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"The Oxford Definition: It's Baaack”

Messages
646
. Post viral fatigue is common. In the vast majority there are no host of secondary symptoms and it resolves naturally in weeks to months. In around one in ten (though up to 8 in 10 depending on the disease perhaps) this goes on to something more serious. That something is what I think ME is. The biochemical and physiological difference between ME and the more common post viral fatigue would be interesting to research.
Are you saying that is the 'only' thing that could be M.E (and M.E being what specifically ? ) and that comparable symptomology, not following a viral infection could not by definition, be M.E ? I also don't understand what you mean by "no host of secondary symptoms" - what symptoms are absent from a prolonged viral infection that are present in M.E/CFS which are not mediated by the effects of chronic incapacity ?

IVI
 

Enid

Senior Member
Messages
3,309
Location
UK
Wha, wha, wha - symptoms come , change in persistance, reach heights, ease, may even go for some of them. this is an illness - sorry IVI etc out of theory here - back to science alone in their findings. And that is well on the way for those of us know the real thing. Many symptoms - get with it.

What on earth are they looking for - nothing consistant as this illness works it's way through.
 

medfeb

Senior Member
Messages
491
Not sure about missing - I think perhaps you may be confusing 'definitive causation' with 'distinctive aetiological process'.IVI

Okay, leveling terminology - I am using the definition of etiology that I have see in a variety of text books and online sources - study of the cause of a disease. I would classify the damage to the myelin sheath as sign or biomarker of the disease, presumably objectively measurable.

I am not sure if you are saying that there must be a 'single cardinal aetiological feature' (biomarker) or not. This was discussed at a recent CFSAC and Mary Ann Fletcher discussed the need to adopt a pattern of biomarkers for ME/CFS and not insist on a single biomarker.

The various claimed ‘bio markers’ have yet to show any consistency of presence across large patient populations, let alone provide any definable explanation of relevance to reported symptoms across a large patient population. In fact the most significant aspect of the various biomarker studies is the sheer lack of consistency. IVI

This is a circular argument - of course, if you start with all the patients and criteria defined under the definition set of ME-ICC, CCC, Fukuda, Empirical and Oxford, you will never find consistent biomarkers because these are random definitions that have been lumped together. Oxford only requires 6 months of fatigue, does not require any other symptoms and allows psychiatric patients to be included. This is a nonsensical clinical entity.

To make an analogy, would it make sense to group cancern patients together with Oxford patients and then say that there are no common biomarkers? Of course not. Same here

But cancer has biomarkers and that is why it wouldnt make sense to group with Oxford, right? True and so does the CCC and the ME-ICC. PEM/PENE is objective and measurable - it is not a random color on a bead. Viral loads, immune system factors including cytokine levels, CPET, autonomic dysfunction are all objective and measurable and starting to drive treatment regimens. We can't expect to find consistent biomarkers across CCC/ME-ICC patients and Oxford patients because they are not dealing with a common disease process any more than Oxford and cancer patients are.

Regarding CCC/ME-ICC and Fukuda - Fukuda will contain both patients with PEM and those without. I dont think we really know what this group of non-PEM Fukuda CFS patients is but again, I dont think it is reasonable to expect they will have the same biomarkers as PEM patients (see the Maes study that compared immune factors across PEM and non-PEM groups).

I am not saying that all ME-ICC/CCC patients will have exactly the same profile across every measurable biomarker. Its a complex disease where factors like the triggers, genetics, onset and the length of illness must be considered. We need to subset out those different factors to better understand these patterns and how to treat patients. But we are not going to get there if we keep moving along with Fukuda and Oxford.

Regarding...
For diagnosis Fukada and NICE are the best we’re likely get until research shows biological characteristics that are demonstrable across large populations. For research Fukada, the CCC, Oxford and NICE may have various roles to play at least until definitive phenomena or comprehensive data requires alternatives.IVI

How many patients have been diagnosed with Fukuda and then told to go out and exercise - all because the doctor didnt recognize or understand the hallmark PEM that CCC requires. Continued use of Fukuda for diagnosis is dangerous to patients. IVI[/quote]
 

Enid

Senior Member
Messages
3,309
Location
UK
IVI - now why did I pass out 3 times - not much to do with your wrangling of who or has not achieved the better diagnostic formula - hey do you know it - it's all there - get science findings for us as these people (lacking experience) scrabble to try and pin down without any understanding.
 

