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BMJ editorial: GET and CBT advised for ME

Sean

Senior Member
Messages
7,378
I agree that, like Simon Wesseley, he seems to have started out with a genuine desire to find a biological mechanism.
You sure about that with Wessely? Not how I remember his earlier papers.

Best I can recall, closest he come to any serious look at biological stuff was some papers on cortisol, which were given the usual psychocausation spin.
 

Jonathan Edwards

"Gibberish"
Messages
5,256
You sure about that with Wessely? Not how I remember his earlier papers.

Best I can recall, closest he come to any serious look at biological stuff was some papers on cortisol, which were given the usual psychocausation spin.

He has his name on papers on lymphocyte activation, MHC genetics, epidemiology, brain imaging and other such things. From 1990 he was saying that CFS needs a neurobiological as well as a psychological explanation. He certainly starts from the assumption that it is primarily a brain problem, maybe unlike Lloyd who seems to have started out from a more immunological angle, but since he starts from a psychiatric training that seems fair enough - at least he emphasised the need to understand the biology.
 

chipmunk1

Senior Member
Messages
765
Cognitive behavioural therapy for patients with chronic fatigue
syndrome is based on the premise that inappropriate cognitive
attributions (thinking patterns) and behaviours help perpetuate
symptoms. It seeks to alter these attributions and modify the
associated behaviour, targeting activity patterns and sleep-wake
behaviours. For example, although primary sleep disorders do not
explain chronic fatigue syndrome,14 patients typically report that
their night-time sleep is unrefreshing, and as fatigue is the dominant symptom, patients may consider that increased sleep will relieve symptoms and aid recovery. This idea commonly leads to frequent daytime naps and a delayed sleep-wake cycle.

How desperate can one become? Are they trying to suggest that the illness is at least partially caused by highly dangerous, injurious, self-inflicted daytime naps and brainwashing them not to nap will make them better?

How does the CBT for this work? Brainwash the patient for several months and have them repeat: "I do not nap. I do not nap...Naps will harm me. Naps willl harm me."
 
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Gijs

Senior Member
Messages
690
He has his name on papers on lymphocyte activation, MHC genetics, epidemiology, brain imaging and other such things. From 1990 he was saying that CFS needs a neurobiological as well as a psychological explanation. He certainly starts from the assumption that it is primarily a brain problem, maybe unlike Lloyd who seems to have started out from a more immunological angle, but since he starts from a psychiatric training that seems fair enough - at least he emphasised the need to understand the biology.

Professor Edwards, Why is it that if the doctor can't find the cause that it is always explained as psychosomatic without any objective prove. How can Wesseley e.a. prove his theory, he can't. It is only a subjective idea. That is why psychology is pseudo science. Karl Popper said it as well. I believe that every serious mental illness is a brain disease.
 

Jonathan Edwards

"Gibberish"
Messages
5,256
Professor Edwards, Why is it that if the doctor can't find the cause that it is always explained as psychosomatic without any objective prove. How can Wesseley e.a. prove his theory, he can't. It is only a subjective idea. That is why psychology is pseudo science. Karl Popper said it as well. I believe that every serious mental illness is a brain disease.

I absolutely agree. But the other explanation given when people can't find a cause is 'a virus'. Everything has to be challenged on an equal basis.
 

duncan

Senior Member
Messages
2,240
Jonathan, I am a little confused when you write that Wesseley "starts from the assumption that it is primarily a brain problem."

Bovine Spongi Encephalopathy is primarily a brain problem. But that is a very different kind of brain problem than is, say, conversion disorder. It's pretty clear that Wesseley is more comfortable speaking to the latter type of brain problem.

But ultimately, he is not speaking much to an organic cause to ME, other than the false illness beliefs somehow occur in some place in the brain, and may or may not be associated with certain cytokines, etc etc.

So that Wesseley's brain problem isn't all that much a brain problem, is it?

Er, well, sorry about that last query: It does leave open so many possibilities...:)
 

chipmunk1

Senior Member
Messages
765
Professor Edwards, Why is it that if the doctor can't find the cause that it is always explained as psychosomatic without any objective prove.

because they believe they are infallible. if they can't find anything it can't have an organic cause and if it isn't organic it can only be psychogenic.

psychogenic usually means:

the don't deserve proper medical treatment(other than psychiatric)
they are causing their problems(most important of all!)
they need to see a psychologist
they need to work on emotional conflicts
they need to make lifestyle changes
they lack insight in their condition

some folks never learn:

http://www.catholic.com/quickquestions/wasn’t-the-catholic-church-wrong-in-condemning-galileo-and-therefore-fallible-in-what
 

anciendaze

Senior Member
Messages
1,841
One could say in a region of £1 million was thus wasted on an overpowered study.
Dolphin's quoted statement is hard to find in this thread, but it illuminates an internal contradiction in PACE. They went to great lengths and expense to make sure the study had adequate statistical power to demonstrate subjective results they wanted to see. At the same time they were so careless with objective tests that they didn't worry about 1/3 of all subjects declining to participate in the 6-minute walk. "Do you feel worse after therapy? Don't worry, we won't test you."

