sign of intense distress, hopelessness and frustration. It's not surprising that when someone is suffering from one of the most extended and intensely distressing and bewildering periods of their lives, that there will be a strong emotional reaction.

This again, makes me asks questions about Jason's research. If the ICC selects the patients with the most distressing symptoms, then it's no surprise that a much higher proportion of patients will have co-morbid psychiatric symptoms.

There is a good discussion in the comments underneath Cort's article.
(I've posted there as "Rob" to avoid confusion with Bob Miller, who posted as "Bob" under another article.)
 

Guido den Broeder

Senior Member
Messages
278
Location
Rotterdam, The Netherlands
The problem with the ICC is that they are symptom criteria. But ME symptoms are none of them unique. It is therefore incorrect to conclude that everyone satisfying the criteria has ME.

Without postviral inflammation of the CNS, it is not ME.
 
Messages
5,238
Location
Sofa, UK
Please forgive my ignorance, but is it even possible to test for inflammation of the CNS? I thought that was only possible after death.
 

parvofighter

Senior Member
Messages
440
Location
Canada
ANOTHER PERSPECTIVE: IS THERE REALLY MORE PSYCH COMORBIDITY IN THE CANADIAN AND INTERNATIONAL CRITERIA FOR M.E.?
Posted in response to http://www.cortjohnson.org/blog/201...elect-for-more-psychiatric-patients/#comments

ARE WE ASKING THE RIGHT QUESTIONS?
Cort, you’ve written a very thought-provoking piece. But I can’t help thinking we need to flesh this topic out, and also ask some tougher questions. I’m having a rare “OK” day, so will make hay while the sun shines and perhaps contribute a related perspective.

1) ISSUE #1: IF WE TREAT THE OSTENSIBLE PSYCH COMORBIDITY, WILL IT RETURN US TO FUNCTION?
For me as a patient, all I ultimately care about is: “What do we have to treat, to restore patients to a modicum of functionality?” And the answer to this question has EVERYTHING to do with whether psychiatric comorbidity (if present) is primary, i.e. integral to M.E. as a disease; or secondary, i.e. a natural sequela to profound disability.
Why is this important? Because if we perseverate on the possibility of profoundly ill patients being depressed, for example, and if we’re sloppy in our assumptions, we can put ourselves in exactly the position that the UK is, where CBT and GET are positioned (despite a lot of arm-waving by the psychs) as the be-all and end-all for ME and CFS patients. I.E. The Psych perspective is being positioned as a fix-all for ME and CFS. To whit, the endemic refusal of biomedical testing, to better understand the biomedical underpinnings of ME and CFS – much less biomed treatment.

I submit that any time psych comorbidity is raised, we have to be meticulous about identifying whether, if we treat that psych comorbidity, that will address the core pathology of ME or CFS, and return the ME or CFS patient a significant measure of functionality. Or whether said psych treatment will just help patients cope better. (And I don’t for a moment believe that treating “false illness beliefs” or graded exercise are safe, much less helpful in ME, even for coping). Consider the number of Rituxan or Ampligen patients who have been able to return to work after treatment – versus those in the PACE trial, which has been consistent in its INABILITY to return patients to work. And this is a big deal, considering – as Dr Unger stated last week about the patients her multi-site research, “What was consistent, was that 75 percent were not working.”

How many of us, for example, have been prescribed antidepressants, only to find them less than useless in affecting our level of disability, much less our abilty to do self-care, or return to work?

And how many of us have been lucky enough to get some biomedical treatment which returned us, dramatically, to a measure of our former lives? I’ve had a small number of blessed but TOTAL remissions on IVIg – unfortunately formulations that are no longer available to me. But I’ve experienced it – from a few days to a week after treatment, spontaneously waking up refreshed in the morning, BOUNCING out of bed, clear of mind, with to-do lists bubbling up with joy; being able to go for walks with the family; able to make meals; tolerating standing up; being cognitively clear enough to dream up all kinds of fun things to do. And being “myself” again, for as long as 3 months after these treatments. With no PEM nor angina. It was like the movie “Awakenings”. Pure joy. Did this affect my mental state? Darn right it did. I felt like myself again.

