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@dave30th I find it much easier listening to podcasts than watching videos. Now that you’re doing more videos (which is great) have you considered doing them as podcasts too – ie, using the he same audio as the videos and uploading them to podcast platforms? I know you’re not much of a techie...

Exactly. The results validate the selection process!

This the letter in question: https://www.thetimes.com/comment/letters-to-editor/article/times-letters-supreme-court-gender-ruling-d270xjch2m Also shared on 'DecodeME in the media' thread: https://www.s4me.info/threads/decodeme-in-the-media.45467/post-631872 [Edited to correct link to thread]...

My (slightly edited) letter in The Times today, and one from Andrew Millar: https://www.thetimes.com/comment/letters-to-editor/article/times-letters-supreme-court-gender-ruling-d270xjch2 Not sure who Andrew Millar is. BlueSky post sharing the letters:

I understand that this is the case but I’ve been struggling to understand why. From the preprint: “Linking GWAS variants to causal genes that may provide biological insights and medical applications remains a challenge for the field (43).” 43. Qi T, Song L, Guo Y, Chen C, Yang J. From genetic...

Statement from BACME: https://www.s4me.info/threads/united-kingdom-news-from-bacme-british-association-of-clinicians-in-me-cfs.7900/page-27#post-631515 Surprisingly good!

I sent your hypothesis paper to Helen Lachmann but no reply. Not sure how well you know her but I’m wondering if she or anyone in her team at the NAC would be interested and in position take things any further.

Not that I’m aware of. But there is quite a lot of evidence that suggests that it’s wrong: This prospective study found that psychological symptoms were not predictive of developing ME/CFS: https://pubmed.ncbi.nlm.nih.gov/33367564/ I think Jason may have done other prospects studies with...

On replicatiion, would it have been useful to exclude, say, 10% of the patient samples from the initial GWAS, and then use those samples to try to replicate only the genetic signals that reached statistical significance? Wasn’t something like that done in a previous study? Am I right in...

Donate to Build on the Work of DecodeME: https://www.s4me.info/threads/donate-to-build-on-the-work-of-decodeme.45500/

I think you’ve missed this one: Direct link the the Daily Mail article: https://www.dailymail.co.uk/health/article-14976305/Scientists-chronic-fatigue-syndrome-breakthrough-cause-effective-treatment.html

Thanks for important correction. I will redo my BlueSky post! Edit: now done: I hope that’s accurate in simple terms.

A trick I discovered is that if you google an FT headline, in this case “Chronic fatigue patients have different genes, study finds”, and click on the FT link from the Google search results, you can read the article for free without signing in. NB if you then copy and paste the URL of the FT...

Further to comments above, I’m very grateful to Tessa Munt for her advocacy and support but unfortunately she doesn’t appear to understand the science. The genes are not “unique” to people with ME/CFS as she suggests and there would be absolutely no point in anybody being tested for these genes...

I’ve been stranded at sea for a long time. I’m hoping that this data will help to get me to dry land!

I’ve posted a response to this on the preprint thread as it’s about the study design and interpretation of the data...

These comments are from the media coverage thread but I’m posting here as they are relevant to the study design and interpretation of data: Given that the study has found genetic associations, does the fact that the study used self-reported symptoms not strengthen the result? I can see that it...

Daily Mail “Scientists FINALLY crack mystery of chronic fatigue syndrome - major breakthrough sparks new hope”: https://www.msn.com/en-ae/news/other/scientists-finally-crack-mystery-of-chronic-fatigue-syndrome-major-breakthrough-sparks-new-hope/ar-AA1K2iLr it’s a shame they call it chronic...

I think we need to be cautious about suggesting some people don’t have ME/CFS, when we don’t know what ME/CFS is physiologically. If someone meets a particular definition, then they have ME/CFS by that definition, even if it transpires that there are subgroups who have different illnesses...

I’m struggling to keep up so apologies if this question has already been asked but I’m wondering if the published data can tell us whether ME/CFS is likely to be one disease which involves the immune system and nervous system, or whether it is possible/likely that there may be two diseases – one...