Agree. It’s a point I’ve repeatedly made. I had a good job, now I can’t do it. If there is a moral duty to get people back into work there’s a moral duty to invest in treatments so they can and in adequate care and support until those treatments are available.
Will you be looking at stratified analysis by severity to see if this changes the genetic signals found or the strength of them? The Data Analysis plan seemed to indicate 2k was enough to do this for co-morbidities.
I suppose you could say they’re a bit like seagulls. Good at regurgitation but you wouldn’t depend on them for reliable deduction.
Well crafted promote definitely help, out of the box their system prompts can give a tendency to be sycophantic, although there are some recent examples of Gemini...
Absolutely this. These tools can create plausible sounding results from anything.
They’re great when used responsibly, for anything which is verifiable, as they can be trained and trained to ensure they behave. That’s why they often make good information retrieval, summarising, code...
There’s more information in the Data Analysis Plan which may help
https://www.decodeme.org.uk/our-gwas-data-analysis-plan/
Check the section of the PDF on Ancestry
https://www.decodeme.org.uk/app/uploads/2024/03/2024-03-15_DecodeME_Data_Analysis_Plan_v2_final.pdf
I’d skip the AI stuff for speculative answers like this. Probably safe to say we don’t know yet and read the great blog post
https://www.decodeme.org.uk/x-marks-the-spot/
Or listen to it if that’s easier for you
https://u.pcloud.link/publink/show?code=kZqX2W5Z4yR8YkHhWUzzghs07AaMamsl6mW7
This seems pretty fair and well edited. The way they have pieced this together is quite entertaining with some selective quoting used to skip the more questionable claims by certain people…
And increased ZNFX1 equates to decreased inflammation or inflammatory signals? So is this something ‘anti-inflammatory’ popping up again?
NLRP3 is apparently expressed predominantly in macrophages. And more ZNFX1 would suppress/inhibit activation here?
I think I see what you mean. Learning about these genes there seems to be a lot about what is let into or out of cells, cleanup and communication between them (particularly neurons).
So in a complex and busy environment having your doormen and your maintenance crews behave just a little ‘off’...
There seems to be lots of things around cell transport and vesicles and synapses cropping up. So could this be not so much about pathogen entry but just subtle differences in neurotransmitter behaviour? One of the many little probabilities shifting slightly which when combined under certain...
Indeed. It is annoying that such rigour is being ignored with empty arguments and in some ways it would be nice to have them corrected in reporting. But tbh for now I don’t think it’s the message people are hearing and I don’t think Chris and co should worry too much about it in their media...
I’d add that the project very clearly did not disclose its criteria for exclusion. This caused a problem with reducing numbers for the GWAS but also with parts of the ME/CFS community because people were not being asked for saliva samples and they did not know why. This is key for the argument...
I’m also extra cautious of any implications of things I’ve come across, as like you @V.R.T. I didn’t do biology past GCSE, made bad decisions with things like smoking and am learning enough to spot patterns and over-enthusiastically link them to hypotheses!
ME/CFS
M/C
Mornington Crescent…...
Definitely. It’s something we’re aware of but the message that most of the public are hearing seems clear: major development in disease I may have vaguely heard about or know someone who has it but haven’t really understood much about.
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