Enid

Senior Member
Messages
3,309
Location
UK
"Definitions" - cut the crap - even historians are reassessing the past in the light of present findings. Oxford or whatever belongs with the dinosaurs. Can you redirect to the Canadian Consensus ?
 
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15,786
In Vitro Infidelium said:
There is no basis for the gross symptomology used in case definitions, diagnostic criteria sets or research criteria sets to have any specificity in terms of relationship to underlying aetiology.
Even if you want to argue that PEM is a symptom and not a sign, it doesn't make sense to disregard it as a defining characteristic of the illness. Unless, of course, you feel that patient perspectives cannot be trusted.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Are you saying that is the 'only' thing that could be M.E (and M.E being what specifically ? ) and that comparable symptomology, not following a viral infection could not by definition, be M.E ? I also don't understand what you mean by "no host of secondary symptoms" - what symptoms are absent from a prolonged viral infection that are present in M.E/CFS which are not mediated by the effects of chronic incapacity ?

IVI

There are no primary symptoms mediated by the effects of chronic incapacity that we are aware of. Some secondary ones arise from reduced activity, but not much can be pinned on this as many sedentary people are less active than we are and do not have our symptom set.

Elsewhere on several occasions I have discussed problems with interpreting the Dubbo studies, I am not going to repeat them again at this point.

During a flu for example we get a host of symptoms. These nearly all resolve in post viral fatigue. That pathogen is gone (low or no viremia), but stamina is down. Immunological responses do not however just end. There are circulating activated immune cells, immune complexes, antibodies, cytokines etc.

In ME however the primary symptom is not chronic fatigue. Its hyperfatigueability including PENE/PEM. Secondary pain symptom arise, additional autonomic (which means neurological) and immunological issues arise. The biochemical basis of PENE/PEMis partly understood now.

Even post viral fatigue patients, so far as I am aware, do not have our secondary consequences. There is still some debate about whether or not diseases like MS have PEM/PENE but I don't think we are ready to answer that yet.

This question of post viral fatigue vs. ME is one that needs investigating. It could be a mirage, but its unlikely. We need science and not presumption to determine what the relationship is. It is possible, but highly improbable in my view, that post viral fatigue has the same symptom set. Most of us have experienced post viral fatigue, and its something like ten times more common than an ME diagnosis. Yet I never hear of OI, severe muscle pain, IBS, insulin resistance, thyroid issues and insomnia in post viral fatigue to name a few. Hypersomnia, yes.

A huge problem in ME research today is that most of the attention is on fatigue. Yet for many of us fatigue is not a very important symptom. Indeed, I wouldn't rate fatigue as higher than the third most important symptom in my case, and probably not even that high ... I have not thought about it much.

Fatigue is perhaps the most common symptom there is, along with pain. Conflating all unknown causes of prolonged fatigue with CFS, as is done in the oxford definition, is tantamount to saying that "I don't know what it is so I will pretend its all the same thing" and further complicated under psychogenic models by " and therefore will presume its a psychogenic illness, without evidence".

Another huge issue is this. In most of these pathogen induced diseases the blood load of pathogen declines. Recovery is delayed beyond that for some time, presumably (in the models I have read) due to persistent immune responses that take time to decline.

ME differs in one huge way. Recently it came to my attention that we have known for some years that enteroviruses at least have three lifecycles, not one. Secondary evidence shows that herpes family viruses might share this feature. In the case of ME patients (actually strictly defined CFS patients I think, this is Chia's work) we have high tissue viral loads of enteroviruses in gut. Yet viremia is not present. This fits with the two alternate viral lifecycles. It also fits with various findings Lerner has made with herpes viruses in strictly defined CFS subsets.

Now its possible these issues arise in post viral fatigue patients. They might. I would like that investigated.

The conflation of post viral fatigue with ME parallels the conflation of chronic fatigue with ME. Its a presumption. If there is some truth to it then the science could show it ... if anyone ever bothered to do adequate research, which means we need more funding, as usual.

