If anyone would like to join the ride for @TimMcKenna01, please get in touch. It's hard to believe this even happened, but it will be so nice to come together and remember Tim, to ride the way he rode, and raise a few quid for Mind. https://t.co/B2Uu6ejF1R These are the dates:

Yesterday was a hard day at 23andMe, and we said goodbye to a number of tremendously talented colleagues. If people have job openings in the genetics space that they'd like me to share with the impacted folks, please do post here.

Thank you to our customers and the @23andMeResearch team for this work on the genetics of #longcovid https://t.co/1UWyDHuJH6

Our blog post on the same work, for the lay reader.

Much-needed data on the genetics of #longCOVID in a new preprint by @23andMeResearch - GWAS of #LongCOVID identified 3 loci pointing to immune and thrombo-inflammatory mechanisms 🔥 @ninaadsc 1) HLA-DQA1–HLA-DQB 2) ABO 3) BPTF–KPAN2–C17orf58 (1/) https://t.co/0MUr9GbDiA

📌Publication alert: In a preprint from the @23andMeResearch team, we conducted one of the largest GWAS study of Long COVID and identified genetic links of chronic conditions with Long COVID. https://t.co/gbVvbFXJTk

🚴🏼‍♀️In less than 2 weeks I'll be in the saddle towards Barcelona with @DominicFurniss & some colleagues, friends, & his family. #O2B Why? To raise 💰for @Sarcoma_UK Why? Have a look here: 👀 https://t.co/utReSxDWIJ Able to donate? Please do here: 👏🏼 https://t.co/5S5pDNX3K7

Thanks to the fantastic Research Team at 23andMe, with a specific shout-out to Dr Jing Shi who impressively led this project to fruition. 🙌

Importantly, levels of Lp(a) are higly genetically regulated, speaking to the need for therapeutics to lower Lp(a) when levels are elevated. This also identifies the value of genetics in identifying individuals who may have high Lp(a) levels.

We found genetically-predicted independent causal effects of Lp(a) on MACE once taking into account the effects of LDL-C or apoB. The implications are that people with elevated Lp(a) are likely to benefit from Lp(a) lowering therapies irrespective of their LDL-C or apoB levels.

Interestingly, for some conditions (eg. aortic stenosis, peripheral arterial disease and dilated cardiomyopathy) the Lp(a) effect was of larger magnitude than that of LDL-C or apoB, when each was scaled to a comparable relative risk of major adverse cardiovascular events (MACE).

We found the effects of Lp(a) to be predominantly confined to cardiovascular conditions. This speaks to the probable absence of target-mediated adverse effects that Lp(a)-lowering therapies will demonstrate.

In a preprint from the @23andMeResearch team, we used Mendelian randomization to explore the genetically-predicted causal effects of Lp(a) on a range (n=489) of human traits and diseases.

Previous papers have shown that drug targets with supporting genetic evidence can have twice the success rate when reaching clinical trials. In our most recent paper ( https://t.co/Rq5ZVaOwgj), we looked at how data from @23andMe can provide additional genetic evidence. 🧵1/8

Excited to share what @drsarahhowles @DominicFurniss @mvholmes, collaborators, and I have been working on: https://t.co/yjevV8I9O5 We used systematic, regional #MendelianRandomisation & #Colocalisation to identify 3 genetic regions where #calcium, #phosphate, & #KSD colocalise.

10-year ASCVD risk prediction leads to older individuals being prioritized for statins missing opportunities for earlier risk recognition & prevention. Our work led by @tigerstatdoc uses genetics & dynamic risk factor trajectories toward intersecting risk *early.*

A preprint from the 23andMe Research Team exploring the multi-ancestry genetics of diarrhea during acute Covid in which we find evidence that IBS subtypes influence risk. Kudos to the 1st author, Ninad Chaudhary @ninaadsc, a postdoc in the Research Team!🙌 https://t.co/lof1kmI43g

A preprint from the @23andMeResearch Team on the genetic architecture of sporadic and recurrent miscarriage and where we evaluate potential causal effects of modifiable exposures TL;DR: we identify 11 novel GWAS loci and evidence smoking and caffeine potentially increase risk

A new preprint from The 23andMe Research Team showcasing our capabilities in recall-by-genotype initiatives. Here we use recall-by-genotype to facilitate enhanced phenotyping in order to characterise a LoF variant in MAP3K15 associated with T2D

In 2018 we published a non-linear Mendelian randomisation (NLMR) study in @ObesitySociety and it is now clear the method we applied is deeply flawed, so in October we published a Perspective correcting it. A 🧵on the cautionary tale of NLMR https://t.co/GZ5D071dEZ