ISSUE #2: WE NEED TO DIG DEEPER TO UNDERSTAND “HOW” THEY ARE DEFINING PSYCHIATRIC COMORBIDITY
I would also argue that any time someone says that psych issues are comorbid, we need to go to their assumptions – i.e. the tools they are using – to see if those are in fact appropriate to our disease or spectrum of diseases. Specifically, we need to know if these tools can differentiate between a depressed patient, and someone who is naturally responding as a result of profound disability.

If you take a peek at Valentijn’s posts at this link: http://forums.phoenixrising.me/inde...n-questionnaires-in-me-cfs.21578/#post-329074 , he provides examples of common depression inventories such as the Multidimensional Fatigue Inventory, the SF36, and the Zung Depression Scale, where a so-called diagnosis of depression could in fact be merely an assertion of significant biomedical disability.

For example, how many ME patients would respond affirmatively to the following – not because they’re depressed, but because they have lost a massive chunk of their quality of life, and have had to contract their life to prevent relapses? Here are just a few of the questions that would peg ME patients as “depressed”:
- “I have a lot of plans”
- “I still enjoy the things I used to do”;
- “I expect my health to get worse”

How many of us expect our health to get worse – not because we’re pessimists, but because we are realistically extrapolating from our past health trajectory, and factoring our slim hopes for imminent treatment? Given how widely used depression inventories are, that have lousy specificity and sensitivity, we must be vigilant about such assumptions about “psychiatric comorbidity”, when applied to a serious multisystem and chronic illness such as ME.

3) MULTISYSTEM SIGNS AND SYMPTOMS CONFLATED WITH SOMATIZATION PAR EXCELLENCE?
Next, while many psych instruments make the assumption that more physical symptoms = somatization (and indeed this skewed assumption is becoming entrenched in psych practice – witness the bastardization of the DSM), anyone with a complex multisystem disease knows differently. But as we saw this year, simply having multiple symptoms, and being concerned about them, will increasingly be taken by the DSM folks as signs of somatization. It’s all in the definition, even if it isn’t supported by science.

Bottom line, I would offer that we need to dig deeper, whenever we see people conflating ME with psychiatric comorbidity, with the ultimate questions always foremost in our minds: “Just how do they arrive at this conclusion of psych comorbidity?”, and “If we treat the so-called psych comorbidity, will this restore the patient to function?”. Proof of principle, in reverse.

4) WHICH ASPECTS OF DEPRESSION – IF PRESENT – ARE FEATURED?
Another consideration is that we need to tease out specifically which aspects of depression – if that is the issue – are coming up as positive in an ME or CFS population. I found it fascinating that at last week’s FDA meeting, Dr Unger made a point of saying that it’s NOT the Role Emotional or mental health that are coming up in her multi-site study of “ME/CFS” patients. Now, even Dr Unger is saying that not all instruments have been validated in CFS, and even she is breaking some paradigms, by saying that Mental Health and Role Emotional are PRESERVED in CFS. Very, very interesting stuff. As she said (from the preliminary transcript on PR):

“In the SF36 … you can see that the bars are all very low except for two of them. And … those two relatively high scores are on … mental health and (role) emotional indicating those areas of function are preserved in CFS and that again is pretty consistent across all of the clinics.” (WOW, just wow… what a change of tune. I thought it was STUNNING to hear the CDC, of all entities, say this)

And more from Dr Unger: “This is also giving us a hint that measures themselves may be limited in their ability to distinguish robust phenotypes and/or robust subgroups, and that’s why we’re proposing to expand this study to some other measures. And it could very well be that other biologic correlates will be needed in order to better define subgroups. The other study — other factor is that the data from these kinds of studies will allow us to evaluate how well these questionnaires work. For example, the MFI general fatigue scale in this population really from a specialty clinics did — was limited by its already reaching the maximum in 40 percent of the patients.”