I am not however saying that this is necessarily the only thing ME is. There is a range of evidence that strongly suggests ME is at least two different diseases, while we know from a number of lines of investigation now that Oxford defined CFS is typically a very mixed cohort.

Nor is ME necessarily induced by viral infection. The issue I am raising is that not all post viral fatigue is ME, not that all ME is necessarily a complication of post viral fatigue. However this latter interpretation might be correct ... something I don't want to discuss just yet, I am thinking about it. This is because of the existence of these two alternate viral lifecycles that have been largely ignored in modern research, though I am not up to date on my virology and want to investigate that more next year.

I think post viral fatigue, CFS and ME can be considered overlapping sets, but they cannot be considered as synonymous. We really need biomarkers to definitively separate these issues. I am hopeful that some of the many biomarkers currently under investigation will prove useful, and that combinations of biomarkers might be definitive.

Bye, Alex
 

Ember

Senior Member
Messages
2,115
The papers I've been reading by Simon Wessely express a similar view, and for similar reasons. To start with, he views ME/CFS as simply being on the extreme end of a continuum of "fatigue". This is a recurring theme, from his earliest work through his latest.
Dr. Unger shares the paradigm whereby an assortment of conditions can somehow be explained by one heterogeneous syndrome through the use of a severity continuum: “It’s a broad umbrella with various degrees of severity.” At CFSAC a year ago, she referenced fatigue specifically in describing her methodology for creating a new definition: “It's not enough to have just fatigue, but how much fatigue.”
Step number two is, if we have good measures of the domains (and as you know, the field is ongoing as to what are the best measures of the domains), then we try to say how can we capture this the best way. We as a field need to be a little schizophrenic and say yes, we can bring people in under a broader umbrella diagnosis, but then we cannot just group cases and controls. We have to be doing some stratification. We have to use a dynamic range in all of those measures. It is not enough to have just fatigue, but how much fatigue?
Dr. Unger rejects any paradigm whereby ME is extricated from the conditions assembled under the CFS umbrella, calling the illness “way too diverse” and demanding instead a unified approach. The problem that she perpetuates is described in the ICP:
Misperceptions have arisen because the name ‘CFS’ and its hybrids ME/CFS, CFS/ME and CFS/CF have been used for widely diverse conditions. Patient sets can include those who are seriously ill with ME, many bedridden and unable to care for themselves, to those who have general fatigue or, under the Reeves criteria, patients are not required to have any physical symptoms. There is a poignant need to untangle the web of confusion caused by mixing diverse and often overly inclusive patient populations in one heterogeneous, multi-rubric pot called ‘chronic fatigue syndrome’. We believe this is the foremost cause of diluted and inconsistent research findings, which hinders progress, fosters scepticism, and wastes limited research monies.
By removing ME from CFS, the ICC/ICP signals a paradigm shift and serves to undo the deception that the CDC began in Incline Village.
 
Messages
646
Okay, leveling terminology - I am using the definition of etiology that I have see in a variety of text books and online sources - study of the cause of a disease. I would classify the damage to the myelin sheath as sign or biomarker of the disease, presumably objectively measurable.
Much as I hate Wikipedia, in this instance it gives a useful summation “In medicine, etiology refers to the many factors coming together to cause an illness” . In MS the damage to the myelin sheath is the distinctive aspect of the condition, without it there would not be an illness called “multiple sclerosis”. Identification (via MRI) of the damage to the myelin is used for diagnosistic purposes, but that is rather like diagnosing a broken leg from an xray – the condition is the diagnosis . For a descriptivel list of the ‘symptoms’, ‘signs’ and tests used in MS diagnosis, see: http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001747/ However as with an xray of a broken leg, the MRI does notreveal what caused the damage only that the damage is there. In the case of M.E/CFS we have no identified ‘damage’ or even process of damage, at least not one that has been identified across a broad ptient population – what we have is a whole collection of oddities which as yet do not make up a coherent picture: here’s a list I made earlier http://en.wikipedia.org/wiki/User:In_Vitro_Infidelium/sandbox#Biomarkers
I am not sure if you are saying that there must be a 'single cardinal aetiological feature' (biomarker) or not. This was discussed at a recent CFSAC and Mary Ann Fletcher discussed the need to adopt a pattern of biomarkers for ME/CFS and not insist on a single biomarker.
No I wasn’t arguing for a single cardinal biomarker – my point was that for MS there is a single cardinal feature without which there would not be a condition called “multiple sclerosis”. Such a single cardinal feature has not been established in M.E/CFS and while (as Alex has argued) PEM/PENE and “hyperfatigueability” are notable features reported by many M.E/CFS patients, we don’t know how these relate to any disease process, in any way that might be comparable to the damage to the myelin sheath, that is evident in MS.

