There needs to be more clarity about what the #NHS10YearPlan offers for patients and what “good enough” looks like in terms of access, along with careful co-design and evaluation of the detail of each of the three shifts.
Full paper: ths.im/4b6oPWp
THIS Summary: ths.im/49oDU4k
Maybe we should stick to a message this simple.
We’re delighted to announce that Professor Trish Greenhalgh @trishgreenhalgh.bsky.social will deliver this year’s CPM Annual Lecture, 'Personalised Medicine: A Primary Care Perspective'
🗓 28 April 2026 | 📍 Maths Institute, Oxford
Find out more and register here: cpm.ox.ac.uk/event/cpm-an...
again- Critiquing language in a press release for @smclondon.bsky.social is part of responsible public engagement. I think we may have reached end of useful exchange in this forum
@emmylooroll.bsky.social said "Gene editing is absolutely a possibility, as is modifying downstream pathways. Genes aren’t all doom & gloom!🧬"
Yes for most of the population it will be modest, looking at the extremes of risk for a population doesnt tell you what the shift in probability would be with intervention for most.
And of course, engineering everyone toward APOE e2/e2 is not entirely benign: that genotype is associated with increased risk of other conditions, which would be expected to rise if such gene therapy were implemented at scale.
Gene therapy in ~95% of the population is the naive concept here: manipulating the genomes of most people for only a modest shift in prob. This why, in public discussion, it is more appropriate to talk about genes as modifying risk alongside other factors, not singular “causes” to be edited away.
Have enjoyed this exchange with you and your coauthors but back into my bluesky dormancy for now!
Publics need to understand not just that the gene matters but how much lifestyle still matters, especially for those who cannot change their genotype. science communication has a responsibility to preserve that distinction
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.
Calling the most common human variant a 'risk allele' is methodologically correct but nosologically problematic—it redefines disease categorisation in a way that obscures rather than clarifies the distinction between genetic susceptibility and modifiable risk pathways.
🧬 How well do ethnicity labels actually work in genomic medicine?
Our new blog explores the challenges - and the pathways to more inclusive, meaningful data.
➡️ cpm.ox.ac.uk/thinking-out...
#Genomics #HealthEquity #DiversityInResearch
You can find out more about the competition and enjoy the amazing winning entries from previous years here: cpm.ox.ac.uk/art-and-scie...
Our 2024–25 Annual Report is now live!
Reflecting on a year of collaboration, engagement, and impact at the CPM. Explore our flagship events, annual lectures, and creative outreach.
➡️ Read more here: cpm.ox.ac.uk/wp-content/u...
well maybe we can agree that epi language and public communication language may need to differ. Like i said for SMC we can say 99% of sunburns are caused by having fair skin. but having fair skin is not a "disease state" causal of burn—sun is still the driver which could be avoided.
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
For public and policy discussion the useful question is how much a variant shifts risk and whether that helps with prediction or intervention, not simply whether we label it as causal from an epidemiological perspective
My view it's more helpful to say different alleles modify risk. in every day language [and I was commenting on press release] 'cause' implies that if you could alter gene you would eliminate disease, which is not how multifactorial conditions work.
I'm really looking forward to this. @CPM we have been fortunate to have absolutely stellar annual lecturers- see here for recordings of the last few years: cpm.ox.ac.uk/series/cpm-a... and @trishgreenhalgh.bsky.social will be no exception
I'll be giving the Annual Guest Lecture for the Oxford Centre for Personalised Medicine. On 28th April 2026 at 5.30 pm.
‘Personalised Medicine, a Primary Care Perspective’.
Open to all.
cpm.ox.ac.uk/event/cpm-an...
And 👏 to Honourable exception 🤭
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
Brilliant! I did not know this paper so thanks from infrequent bluesky user for this nugget reposted.
Have you got a patent application in? Have you been to Sandhill Road in Palo Alto for funding? Why not???
BTW add the strong prediction that the kid will drink milk!
We get the politics the few pay for.
#democracy - it would be a good idea
www.theguardian.com/politics/202...
Worried that using ChatGPT harms the planet? A new analysis shows each query uses less energy than a Google search – and far less than lighting a bulb or streaming TV.
@eastangliabylines.co.uk
“This thing is definitely bad for us but no one can say what it is”
My test is 99% accurate and predicts that your child will grow to between 5 and 6.5 feet have an IQ between 80 and 130 and live 60-90 years. AND I don’t need any DNA to do my test…