There is a pattern to this manipulation.

Do actimeters show patients displacing activity from a fixed energy budget?
Drop actimeters entirely.
Do patients report setbacks following exercise that last one week?
Change criteria for adverse responses to require over two weeks of setback.
Do preliminary results fail to validate your preconceptions?
Change entry criteria for the study without changing recovery criteria.

The only statistically-significant results which remain are those which demonstrate that researchers can bullyrag patients into saying they are better, if the consequences of disagreeing might be loss of benefits for noncompliance with treatment.

If you flatly refuse to notice that anyone might be made worse, except by the traditional medical standard of dropping dead, you can always find random variation in a positive direction. Do not expect to validate such results. Do not expect them to last.
 

Gijs

Senior Member
Messages
690
I still wonder where all these recovered happy ME/CFS patiënts are? I never hear anyone getting better after CBT, and i know many patiënts. It is all about fatique and selection bias. It is fraud and they made a lot of money.
 

chipmunk1

Senior Member
Messages
765
I still wonder where all these recovered happy ME/CFS patiënts are? I never hear anyone getting better after CBT, and i know many patiënts. It is all about fatique and selection bias. It is fraud and they made a lot of money

there no recovered "happy" patients. there are only "recovered" brainwashed patients.
 
Messages
13,774
there no recovered "happy" patients. there are only "recovered" brainwashed patients.

It wouldn't surprise me if there were a lot of patients who had recovered while doing CBT/GET, especially teenagers/those not ill for long who have high recovery rates for natural course. There are lots of people claiming all-sorts helped them to recovery from CFS.
 

Snow Leopard

Hibernating
Messages
5,902
Location
South Australia
It wouldn't surprise me if there were a lot of patients who had recovered while doing CBT/GET, especially teenagers/those not ill for long who have high recovery rates for natural course. There are lots of people claiming all-sorts helped them to recovery from CFS.

Just a note that "lots" can be derived by just a few recovering out of a large number of people who came down with the illness...
 

anciendaze

Senior Member
Messages
1,841
Just because this thread has brought thoughts about PACE back to mind, I want to clarify one aspect of my criticism. This concerns one statement I made above.
Do preliminary results fail to validate your preconceptions?
Change entry criteria for the study without changing recovery criteria.
Malcolm Hooper has accused them of allowing patients to enter the study with a score of 65, drop to 60, and then count them as recovered as a result of therapy. My guess is that this obvious malfeasance would cause the authors serious problems with cognitive dissonance, even if there were no defectors to cry "fraud".

What I believe they did was to run two separate studies with different criteria for entry and recovery, then pool the results.

There is a simple solution which they did not use: run the whole study with consistent criteria, as though these had been chosen at the start. Patients who entered the study with scores of 60 would certainly have qualified as patients in a study that set the bar for entry at 65. Nobody would be arguing about this particular anomaly. The problem would then be that raising the score above 60 would not count as recovery unless it was also above 65. Note that the metric they were using can't measure changes smaller than 5 points.

My guess, in the absence of actual data, is that the results with the bar for recovery of all patients set at the height required by the second cohort of patients were too poor to allow spin doctoring. I'm suggesting this peculiar behavior tells us that the bulk of the "recovered" patients experienced improvements of about the minimum which might be charitably considered recovery by anyone.
 

user9876

Senior Member
Messages
4,556
Just because this thread has brought thoughts about PACE back to mind, I want to clarify one aspect of my criticism. This concerns one statement I made above.
Malcolm Hooper has accused them of allowing patients to enter the study with a score of 65, drop to 60, and then count them as recovered as a result of therapy. My guess is that this obvious malfeasance would cause the authors serious problems with cognitive dissonance, even if there were no defectors to cry "fraud".

What I believe they did was to run two separate studies with different criteria for entry and recovery, then pool the results.

There is a simple solution which they did not use: run the whole study with consistent criteria, as though these had been chosen at the start. Patients who entered the study with scores of 60 would certainly have qualified as patients in a study that set the bar for entry at 65. Nobody would be arguing about this particular anomaly. The problem would then be that raising the score above 60 would not count as recovery unless it was also above 65. Note that the metric they were using can't measure changes smaller than 5 points.