At this stage, reasoned consideration requires that we consider M.E/CFS as heterogenous – that is there is more than one underlying aetiology that is producing a common surface phenomenon . What ‘biomarkers’ may turn out to be relevant and how they might relate to differing aetiologies can’t be a priori defined. However if one accepts heterogeneity, then clearly multiple biomarkers should be expected to have relevance – but at this stage no one could assign specificity to any hypothesised grouping of markers, in terms of defining underlying pathologies.
This is a circular argument - of course, if you start with all the patients and criteria defined under the definition set of ME-ICC, CCC, Fukuda, Empirical and Oxford, you will never find consistent biomarkers because these are random definitions that have been lumped together. Oxford only requires 6 months of fatigue, does not require any other symptoms and allows psychiatric patients to be included. This is a nonsensical clinical entity.
To make an analogy, would it make sense to group cancern patients together with Oxford patients and then say that there are no common biomarkers? Of course not. Same here
But cancer has biomarkers and that is why it wouldnt make sense to group with Oxford, right? True and so does the CCC and the ME-ICC. PEM/PENE is objective and measurable - it is not a random color on a bead. Viral loads, immune system factors including cytokine levels, CPET, autonomic dysfunction are all objective and measurable and starting to drive treatment regimens. We can't expect to find consistent biomarkers across CCC/ME-ICC patients and Oxford patients because they are not dealing with a common disease process any more than Oxford and cancer patients are.
Regarding CCC/ME-ICC and Fukuda - Fukuda will contain both patients with PEM and those without. I dont think we really know what this group of non-PEM Fukuda CFS patients is but again, I dont think it is reasonable to expect they will have the same biomarkers as PEM patients (see the Maes study that compared immune factors across PEM and non-PEM groups).
I am not saying that all ME-ICC/CCC patients will have exactly the same profile across every measurable biomarker. Its a complex disease where factors like the triggers, genetics, onset and the length of illness must be considered. We need to subset out those different factors to better understand these patterns and how to treat patients. But we are not going to get there if we keep moving along with Fukuda and Oxford.
I can’t really follow what you are getting at. You seem to be making a false equivalence between cancer and some notional cohort of M.E/CFS patients who have a common set of biomarkers. Cancers are defined by definitive aetiologies, some excessive growth of cells has to be evidenced somewhere or else cancer wouldn't be diagnosed – we are back to the broken leg, tests and investigations may not tell us the cause of the break, but the break of itself defines the illness. This is very different from unusual measures of FoxP3 or IL10 which have no certain meaning, not to mention that they are not even consistently recorded as unusual across the patient population. The idea that treatment regimes can be derived from a few small scale studies, with no replication and in many cases carried out without stringent external oversight, is crazy. It certainly isn’t going to advance science in any meaningful way.
How many patients have been diagnosed with Fukuda and then told to go out and exercise - all because the doctor didnt recognize or understand the hallmark PEM that CCC requires. Continued use of Fukuda for diagnosis is dangerous to patients.
What has poor primary care got to do with diagnostic criteria ? Whether someone is diagnosed under Fukada/NICE or CCC shouldn’t impact upon what medical advice they are given. And certainly this nothing to do with whether Oxford has any relevance because it was only ever intended as a research protocol.

