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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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I guess this could be regression to a mean, where patients who wouldn't normally be severe enough to qualify for the trial are included if they happen to be in a relapse, then appear to 'improve' as they recover from the relapse independently of any treatment. The converse, counterbalancing example is a patient who would normally be severe enough to qualify, but didn't get selected because they happened to be in remission. But because they aren't selected for the trial you lose the counterbalancing effect.However, another point to all this is that it's just one moment in time in a relapsing-remitting condition.
Thanks for that. I thought it might help if I put the data you used below:Don't know if this has been posted before but here is a table containing CIS-20, CHQ, and school attendance of healthy controls and adolescent CFS from the paper cited in the FITNET paper regarding:
"Recovery was defined post hoc, in relation to healthy peers (2 SD), as having a fatigue severity score of less than 40, physical functioning score of 85% or more, and school absence of 10% or less in the past 2 weeks, all assessed at 6 months."
Table: Morbidity of Adolescents With CFS Reported by Pediatric Departments in 2008
http://pediatrics.aappublications.org/content/127/5/e1169/T1.expansion.html
CIS-20 score and school attendance of those who recovered on FITNET at 6 months (2 SD) is the same as the scores of these healthy controls. CHQ score is a little lower...
On the other hand, only about half of the patients considered recovered by the 1 SD cutoff considered themselves "completely recovered". This is even though the 1 SD recovered group scored the same as healthy controls on the CIS-20 and school attendance. I don't think half of healthy controls with the same scores would call themselves the equivalent of not completely recovered.
Anyways, 2 SD.. I think in a normal distribution, that means about 5% falls beyond the cutoff, including upper and lower ends, so assuming only the lower end applies to CFS patients recovering compared to healthy controls, that means the 2 SD recovery cutoff corresponds to the 2nd percentile of "healthy" controls, if I'm understanding this correctly, which is borderline not healthy, but I guess that actually makes the cutoff similar to the healthy/not healthy distinction.
Attend | Function | Fatigue | |
---|---|---|---|
FITNET, Recovered, 12months: mean | 96.3% | 89.8 | 21.0 |
FITNET, SD | 8.6 | 18.6 | 10.7 |
'Healthy' population mean (Nijhof 2012) | 98% | 95 | 30 |
healthy, SD (1) | 4 | 5 | 5 |
Healthy mean (Nijhof 2011) | 98.5% | 95.1 | 22.6 |
healthy , SD | 3.9 | 7.6 | 10.6 |
The cutoff point for impaired physical functioning was set at ?85 (healthy population's mean of 96.8 minus 2 SDs [2 5.4]).19 As a reference group, students at a Dutch secondary school (de Breul, Zeist) were invited to participate. Adolescents who were suffering from a chronic illness and adolescents currently under treatment were excluded [my note: ie a proper healthy population, wiht chronically ill excluded]. The participation rate was 85%. From this group of students we randomly selected individuals for a control group matched for age and gender (n = 144; mean age: 15.3 0.6 years; 79% girls).
Let's be honest, if these kind of results were found in a study that was looking at bio-medical causes we would stand up and take notice (as has happened with the Rituximab trial). This seems to be far more clear cut than the PACE trial, whatever the cause of this illness is, it seems that there is some subset of people who suffer with idiopathic chronic fatigue for whom this kind of intervention is effective. I feel both sides of the argument are culpable in preventing progress, because one side is so adamant that the cause is not psychological that they flatly dismiss any finding which would implicate that hypothesis, but the other side doesn't even acknowledge that there may be a spectrum of different illnesses, and that applying the results of studies done on patients with idiopathic fatigue to people with chronic ME/CFS is misleading and utterly useless. I think the future is very bleak indeed if we can't separate and define these illnesses properly.
Let's be honest, if these kind of results were found in a study that was looking at bio-medical causes we would stand up and take notice (as has happened with the Rituximab trial).
Thanks for exploring that - regression to the mean is one point.I guess this could be regression to a mean, where patients who wouldn't normally be severe enough to qualify for the trial are included if they happen to be in a relapse, then appear to 'improve' as they recover from the relapse independently of any treatment. The converse, counterbalancing example is a patient who would normally be severe enough to qualify, but didn't get selected because they happened to be in remission. But because they aren't selected for the trial you lose the counterbalancing effect.Dolphin said:However, another point to all this is that it's just one moment in time in a relapsing-remitting condition.
This effect should apply equally to control and treatment groups in a randomised trial, at least on average, but may be the explanation for some unusually good results.
He gave more info:(To nobody in particular)
Saw this posted on a discussion on the CAA's FB by Danny Ze-dog:
The danger of relying on self-report rather than objective measures to assess physical function has been noted many times before. For example, Barber (1991) studied the correlation between subjective health questionnaire reports and cardiac function in adolescent patients and found that "questionnaire data significantly overestimated exercise ability in 67% and underestimated it in 3% of the subjects".
