Michael V Holmes (he/him)

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Michael V Holmes (he/him)

Michael V Holmes (he/him)

@mvholmes

Pharmaceutical physician & epidemiologist, MD/PhD Genentech. Opinions are my own.

Bay Area, USA Katılım Mayıs 2009
1.5K Takip Edilen1.8K Takipçiler
Michael V Holmes (he/him) retweetledi
Anna Hughes
Anna Hughes@EatSleepCycle·
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. timcyclesthecoast.com These are the dates:
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Dave Feldman
Dave Feldman@realDaveFeldman·
With due respect @BioLayne, I again want to point out we can't make the claim that lifelong low LDL cholesterol supports the hypothesis of longevity. If this were the case, those with genetic abnormalities (ie PCSK9 Loss of Function) would have a clear signal of benefit in longevity. I think the data supports these populations do have less ASCVD. But if this reduction in ASCVD came at no trade off in other non-ASCVD diseases, we should definitely see a clear longevity signal in these populations. You're completely right to point out correlation shouldn't be mistaken for causation – but stating something is reverse causation is itself a causal claim. And if holding to Bradford Hill criteria (particularly Consistency), then these data showing lifelong LDL *not* having a signal of longevity is why we can't have high confidence in that conclusion. As always, this is in no way making a counter-causal claim – on the contrary – I'm pointing to why we can't have confidence in LDL having a clear linear, causal association with regard to All Cause Mortality outside confounders and adjustments.
Layne Norton, PhD@BioLayne

LDL Cholesterol Saves Lives! What a fantastic example of cherry picking! Yes this person is right, in ELDERLY people, all cause mortality is greater amongst those with low LDL cholesterol… but WHY? And why didn’t he bring up all cause mortality with LDL levels amongst those who are not elderly? Oh because he doesn’t like that data. This is a textbook example of reverse causality. LDL Cholesterol is not protecting people from disease, but rather people with wasting diseases like cancer are more likely to be resistant to wasting if LDL is not low, indicating that they are not emaciated. But if we zoom out of the elderly and look at lifelong LDL exposure & the risk of mortality, it tells a very different story. Lifelong LDL cholesterol exposure has a LINEAR association with increased mortality, especially from cardiovascular disease (CVD) (PMIDs: 23083789, 38241044, & 30694319). In fact, reduced LDL exposure early in life throughout adulthood can reduce the chance of mortality from CVD by up to 3 times! Gee I wonder why he didn’t mention that. Additionally, the unremarkable results from many statin trials comes from the fact that often these are prescribed after a CVD event or later in life when someone has already done significant damage to their blood vessels. But even with that being the case we do see a clinically significant benefit in lowering the risk of mortality with statin use (PMIDs: 36233511 & 37368941). That said, statins can have some side effects & are not appropriate for everyone & you should speak to a cardiologist about your options if you have high LDL But this is a textbook example of carnivore zealots trying to do f***ery with science & giving you a 3rd of the info to try to trick you into believing their nonsense

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Adam Auton
Adam Auton@adamauton·
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.
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23andMe Research
23andMe Research@23andMeResearch·
Our blog post on the same work, for the lay reader. blog.23andme.com/articles/genet…
Prof. Akiko Iwasaki@VirusesImmunity

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/) medrxiv.org/content/10.110…

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Ninad Chaudhary
Ninad Chaudhary@ninaadsc·
📌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. medrxiv.org/content/10.110…
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Michael V Holmes (he/him)
Michael V Holmes (he/him)@mvholmes·
Thanks to the fantastic Research Team at 23andMe, with a specific shout-out to Dr Jing Shi who impressively led this project to fruition. 🙌
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Michael V Holmes (he/him)
Michael V Holmes (he/him)@mvholmes·
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.
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Xin Wang
Xin Wang@XWang829·
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 (medrxiv.org/content/10.110…), we looked at how data from @23andMe can provide additional genetic evidence. 🧵1/8
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CEL
CEL@CELovegrove·
Excited to share what @drsarahhowles @DominicFurniss @mvholmes, collaborators, and I have been working on: medrxiv.org/content/10.110… We used systematic, regional #MendelianRandomisation & #Colocalisation to identify 3 genetic regions where #calcium, #phosphate, & #KSD colocalise.
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medRxiv@medrxivpreprint

Genetic variants predisposing to increased risk of kidney stone disease medrxiv.org/cgi/content/sh… #medRxiv

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Pradeep Natarajan
Pradeep Natarajan@pnatarajanmd·
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.* nature.com/articles/s4146… @NatureComms
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Michael V Holmes (he/him)
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!🙌medrxiv.org/content/10.110…
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