Search results

I don't know, I thought 0.4 was higher than you normally get from things like that. But I still think that using a sensible measure would give us a clear answer.

I agree that symptom count is a weird measure, and wouldn't expect it to show much, so r=0.4 is quite impressive. It would be great to see this work done measuring the overall symptom severity/burden on standing. Maybe there is something impressive to find here

As you say, the combinatorial principle is straightforward. The trick is finding a good way to search the "computational space". And that's where their proprietary, black box method comes in. Which means it's not possible to validate it. They point to quite a lot of evidence for validity in...

I agree with all of that. And this conversation is complicated by not knowing what dME will report. However, after the ambush of CP on R4, I think we can assume that SMC is likely to try to undermine DecodeME, regardless of its findings. It would be wise to be prepared for this. If the study...

Doesn't look like they've done Mendelian randomisation properly. At the heart of Mendelian randomisation is the "instrumental variable", IV. This is a genetic factor that you know impacts the outcome of interest. This is one example I know: – George Davey Smith, a pioneer of Mendelian...

Yes, I found the same thing. But how do we know the cases really do have ME/CFS? UKB has over 5000 CFS cases, but the recent Samms/Ponting paper on cohort quality, showed there were numerous concerning features of the data. I'm not sure there is better data out there (though there is a Finnish...

The usual question applies: how good is the underlying data? There is only one source of trustworthy ME/CFS GWAS data I know of, and it hasn't reported yet or made its data available more widely for GWAS analysis

Of course we do, and I'm well aware of that. And yet it hasn't gone away, not least because of the overwhelming popularity of mind body explanations. Well, yes. But to change minds that are already firmly made up, I think we need a stronger result. It's no good saying "that's not good...

It has been tried before, without success The BPS advantage is that most scientists, doctors (and people) instinctively accept the BPS view, the mind can be responsible for anything we can't explain (kind of like witchcraft in medieval times). Because BPS has, at least, been clear that what...

I agree, and that's why I was joining the discussion GWAS are good at providing causal evidence. If there is a link to anxiety-related genes, or other relevant jeans – even if subthreshold in. DecodeME – that coup support the BPS claim to a degree. They've always accepted that they are...

Sorry, I see what you mean. I'm not sure what case BPS proponents would make, so this feels like shadow boxing. And I don't think we can award the non-BPS view a knockout win without knowing BPS arguments. I expect that, at least, they would argue for the 'success' of CBT (which takes us back to...

? I'm not sure what you said, I was responding to Robert.. But is surely depends on the results. If anxiety-related genes show up in DecodeME, or at least are prominent if not significant at the threshold, wouldn't that make it hard to rule out a role for them? (I don't know what the results...

I think it might be quite difficult to prove that there isn't a substantial role for the mind. My reading of CBT in particular is that it's built on the idea of anxiety about symptoms. So you might expect to see anxiety-related genes in a GWAS. Possibly, you would expect to see such things as...

I think that's the most important point. Based on the discussion here, it's still not clear what the best way is to respond , or how best to present an argument. I am very wary of the risk going down mind/body rabbit holes. I think we can be sure that those wedded to a psychosocial...

I'm sure that's the journal, so that must be it, thanks.

I suspect this has been covered before, but I'm looking for a paper/journal piece penned by SW, possibly in 1999 (maybe later). In it, IIRC, he reflects on how the BPS model has held up and concludes, 'pretty well', though he concedes that his original suggestion that CFS was a form of...

Abstract: >We applied this method to a very homogeneous sample of patients belonging to a unique and clinically well-characterized multigenerational pedigree with one of the most severe forms of early onset AD, carrying the PSEN1 p.Glu280Ala mutation (often referred to as E280A mutation), which...

I will be interested to see how this holds up in DecodeME. With only 77 cases, the WES looks underpowered to me.

An SF 36 physical function of under 30 is lower than usual in clinical cohorts, I think. IIRC, the pace trial was mid 30s. Similarly, 97.5 is above average for the population. Maybe that's because it's specifically healthy controls, but it looks like there's been no attempt to control for...

I think that's the key point: we need replication. These are all interesting findings. But there are hundreds, if not thousands, of interesting findings out there. Almost none of them have been replicated, so we can't rely on them. What we need are more independent replications, like this...