The everyday understanding of cause and the epidemiological understanding of cause are similar. Virtually ubiquitous exposures can obviously have large contributions to disease in the population.
Gene editing is absolutely a possibility, as is modifying downstream pathways. Genes aren’t all doom & gloom!🧬 The public don’t need patronising or protecting, they want to see that good science is being done and real progress is happening. Nice chatting Anneka, over & out! 😁 3/3
yep and as I said, fine in that setting- it was the press release I was responding to-'most alzheimer's cases linked to single gene' we lose the nuance that for 95% population carrying E3/E4, modifiable lifestyle factors remain the dominant lever for prevention.
Gene editing is absolutely a possibility, as is modifying downstream pathways. Genes aren’t all doom & gloom!🧬 The public don’t need patronising or protecting, they want to see that good science is being done and real progress is happening. Nice chatting Anneka, over & out! 😁 3/3
The whole point of our paper is to challenge the current line of thinking - APOE is clearly a predominant cause for almost all AD, and we should be looking at APOE based interventions. 2/3
Except that there is mostly extremely poor, and at best, very mixed, evidence for almost all lifestyle risk factors for AD, other than educational attainment. 1/3
I think we're talking difference between "cause" in epidemiology and what pple understand in everyday speech. IMO "cause" misleads into thinking gene more deterministic than it is. for single dominant risk like smoking, "cause" is fine, but for multifactorial conditions "modifies risk" is better
3/3: I think you’re trying to contrast modifiable (sun exposure) vs non-modifiable (fair skin) risk factors (??), potentially implying genes or their downstream effects aren’t modifiable. But we know they are, and both modifiable and non-modifiable risk factors remain causes of disease.
2/3: A ‘cause’ doesn’t require the exposure to be the sole driver; it simply means it changes the probability of disease. You can call fair skin a cause of sunburn, just as you can call APOE a cause of AD.
1/3: Well, we did write the paper to be published in a scientific (epi) journal… 🤣 And respectfully, that example actually reinforces my point rather than undermines it: having fair skin modifies your risk of sunburn—just like APOE modifies risk of Alzheimer’s. Hence both are causes of disease.
A ‘cause’ doesn’t require that the exposure be the *sole* driver, it simply means it changes the probability of disease. You can still call fair skin a cause of sunburn, just as you can call APOE a cause of AD. 2/2
My fave commentary on our paper in the Mail last week
Interested to know what @alucassen.bsky.social uses as a definition of causation though!
Here's mine: ajph.aphapublications.org/doi/full/10....
Further reading WRT the topic: zenodo.org/records/1796...
Thanks for waking me out of bluesky inactivity! Presume this on the back of my SMC quote? My point was that if >95% population have a genotype, it is pretty meaningless to talk about it being causative of disease. Quite happy with apoE alleles *modifying risk* of Alzheimer’s
In epidemiology, ‘cause’ literally just means ‘modifies risk’—it never implies determinism. Both AD and smoking-related lung cancers are multifactorial, and in both cases most exposed people don’t get the disease. So I’m not entirely sure i follow. We’ll have to agree to disagree :-)
’Cause’ doesn’t imply you can eliminate disease, for alleles or any other risk factors. Sticking with the smoking analogy, if we wipe out all smoking tomorrow, some people will still get lung cancer. Smoking is still the biggest cause of lung cancer. I think you’re thinking more about prediction?
And if a genotype (or any other risk factor) *modifies* risk of disease, it is, by definition, causal? I’m not sure I understand your comment Anneke, would be keen to try understand what you mean! :-)
Out now!!
www.nature.com/articles/s44...
Intro to this paper pictured below
Huge thanks to collaborators @neilmdavies.bsky.social, @emmylooroll.bsky.social at @uclbrainscience.bsky.social & Sami Heikkinen and Mikko Hiltunen at @uniuef.bsky.social ...
#endalz #episky #medsky
Causality is about whether changing the factor changes the risk, not how frequent it is… If everyone in the population started smoking tomorrow, smoking would still cause lung cancer—it would just be ubiquitous. A highly prevalent genotype can still be causal for disease.
Last chance to sign up for our MR course next week folks!
jesus christ
⏰Post-doctoral #qualitative job alert! (closes 14/9/25).
@uclpsychiatry.bsky.social is recruiting for a #Qualitative Post‑Doctoral Research Associate to join our #suicide & #selfharm research team on a @nihr.bsky.social grant investigating acceptability of close obs www.ucl.ac.uk/work-at-ucl/...
I wonder if they know their pics are being sent to you 😂 so strange!
Impressive work by our *brilliant* MSc student Christina Kushnir on the potential for anti-inflammatory targets for reducing Alzheimer's disease risk.
www.medrxiv.org/content/10.1...
New 29 month postdoc position available at Newcastle with Dr Oli Shannon for an exciting new project funded by ARUK 🥳
🔬 Investigating whether following UK-specific dietary guidelines is linked to lower dementia risk
shorturl.at/6WZFd
Our in-person Mendelian randomisation course is back at University College London this autumn. Join us in Bloomsbury, 16th-18th September 2025.
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Guest lecturer: Eleanor Sanderson
onlinestore.ucl.ac.uk/conferences-...
Postdoc in dementia research at Karolinska Institutet, Solna, with Dr Shireen Sindi and Prof Miia Kivipelto exploring sex differences and biomarkers in Alzheimer’s disease. Closing date: 6th July
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University of Exeter (David Llewellyn, Janice Ranson), and University of Cambridge (Tim Rittman).
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📧 Check out the job advert above and please reach out to me via email (oliver.shannon@newcastle.ac.uk) if you have any questions
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👍 You will be working as part of a multidisciplinary team spanning Newcastle University (Oli Shannon, Rebecca Townsend, Dr Andrea Fairley, Emma Stevenson), University College London (@emmylooroll), University of Edinburgh (Graciela Muniz Terrera, Sarah Gregory)...
⭐ We're hoping to hire a dedicated, collegiate and enthusiastic researcher
💻 Analysing data from large observational cohorts
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New 29 month postdoc position available at Newcastle with Dr Oli Shannon for an exciting new project funded by ARUK 🥳
🔬 Investigating whether following UK-specific dietary guidelines is linked to lower dementia risk
shorturl.at/6WZFd