5) A CARDIAC EXAMPLE – THE WOMEN’S ISCHEMIA SYNDROME EVALUATION (WISE study)
There’s another example of assumptions-gone-wild in the Women’s Ischemia Syndrome Evaluation, a massive NIH initiative looking at women with chest pain, but often clear-as-a-bell coronary arteries. These women nevertheless present with cardiac ischemia; and these women are at TEN TIMES the risk of cardiovascular events (death, myocardial infarction, stroke, etc) from those without chest pain. As it turns out, this population is heavily represented by multiple comorbidities, with chronic pain conditions such as FM, “CFS”, IBS, interstitial cystitis, migraine, and Raynaud’s – exactly the constellation of comorbidities associated with “ME/CFS”. In other words, ME and CFS are likely well represented in this WISE population of women who are dying prematurely from heart disease. And indeed, that’s what the work of Dr Newton and her team at the U of Dundee would suggest (http://www.meresearch.org.uk/research/studies/2012/endofunction.html ).

This makes one finding from the WISE study stand out: the WISE researchers found that, “Anhedonia Predicts Major Adverse Cardiac Events and Mortality in Patients 1 Year After Acute Coronary Syndrome (ACS)” (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058237 )
“Depression is a consistent predictor of recurrent events and mortality in ACS patients, but it has 2 core diagnostic criteria with distinct biological correlates—depressed mood and anhedonia… anhedonia and MDE (Major Depressive Episode) were significant predictors of combined Major Adverse Cardiac Events (MACE)/ All Cause Mortality (ACM), BUT DEPRESSED MOOD WAS NOT.”

“… Anhedonia identifies risk for MACE/ACM beyond that of established medical prognostic indicators. Biological correlates of anhedonia may add to the understanding of the link between depression and heart disease.”
IMO, the most pressing “biological correlate” of anhedonia that I can think of in this population, heavily represented by “chronic pain conditions” such as ME and CFS, is Post-Exertional Neuro-Immune Exhaustion – mislabeled as “anhedonia”. In other words, the WISE researchers need to start cross-pollenating with “ME/CFS” research, and start measuring for NK cell dysfunction, RNase-L abnormalities, cytokine profiles, etc.

This is an assumption about depression, among the massive team of WISE researchers that so far has gone unchecked.

6) THE KEY MESSAGE: WE NEED TO CHALLENGE GRATUITIOUS ASSUMPTIONS ABOUT COMORBIDITY
So will there be psych comorbidities in any chronic illness, particularly one with neurocognitive involvement? Absolutely? But let’s be aware that entrenched forces have a tendency to overstate that linkage in ME and CFS.

Specifically, let’s come back to this subgroup of CBT/GET practitioners whose “business is rehabilitation” (Wessely’s comment from this BMJ Group Podcast http://www.bmj.com/podcast/2010/03/05/chronic-fatigue-syndrome – see 11 minute, 15 seconds for his quote). It needs saying that this is an all-out war for market share and credibility, and for the psychiatric paradigm of “CFS”, this tenuous hold on credibility requires that they keep the largest and most expansive definition of the disease(s). We feed into this grab for market share, if we don’t ask tough enough questions, whenever psych comorbidity is conflated with ME or even CFS. Just how are they arriving at this linkage?

I do find it deeply worrisome that so many people are comfortable making the implied leap that just because there is a hint that significantly disabled patients despair at times, that the treatment must equal psychiatric. It is a massive leap of logic that is not justified by science. True, there are other neurocognitive aspects of this disease that might blur into psych domains. But we need to be precise when discussing this.

All I’m sayin’ is that we need to probe a little deeper, and DEMAND treatment that “fixes” us – not window dressing. And this starts with dissection of the assumptions that drive our historically limited treatment options.