Barber G, Heise CT: Subjective estimates of exercise ability: Comparison to objective measurements. Ped Exerc Sci 3:327-332, 1991
Another one you may find interesting, which used the same questionnaire and found the results did not correlate with cardiac function:
Ginsberg JP, Cnaan A, Zhao H et al. Using health-related quality of life measures to predict cardiac function in survivors exposed to anthracyclines. J Clin Oncol 2004;22:3149-3155."
I'm willing to believe activity questionnaires can have a value in people who don't have ME/CFS and who haven't been put through particular programs.Thanks, Sam.
Subjective Estimates of Exercise Ability: Comparison to Objective Measurements
However, a couple of more recent papers on adolescents and adults with heart disease found decent correlation of r = 0.521 and r=0.435 (see fig 3), with Physical Functioning questionnaire scores. I'm also not sure how precise a correlation there should be between general physical capability (e.g. ability to climb a flight of stairs) with peak oxygen uptake.
but it's certainly useful evidence of the problems of relying on questionnaires to assess physical function.
I certainly agree there is an important difference between recovery and improvement. I take you point that although you could do quiite a bit while in education, you couldn't live a full life yet they might have counted you as 'recovered'.However, there is in my view a difference between "improvement" and "recovery". If you recover from a condition in my book, you don't have it again. It's history. Being well for a period in a relapsing-remitting condition (in my book) isn't recovery esp. if the person isn't being "stressed". If they can play competitive sports for a year, say, I'd be more happy with that being called recovery.
I was in full-time education for over 4 years with the condition. Even managed to build up to a reasonably large amount of exercise (1000m swimming or 6 miles cycling every two days). But I couldn't live the life I wanted to live. I couldn't have much of a social life. I couldn't live the life of a young person. I had some cognitive problems. I wasn't recovered. Occasionally (I wasn't undiagnosed) I'd play an (uncompetitive) game of football and I'd feel terrible the next day - I couldn't do it. Eventually I relapsed. And am now severe. By their criteria, I almost certainly would have been classed as recovered.
Let's be honest, if these kind of results were found in a study that was looking at bio-medical causes we would stand up and take notice (as has happened with the Rituximab trial). This seems to be far more clear cut than the PACE trial, whatever the cause of this illness is, it seems that there is some subset of people who suffer with idiopathic chronic fatigue for whom this kind of intervention is effective. I feel both sides of the argument are culpable in preventing progress, because one side is so adamant that the cause is not psychological that they flatly dismiss any finding which would implicate that hypothesis, but the other side doesn't even acknowledge that there may be a spectrum of different illnesses, and that applying the results of studies done on patients with idiopathic fatigue to people with chronic ME/CFS is misleading and utterly useless. I think the future is very bleak indeed if we can't separate and define these illnesses properly.
I think I know where I fit - I'm in the screwed up stress response group. Others may be in the pathogen fluey completely wiped out group.
Remember that there is no proper control group in this study. We don't know how many would have recovered without any treatment whatsoever.Let's be honest, if these kind of results were found in a study that was looking at bio-medical causes we would stand up and take notice (as has happened with the Rituximab trial). This seems to be far more clear cut than the PACE trial, whatever the cause of this illness is, it seems that there is some subset of people who suffer with idiopathic chronic fatigue for whom this kind of intervention is effective. (...)
We always assume that if CBT or another behavioral treatment helps that it means this disorder is psychological. But what if the Lights theory is correct - that the sensory nerves are blasting the brain with signals - sending pain and sensation levels upwards - with every activity? And/or what if the autonomic nervous system - which controls blood flows and regulates the immune system and is an important part of the stress response is dysfunctional?
it is undeniably the case that people do experience a full recovery with these talking therapies on a regular basis (be it CBT, MT, LP etc.)
Because despite the rather shoddy definitions of recovery used in many of these studies it is undeniably the case that people do experience a full recovery with these talking therapies on a regular basis (be it CBT, MT, LP etc.), if there was an underlying neurological abnormality as the Lights postulate then it seems that the best these techniques could hope to achieve is a reduction in symptoms, as reducing stress via altering thought patterns would only be masking the underlying physiological issue. I suspect the primary cause within a significant portion of the CFS spectrum really is psychological, or neuro-psychiatric to be more precise, and if that were the case we are wasting our time trying to incorporate that subset within ME, we would be better admitting that for that subset the psychologists are correct in their evaluation and to let them get on with it, while we get on with solving ME. I don't see any way forward while the different subsets remain conflated as they currently are. I should clarify that I wasn't trying to accuse people of bias, I appreciate the efforts people make here to analyse each study in meticulous detail.