IVI
 
Messages
646
Even if you want to argue that PEM is a symptom and not a sign, it doesn't make sense to disregard it as a defining characteristic of the illness. Unless, of course, you feel that patient perspectives cannot be trusted.
Where did I suggest it should be disregarded. The issue here isn't what may or may not be important, the issue is (as per the thread subject taken from MK's blog) is what is meaningful in terms of patient populations from which research subjects are selected. Whatever PEM/PENE may be at present it offers no means to establish specificity for the indentification of underlying aetiology.

Patient perspectives whilst very important in structuring and in providing treatment/service delivery, and potentially in defining research priorities, can only ever have a very limited role in the conduct of research. The point of all research is 'trust nothing unless it can be repeated' - on that basis if the context is reserch, then patient perspectives have to be considered as inherently open to perpetual question.

IVI
 
Messages
15,786
Where did I suggest it should be disregarded. The issue here isn't what may or may not be important, the issue is (as per the thread subject taken from MK's blog) is what is meaningful in terms of patient populations from which research subjects are selected. Whatever PEM/PENE may be at present it offers no means to establish specificity for the indentification of underlying aetiology.

Patient perspectives whilst very important in structuring and in providing treatment/service delivery, and potentially in defining research priorities, can only ever have a very limited role in the conduct of research. The point of all research is 'trust nothing unless it can be repeated' - on that basis if the context is reserch, then patient perspectives have to be considered as inherently open to perpetual question.

The alternative, in the Oxford and CDC definitions which you seem to prefer, is focusing on fatigue. As others have already mentioned, patients with symptoms like PEM and OI and hypersensitivities and pain and sleep problems really don't give a rat's ass about "fatigue".

And as far as things being subjective - fatigue is a far worse transgressor than most other symptoms. PEM related abnormalities can be detected. OI can be diagnosed with a TTT. I can show you my arms swelling up when I eat the wrong foods, etc. Fatigue is just confined to questionnaires, which is why proponents of psychological models seem to be so fond of it - they don't have to bother engaging in real science.
 
Messages
646
There are no primary symptoms mediated by the effects of chronic incapacity that we are aware of. Some secondary ones arise from reduced activity, but not much can be pinned on this as many sedentary people are less active than we are and do not have our symptom set.
Elsewhere on several occasions I have discussed problems with interpreting the Dubbo studies, I am not going to repeat them again at this point.
During a flu for example we get a host of symptoms. These nearly all resolve in post viral fatigue. That pathogen is gone (low or no viremia), but stamina is down. Immunological responses do not however just end. There are circulating activated immune cells, immune complexes, antibodies, cytokines etc.
In ME however the primary symptom is not chronic fatigue. Its hyperfatigueability including PENE/PEM. Secondary pain symptom arise, additional autonomic (which means neurological) and immunological issues arise. The biochemical basis of PENE/PEMis partly understood now.
Even post viral fatigue patients, so far as I am aware, do not have our secondary consequences. There is still some debate about whether or not diseases like MS have PEM/PENE but I don't think we are ready to answer that yet.
This question of post viral fatigue vs. ME is one that needs investigating.
I think that is a very interesting hypothesis and very much agree that “This question of post viral fatigue vs. ME is one that needs investigating” and although I understand may patients will be uncomfortable with the connection, that direction of research may well be facilitated by the evolving interest in ‘fatigue’ as a medical (not psychiatric, at least not exclusively) phenomenon.

