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I'm not sure what you are refering to? You have WGS data from one set using one technology and WGS data from another set of people using a different technology. Presumably any differences introduced by the setups are handled similarly as they were in DecodeME study (which introduces some loss).

Yes, we won't have to wait too long for replication, at the same time I think it can probably just as well be argued the opposite way, given that the UK biobank samples didn't replicate very strongly in the DecodeME data: It suggests that it's possible to pick up confounders (that aren't...

Should we take the precision Life data from the UK biobank serious? From what we know the DecodeME findings didn't very clearly replicate in the UK biobank sample and others have already mentioned that there's reason to believe that this data represents other things not necessarily representing...

Maybe they would just argue that the possibility of Münchhausen by proxy makes a study unfeasible, because you'd have lower chances of ending up with the cohort you want to study (but Altmann's quote suggests something quite different).

Maybe they are referring to Münchhausen by proxy?

How do the technological methods (not recruitment) between WGS differ and how can this influence replication? I'm asking that because if one was to do WGS on (a subset) of DecodeME participants one could then only compare the results to WGS results in only very few cohorts (for example people in...

I remember looking into the a while ago. Looks like they didn't gather data on whether patients believed they received placebo or the actual drug? I always wonder why researchers would do this, if the ybelieve that the placebo is actually blinding, I see no reason not to.

No need to publish data on the hundreds of people that have undergone a 2-day CPET at your facility if you have this kind of groundbreaking work happening.

Lessons Learned?

Novartis announces both ianalumab Phase III clinical trials met primary endpoint in patients with Sjögren’s disease Aug 11, 2025 Ad hoc announcement pursuant to Art. 53 LR NEPTUNUS-1 and NEPTUNUS-2 are the first ever global phase III trials to demonstrate statistically significant reduction...

I'm no machine learning expert and also no statistician and don't have access to this exact paper, but we're seeing this approach a lot in ME/CFS research and in other papers, which I had access to, there were often large concerns about this approach (not just related to the biology behind...

Yes, that is what I meant. What I meant with a "German DecodeME cohort" would be to just repeat this procedure (supposedly without telling them that you're doing this) and also have a clinical cohort as comparison (that also undergoes the questionnaire screening).

Yes but how would that work? If you'd just include people with MS, or Ank Spond in your ME/CFS cohort you might artificially just get more significant findings but your diagnostic criteria to get there will mean that you're not actually doing anything meaningful anymore. Maybe a certain Fukuda...

Doesn't this already happen? Look at risk genes (or location) and look at spread across the study population. The easiest example would be where you have 2 extremely significant risk genes and see that people on average only have 1, suggesting that there may be 2 different underlying pathways...

But why? People without the risk genes for MS have MS just like those with the risk gene?

I saw that the rate of muscle pain was mentioned (presumably because it was the highest) but didn't find data on the other pain questions (for example the 2 joint pain questions). Presumably this will still follow at some point in time or the data can be requested, but having this data at some...

I suspect that viewing it purely as genetic vs environmental might be to simplistic when you have complex dynamical interactions to account for which have to include stochasticity which may be neither (not genetic nor environmental).

All of them!

I tend to think of it as a "group signal" vs an "individual signal". There will be people in the DecodeME's cohort that don't have any of the signals and there will be healthy people that have all of them. It is more so that on average people with ME/CFS status are as associated with these...

But isn't this then just the argument that is already presented? That genes related to pain can be part of different illnesses associated to pain in various ways?