My guess, in the absence of actual data, is that the results with the bar for recovery of all patients set at the height required by the second cohort of patients were too poor to allow spin doctoring. I'm suggesting this peculiar behavior tells us that the bulk of the "recovered" patients experienced improvements of about the minimum which might be charitably considered recovery by anyone.

In the protocol they defined recovery as including an SF36-pf score of 85 but at some point that they reduced this to 60 for reasons what we know are wrong. We are not allowed to know when they made these changes because to ask is vexatious harassment and its completely unreasonable that an academic should have their trail discredited by answering such questions.

The entry criteria was 65 for the SF36-pf scale.

From things they have published it appears they never actually tracked patients through the trial and didn't look at individuals changes or at least with respect to recovery. They claim not to have even correlated say the walking tests with the sf36 results which shows a remarkable lack of curiosity and lack of quality control. However, given they seem to have issues with basic stats within a statistics package (evidenced by their FoI responses) then maybe it is technically too hard for them to really carefully examine their data. Or maybe the are just sticking their fingers in their ears and singing la la la so that they can't hear the data shouting spin spin spin.

But there were not two different sets of data just two thresholds with no one looking at what changes happened.
 

anciendaze

Senior Member
Messages
1,841
I'm still perplexed by the problem of two thresholds which were apparently used for data collected at different times. If the recovery threshold was actually 60 for all patients, then Hooper's criticism is valid. If they used different thresholds for patients who entered the trial after the change in entry criteria, then the effect is the same as if they ran separate cohorts and pooled the data on recovery.

I think we can all agree that such games would not be necessary if they had much evidence of changes beyond the minimum change measurable on that scale.

I do not say they were incapable of understanding the statistical issues. My contention is that reporting the threshold as one standard deviation below the mean was a deliberate attempt to exploit medical prejudice about "CFS" and mislead peer readers who did not check to see that the population data were very far from normally distributed. Later changing that threshold also indicates that the number didn't mean very much to the authors themselves.

Changing the entry and recovery criteria after seeing much of the data also massively violates the assumption of independent sampling needed to say the distributions in groups were normal. This pretty well destroys the arguments about statistical significance, leaving the problem of clinically-significant changes.
 

user9876

Senior Member
Messages
4,556
I'm still perplexed by the problem of two thresholds which were apparently used for data collected at different times. If the recovery threshold was actually 60 for all patients, then Hooper's criticism is valid. If they used different thresholds for patients who entered the trial after the change in entry criteria, then the effect is the same as if they ran separate cohorts and pooled the data on recovery.

I think we can all agree that such games would not be necessary if they had much evidence of changes beyond the minimum change measurable on that scale.

I do not say they were incapable of understanding the statistical issues. My contention is that reporting the threshold as one standard deviation below the mean was a deliberate attempt to exploit medical prejudice about "CFS" and mislead peer readers who did not check to see that the population data were very far from normally distributed. Later changing that threshold also indicates that the number didn't mean very much to the authors themselves.

Changing the entry and recovery criteria after seeing much of the data also massively violates the assumption of independent sampling needed to say the distributions in groups were normal. This pretty well destroys the arguments about statistical significance, leaving the problem of clinically-significant changes.

When they changed the entry criteria as a condition of being allowed they were told to change other criteria however, this got ignored when they published results. It is not clear that they had approval from the trial steering committee to change the recovery criteria - my guess from what is said is that they didn't but we are not allowed to know. They have never talked about having separate sets of data so I'm pretty sure they didn't.

I genuinely don't think they understand statistics but I'm not convinced they tried when they claimed 1/2 the population were below 85 on the sf36-pf scale and used mean-SD I think that just gave them results they were happy with. Any slight sanity check that they should have carried out would have told them it was dodgy. In engineering you would be expected to have some sort of QA processes to check results are correct but I don't think that is the case in a medical trial - perhaps that's why bridges tend not to fall down but medicines don't always work!

Its not clear at what point they changed the recovery criteria they claim it was before the statistician was unblinded as to which data set was which. But does this mean they had analysed the datasets blind in which case a guess would be pretty easy. Even if this is not the case the trial was not blinded so they would have an idea for how it was going.

The whole methodology is dodgy anyway.
 

Dolphin

Senior Member
Messages
17,567
There are now two rapid responses up, from Dr. Jonathan Kerr and Stephen Hawkins (a patient), replying to this week's BMJ editorial.

Plenty of scope for other points to be raised.
The BMJ has posted most e-letters over the years including ones that don't have any references.

However, it is a lot harder to get in the print edition. Responses should include five or fewer references (incl. original paper) and include fewer than 300 words (ideally fewer than around 220-230 words I would say).

http://www.bmj.com/content/350/bmj.h2087/rapid-responses