However, in advance of further research I don’t see how this allows the CCC to achieve greater specificity of aetiology than Fukada, beyond an hypothesis. We don’t know what a presentation of PEM/PENE means, we don’t know if some individuals suffer from the same underlying illness but happen to have inherent protection or endogenous amelioration against/of PEM/PENE, we don’t know if some people are simply better at unconsciously managing the limitations of PEM/PENE or whether age or social circumstances provide ameliorative or degenerative impacts, all which makes PEM/PENE highly problematic as a signal criterion for any proposed condition.
The conflation of post viral fatigue with ME parallels the conflation of chronic fatigue with ME. Its a presumption. If there is some truth to it then the science could show it ... if anyone ever bothered to do adequate research, which means we need more funding, as usual.
I am not however saying that this is necessarily the only thing ME is. There is a range of evidence that strongly suggests ME is at least two different diseases, while we know from a number of lines of investigation now that Oxford defined CFS is typically a very mixed cohort.
‘We’ don’t ‘know’ that Oxford defined cohorts are ‘mixed’, in that we have no means to distinguish underlying aetiologies, the mix provided by Oxford could be just as meaningful as the CCC in terms of what is actually causative or in terms of disease processes. I don’t know why researchers would want to use Oxford in addition to, or as an alternative to, Fukada/NICE but to suggest that somehow this ‘mix’ produces bad science is to misunderstand the research process. It’s not as if there is any evidence of M.E/CFS being drowned out by ‘noise’ from other conditions – the various biomarker studies (Light, Fletcher, Brenu) have no difficulty in identifying abnormalities – the problem is that abnormalities are not consistent across studies.
Nor is ME necessarily induced by viral infection. The issue I am raising is that not all post viral fatigue is ME, not that all ME is necessarily a complication of post viral fatigue. However this latter interpretation might be correct ... something I don't want to discuss just yet, I am thinking about it. This is because of the existence of these two alternate viral lifecycles that have been largely ignored in modern research, though I am not up to date on my virology and want to investigate that more next year.
I think post viral fatigue, CFS and ME can be considered overlapping sets, but they cannot be considered as synonymous. We really need biomarkers to definitively separate these issues. I am hopeful that some of the many biomarkers currently under investigation will prove useful, and that combinations of biomarkers might be definitive.
This is where I have problem – to demand the establishment of distinctive cohorts prior to biomarker identification is to put the cart before the horse. And to then come up with a notion of CFS being a definitive entity, that is distinct from M.E, is a semantic resolution based on ‘a priori’ reasoning. As things stand we have a broad pool of people who are ill – we have no clinical means to distinguish between any one of us who is in that pool and any other individual who is in the pool. I don’t understand the thinking and apparent anxiety of those who insist that Fukada and NICE (or even Oxford) produce research cohorts that preclude research advance, nor do I understand why the CCC or ICC are thought to be resolutions of that problem. Differentiating between M.E and CFS is just another ‘a priori’ justification of the CCC and ICC being ‘more right’ than Fukada and NICE.

Personally I’m not optimistic that simple biochemical markers or patient function tests will yield definitive population level results in the short term, rather the picture will be one of continuing complexity with definitive evidence of active disease processes in individuals but little coherence at a population level – lots going on but no definitive patterns. If I had to ‘bet the farm’ on the source of any break through it would be on something from outside M.E/CFS research - probably autoimmune studies or the genetics of cancer. That isn’t to say M.E/CFS research isn’t important – we need more of it and to not fuss about ‘a priori’ definitions of what illness might be what, and who qualifies with what symptoms for what definition.

IVI
 
Messages
646
The alternative, in the Oxford and CDC definitions which you seem to prefer, is focusing on fatigue. As others have already mentioned, patients with symptoms like PEM and OI and hypersensitivities and pain and sleep problems really don't give a rat's ass about "fatigue".
Why personalise the issue to "which you seem to prefer" ? I don't have a preference. That's not the issue; it's a matter of research 'facility' - what works and and 'why'. What patient's 'care about' is interesting and in context, very important, but for matters of research patient concerns may not have substantial informational power.
And as far as things being subjective - fatigue is a far worse transgressor than most other symptoms. PEM related abnormalities can be detected. OI can be diagnosed with a TTT. I can show you my arms swelling up when I eat the wrong foods, etc. Fatigue is just confined to questionnaires, which is why proponents of psychological models seem to be so fond of it - they don't have to bother engaging in real science.
You seem to be arguing that research populations must be constructed so as to purposely confound psychiatric studies - I don't think that's going to be taken seriously by the CDC or any other major research commissioning agency. You may not like it but fatigue is likely to be a growing area of research interest, and from the M.E/CFS perspective it's going to be a question of getting on board or waiting another 20 years for some passing ship to to offer rescue http://www.tandfonline.com/doi/full/10.1080/21641846.2012.746490, but then splendid isolation does have a certain perverse emotional reward. IMO the perfect science of M.E is never going to happen - progress will be made in a messy conflation of piggyback studies, serendipitous discoveries in unconnected fields, sort of in the right direction work, and some bog standard boring stuff that'll happen on something useful.
 
