2025: The 2019/24 Cochrane Larun review Exercise Therapy for CFS - including IAG, campaign, petition, comments and articles

You are assuming that there's a focus on one single issue but there's no evidence of that.

Beyond that, I don't have anything further to add at this point.

 

FYI, this phrasing makes it seem like you’re saying that the wider inclusion criteria is acceptable because you like the results and want to apply them to a narrower case.

What we want is irrelevant.

 

Interesting data but these 'others' would presumably have been diagnosed as having these other conditions rather than CFS or ME/CFS. I don't think it suggests that people like Peter Denton White were managing many people as 'CFS' or 'CF' who did not in fact have ME/CFS.
They would not have recruited to PACE people they had identified as having depression instead.

 

But it doesn't @Medfeb.

If an anti-inflammatory analgesic is studied in large trials of joint pain do we then say that it should not be prescribed for rheumatoid arthritis because the trials did not require symmetrical joint swelling or a raised ESR? No, we use most drugs test on brand categories for all sorts of more restricted subsets.

If PACE had had a positive outcome based on adequate methodology it would have been gerrymandering to argue that it did not apply to ME/CFS because the criteria were not explicitly the same. Exactly the sort of gerrymandering the BPS people are accused of. Their defence of their criteria is entirely reasonable and it is a huge distraction that people are arguing against it.

 

Here’s another angle that might explain why there’s focus on the diagnostic criteria:

If you study a group that may or may not have PEM, then you can’t deduce that any positive results regarding effect or safety would apply to everyone with PEM. Why? Because PEM acts differently in relation to exertion, compared to non-PEM. So it’s reasonable and plausible to expect that a pure PEM study could yield different results.

MAGENTA is different. They showed that an exertion-based approach was harmful even for non-PEM patients. There is no reason to believe that PEM-patients would respond fundamentally different from the studied group.

«This is how it’s usually done» is not a valid argument. That’s what the BPS lobby argues with regards to using subjective outcomes.

 

Nobody is labelling people who do to conform to ME/CFS criteria as ME/CFS, any more than they are labelling people with joint pain by not RA, RA.

One very unfortunate by product of this sort of debate I see is that if there are indeed a lot of people with 'chronic fatigue syndrome' who do not conform to criteria for ME/CFS, as seems to be suggested, these people no longer have any NICE Guidelines for their care. That to me is pretty much a violation of human rights. Advocated for people with ME/CFS do not have the right to trample over the interests of people who do not!

Diagnostic pigeonholes can cause a lot of harm.

 

They apply to the narrower case until proved otherwise by the nature of set theory @Utsikt. I thin you have still got this back to front - maybe because you are unhappy about the implications of getting it the right way around?!!

 

What about the argument that strictly defined ME/CFS with clear PEM would have been more likely to have shown adverse effects in GET/CBT trials. That might overshadow any positive results and explain why the BPS people preferred to focus on broad criteria with unexplained fatigue.

As Jonathan said, if you follow their reasoning about deconditioning and false illness beliefs, the more severe ME/CFS patients would have been the best study subjects who should improve the most. Instead, BPS'ers preferred to focus on patients with unexplained fatigue using the Oxford criteria.

 

I don’t care what the result of my thinking is. I care about understanding the underlying mechanisms. And I currently don’t understand it.

I stated earlier in the thread that I don’t have an opinion because I recognize that I don’t understand the full picture yet. Besides, the conclusion would still be that GET shouldn’t be recommended on the basis of the studies in the review. Either due to a lack of evidence, or due to evidence that it doesn’t work/is harmful.

So the implication in this case is irrelevant.

 

That's right @Trish, but, as discussed with @Utsikt, examples like this are what I call 'special pleading' and although they may be valid, if we don't know they are, the default probability estimation remains. Basically NICE cannot alter a recommendation on the basis of 'what if we think of this scenario' arguments - although it could certainly raise a caution.

 

I just want to be very clear: I am not claiming that indirectness is the main issue with PACE or the Cochrane review.

I’m also not claiming that arguing about indirectness is the strategic approach from the different parties involved.

What I am doing, is tryingy to understand why indirectness is not a fatal flaw to the study design. I want to learn. I want to understand. And I’m not arguing against anyone here because I disagree, but because I don’t understand. And that’s provably a me-problem.

 

Not so sure because their concept of ME/CFS might differ and be more inclusive than ours.

I've heard some interesting stories from ME/CFS patients in Belgium. In the early 2000s that country financed CFS centres where patients were treated with GET/CBT. You had to meet CFS criteria (Fukuda) in order to be eligible. Some of the treatments sessions or the initiation was done in group form where patients could meet.

Several ME/CFS patients reported that this was frustrating because many other participants did not have ME/CFS as we would see it today: with PEM, OI and other characteristic symptoms such as light and sound sensitivity.

It included people who were fatigued, depressed, or burned-out, who were much more active and didn't get severe crashes. Many thought their symptoms were stress-related. It also seem to include people who's primary issue was a sleep disorder or pain which in turn also caused fatigue which led them to get a CFS diagnosis.

Later the physicians at the CFS centre admitted they were initially too loose in applying CFS criteria, for example by including too many people with sleep disorders. This was because everything was new for them, etc.

I suspect BPS'ers might have done something similar in their trials to avoid too many ME/CFS patients with clear PEM who might worsen or drop out during treatment.

 

I appreciate that. And I think it is useful for us all to realise how hard it can be to see what one might call mathematical necessities - like in set theory. But I think the example of using painkillers for RA on the basis of them working for joint pain is a pretty simple demonstration that 'indirectness' need not be a problem at all.

Sometimes these things are hard to follow and suddenly become clear. I love Roger Penrose's explanation for why 3x4 = 4x3. You might say why should it have to? How can we be sure that 567x439=439x567. As he points out the answer is that if you lay beads out in arrays of 3 by 4 you have by definition laid them out in arrays of 4 by 3 and the same for 567x439.

Extrapolating to subsets is legitimate by default in a probabilistic analysis. Extrapolation to supersets is the problem.

 

It might indeed, and it sounds as if they had to scrape the barrel to recruit. I am just saying, though, that those figures for people referred with suspected ME/CFS may not be directly relevant if they were actually given different diagnoses from CFS.

 

There are still no comments appearing on the MEAction blog post on Cochrane’s abandoning the new exercise review and their redating of the old review. I discovered that adding a new comment enabled seeing the old comments in moderation, so added a new comment just now in order to access what I had already posted:

Am posting them here as a record in case they end up getting lost indefinitely. With the Viriology Blog some time ago comments would occasionally get eaten up by the software, though they seem to have now sorted whatever the problem was.

 

@Jonathan Edwards I appreciate your patience!

If you say that you study mammals, but only study rats, can you extrapolate those findings to humans because the humans are a subset of mammals?

If yes, why do we need human drug trials?