Now to throw a spanner in the works. In my earlier life, I used to research corporate health outcomes, and saw – in insurance payouts – the impact of psychosocial factors on health cost and health outcomes. For example, in workplaces where employees had poor control over how they did their work, and high demands, combined with high effort and low reward (“high stress workplaces”), we saw an increase in colorectal cancer by a factor of 6; back pain by a factor of 3; injuries and infections by a factor of 2-3, and so on. So I DO believe that psychosocial factors can drive and influence health outcomes – I’ve seen it in the corporate health numbers. BUT never in a million years, however, would I support that any disease precipitated, influenced, or exacerbated by psychosocial factors – aka epigenetic changes – have its treatment LIMITED to psych therapy. That’s just silly.

Just think how ludicrous it would be to tell a colorectal cancer patient that they are going to receive ONLY GET and CBT, AND no more biomedical testing nor treatment because psychosocial factors may have precipitated or worsened their disease. But somehow society has allowed this runaway train, especially in the UK, to run amok, and to make this grandiose and unsupported leap of logic, where it pertains to ME and CFS. This, we have to stop. And a first step might be in demanding precision, whenever psych issues are conflated with ME/CFS. “Just how are you defining this?” “What are your underlying assumptions”?

We need to dig deeper.

Parvofighter
 

Lynne B

Senior Member
Messages
126
Location
sydney, australia
Great stuff, Parvofighter! Couldn't agree more.

It's so frustrating to tell an immunologist that sometimes I feel anxious, like if I'm worried about driving after I become tired from some other activity, and for him to turn round and suggest that my anxiety is part of a psychological problem. Good grief, and he's an immunologist! You'd think he'd know better.

Sorry, rave over... But your post is just inspirational. It wasn't till I convinced this particular immunologist to give me blood tests for NK cell function and cytokine levels, and so on, that the results finally convinced him I actually had the disease. But then he offered no treatment other than CBT and GET! I do wish there was a specialist in Sydney Australia who had something to offer other than those or alternative medicine. There seems to be no one willing to work with the patient on some of the therapies suggested as a result of the research highlighted on Phoenix Rising and Health Rising. It's such a waste of years of our lives.

Lynne
 

Firestormm

Senior Member
Messages
5,055
Location
Cornwall England
If a criteria is meant (at least in large part) to define a specific disease - and it is shown to also en-capture patients with a comorbidity - then doesn't it reduce the uniqueness of the disease? Shouldn't a criteria for ME define ME and not anything else?

All a bit redundant these things if you ask me and for what it's worth in the absence of a biomarker or markers. What I mean is: if as an example a biomarker is discovered for 'fatigue' or something else that is found to cause an agreed upon common and/or defining symptom; we and others could then be assessed as having or not having said marker and where on any resulting 'scale' or spectrum we might 'fit'.

Depression for example is commonly acknowledged as a common comorbidity, not a key aspect of the disease ME, but a likely consequence: this prevalence may indeed decrease should a ME biomarker(s) be found. If a biomarker could be found for 'PENE' and it was agreed that (along with other markers and symptoms) 'PENE' was what defined ME from, say, MS or Depression; then it would be unsurprising to my naive little mind, if the number of psychiatric comorbidities and indeed misdiagnoses decreased and ME criteria became far more relevant and unique.

The ICC jumped the gun and the research generated does not appear to have been unpredicted (see e.g. Wessely). I can't get excited about any new or tinkered criteria that attempt to 'improve' upon what we already have by way of symptom-based definitions. Not until we have biomarkers. And not until those biomarkers point towards some better and more relevant means of treatment (hopefully). Of course we may not get the kind of biomarkers we would all like; but we deserve to be better served than we are by these current improvements.
 

snowathlete

Senior Member
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5,374
Location
UK
It'll be interesting one day to test these different criteria against known biomarkers, see accurately which were good or bad.
 
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13,774
Even if we found a biomarker for 'fatigue', it's likely that there are many different illnesses which would cause this fatigue. I think that all CFS research should be looking for different sub-types, rather than assuming that any criteria is likely to have identified a meaningfully defined syndrome which allows patients to be lumped together.