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15,786
You seem to be arguing that research populations must be constructed so as to purposely confound psychiatric studies - I don't think that's going to be taken seriously by the CDC or any other major research commissioning agency.

No, I'm arguing that it makes more sense to focus research based on symptoms with an objective aspect which is highly debilitating, very concerning, and relatively rare.

Focusing on fatigue is ridiculous. It's an extremely common symptom in people with physiological illness, mental illness, or no illness at all. Insisting that it somehow has more utility in the context of ME than PEM does is senseless.
 

Firestormm

Senior Member
Messages
5,055
Location
Cornwall England
Out of interest has anyone seen a study that links PEM to ME as a discrete symptom i.e. one that is not seen elsewhere? I have lost the plot on such things. I tend to think my Mum has PEM with her osteoarthritis - but then I'm biased I suppose. Then if you want to hear pain and discomfort and 'fatigue' post-exertion - you should hear the poor woman. Nothing quite like hearing one's Mum screaming in agony in the night etc.
 

Nielk

Senior Member
Messages
6,970
No one is claiming it is unique - but it's quite rare and distinct, compared to fatigue.

I think that it is distinct to "physical" illness as opposed to "mental" illness. For example, if one is suffering from fatigue due to depression, exercise is healing as it increases endorphines and in general makes one feel better. On the opposite side, if one suffers from ME/CFS exercise will usually exacerbation the condition.
 

SOC

Senior Member
Messages
7,849
That seems to be the ICP solution: “Not only is it common sense to extricate ME patients from the assortment of conditions assembled under the CFS umbrella, it is compliant with the WHO classification rule that a disease cannot be classified under more than one rubric.”

Yes, the ICP does exactly what we need, imo. Now if we could only get the US medical authorities to accept that. But no, we have to waste a bunch of time and money for the CDC to reinvent the wheel (and probably do a bad job of it). :rolleyes:
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
This is where I have problem – to demand the establishment of distinctive cohorts prior to biomarker identification is to put the cart before the horse. And to then come up with a notion of CFS being a definitive entity, that is distinct from M.E, is a semantic resolution based on ‘a priori’ reasoning. As things stand we have a broad pool of people who are ill – we have no clinical means to distinguish between any one of us who is in that pool and any other individual who is in the pool. I don’t understand the thinking and apparent anxiety of those who insist that Fukada and NICE (or even Oxford) produce research cohorts that preclude research advance, nor do I understand why the CCC or ICC are thought to be resolutions of that problem. Differentiating between M.E and CFS is just another ‘a priori’ justification of the CCC and ICC being ‘more right’ than Fukada and NICE.
IVI

Which is why I said that they can be considered overlapping sets, but can't be considered synonymous. This is the best fit for the current data. It is also why I pointed out that even ME might have to be considered, and here I will use set theory instead of my other explanation, as two overlapping sets.

I am also talking about definitions, not distinct entities. What the entities are is still unclear. In any case, it is entirely possible that we are talking multidimensional spectrums and no clear entities will emerge except by definition. We impose identity sometimes because it suits our purpose or our brain neuronal structures - its easier to think about.

What is clear is that patient cohorts selected under one definition do not match patient cohorts selected under another. In the case of something like ICP this is still largely untested, but Oxford, Fukuda and CCC have been used a lot. There are differences in the cohorts. This means that the best fit is overlapping sets, not congruent or nested sets. Biomarkers will make the difference here.

The other point about biomarkers is they do not have to be diagnostic. Anything that discriminates between subsets is valuable data that can be used in research. How useful they are then depends on the results from that research.

As to breakthroughs outside ME, the one that has my attention at the moment is from virology. The enteroviruses were ruled out as a cause of ME because ME patterns do not fit the entervirus lifecycle. Now we know this is not true. Enterviruses have three distinct lifecycles. Two of those match empirical findings from Chia. Similar data by Lerner on herpes viruses might also fit this picture. Persistent and widespread non-viremic viral infection has to do something to our immune system. What is unknown at this point, presuming that all of this can be adequately validated and tested, is whether this is all due to opporunistic infection (from poor immunity) or has some causal role.

Bye, Alex