Naomi Harvey PhD

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Re: @decodemestudy.bsky.social asking; 'Were you told it was in your head, and if so what do these findings mean to you?'
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It’s drawn way out of proportion. It’s not even comparing the same thing. ‘Long Covid’ and Covid induced ME are very different things.

It’s ridiculous! Being blown way out of proportion.

Genome-wide association study of long COVID - Nature Genetics A genome-wide study by the Long COVID Host Genetics Initiative identifies an association between the FOXP4 locus and long COVID, implicating altered lung function in its pathophysiology.

Importantly, whilst the Long Covid study they reference had over 6,000 samples, which is well powered, it was NOT of people with Covid induced ME. It was a wide pool of people simply with long Covid, so it is not directly comparable. www.nature.com/articles/s41...

Long COVID, a condition with similar symptoms and starting, like most cases of ME/CFS, after an infection, has one genetic association near FOXP4 (72), but this was not shared with ME/CFS (p = 0.59 for rs9367106).

I finally checked the DecodeME preprint to verify the ‘no overlap with LC’ claim:

1) DecodeME only had 462 people with C19 caused ME

2) they did not run a separate GWAS on the LC cohort (it’s too small)

3) this is the piece of text people are referring to: it’s just a reference to another study

Importantly, whilst the Long Covid study had over 6,000 samples, which is well powered, it was NOT of people with Covid induced ME. It was a wide pool of people simply with long Covid, so it is not at all comparable.

Long COVID, a condition with similar symptoms and starting, like most cases of ME/CFS, after an infection, has one genetic association near FOXP4 (72), but this was not shared with ME/CFS (p = 0.59 for rs9367106).

Hi 👋🏻 I finally checked the preprint and I see why things were confused:

1) DecodeME did only have 462 people with C19 caused ME

2) they did not run a separate GWAS on the LC cohort

3) this is the piece of text people are referring to, as you say, it’s a reference to another study 👍🏻

It’s what would be called ‘underpowered’. There isn’t enough power in the sample size to detect these kinds of tiny associations. They may very be there, they just can’t be seen in such a small sample.

I believe there was but what I’m saying is it was too small. A GWAS needs thousands of samples. You can do them on 400, but it would be like looking in pitch darkness with a really weak glow stick instead of a powerful lamp.

Posthumous album of singer Kara Jane released on Severe ME Awareness Day - The Sick Times This month, on August 8, the posthumous album of a young singer was released to mark Severe ME Awareness Day. Kara Jane, from Derbyshire in the U.K., had myalgic encephalomyelitis (ME) for most of her...

Today, on Severe ME Awareness Day, @thesicktimes.org is proud to publish this piece by @naomiwhitt.bsky.social sharing the story of singer Kara Jane and her new album, released posthumously by her family. thesicktimes.org/2025/08/08/p...

We cannot take that finding with any real meaning, because the sample size for the ME-LC group was so small. It was only just over 400 people when for this type of analysis you need ten times that, minimum. It’s a meaningless result essentially.

No, the paper didn’t include the rs numbers. There were over 40 SNP’s identified in 8 gene regions.

As you can see from the 23andMe data, each gene has a lot of different SNP’s and at the moment we don’t know which ones are flagged in this study.

You’re welcome, glad it was useful x

In this case it deletes the image as soon as it’s estimated your age. Or at least it’s supposed to, so there’s obviously an element of trust there.

But the way genes work, that weakness that risks ME, may be a benefit for something else. Like maybe it reduces the chances of another disease.

You’re right that we can’t know that from the details we have. But, in terms of the risk for ME, they presumably provide cumulative a weakness in their systems they’re in that increases the risk of the system collapse and disease process.

It did! I’m officially old, lol. Thank goodness they don’t show you the age the system estimates 🤣

🤣 really? That’s so funny! I assumed it would want a copy of my ID which I’m not comfortable uploading to websites given how often they’re hacked.

Ah I don’t I’m afraid, sorry! That sounds like a good idea though.

Just checked and I can’t access them, sorry.

Sure, not sure if my DM’s even work at the moment though as I’ve heard some are blocked by this new ID thing.

Pretty much 😄 it needs proper research funding like other big diseases get.

Not at all! The results help to form a map of the systems that are implicated in the disease. We know these genes 🧬 and the areas they’re linked to are where things are going wrong/being damaged. So they provide a map for future research to focus on.

Huge thank you to Chris Ponting and the @decodemestudy.bsky.social team for all their work on this project, and the work still to come.

These results are a great foundation and provide a lot of validation for patients across the world 🩵

A screenshot of Google news results showing headlines from 7 different news sources about the latest DecodeME results, Google me cfs news 4- Channel 4 ME linked to your genetics - early study indicates 1 hour ago The Guardian Scientists find link between genes and ME/chronic fatigue syndrome 1 hour ago The Times Breakthrough genetic study offers treatment hope for ME patients 1 hour ago The Independent The key genetic difference ME sufferers have from others - and what it means 1 hour ago New Scientist Key genetic differences found in people with chronic fatigue syndrome 1 hour ago The Telegraph ME is a real illness, genetic study shows 1 hour ago Financial Times Chronic fatigue sufferers have different genes, study finds 1 hour ago

Look 👀 at this - five of the news outlets are actually using ‘ME’ in their headline, and four of those are using it exclusively, without CFS!! That’s real change right there.

This is just like genes that increase risk for cancer and Alzheimer’s.

You can develop both without any of the risk genes.

Or you can have all the genes and never get cancer or Alzheimer’s (such as when one identical twin develops a disease and the other does not).

There were more than 40 genes found, in 8 regions.

Genetic risk like this is cumulative, between 0-100%.

Each gene carries a tiny risk, say +6% increased risk of ME, some reduce the risk like -8%.

Each persons individual combination affects their overall risk.

You can think of our bodies like a house. If the hot water system and the windows are not functioning well to begin with, then when a storm rolls in, they’re more likely to be left with damage than a house with strongly built systems.

Yes, the areas the genes are in line up with the areas that go wrong in ME.

This is likely because having wonky genes in those areas weakens their genetic foundations, increasing risk of damage when under immune stress (from infections).

There will be people with very few of these genes that still get ME.

And there will be people (like our own relatives perhaps) who might have a lot of them, but never develop the disease.

It is not diagnostic, and it is not genetically caused.