Peter Adams🇪🇺🇺🇳

1.6K posts

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Peter Adams🇪🇺🇺🇳

Peter Adams🇪🇺🇺🇳

@AdamsBioAging

Director NCI-designated Cancer Genome and Epigenetics Program at SBP, Co-Editor-in-Chief Aging Biology Journal, Road/Gravel/Mtn Cycling, Wolf Pack Cycling.

San Diego, CA Katılım Ağustos 2020
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Peter Adams🇪🇺🇺🇳
Peter Adams🇪🇺🇺🇳@AdamsBioAging·
New road bike. S-WORKS Tarmac SL7, Campy SR wireless and disc, Campy Bora Ultra WTO wheels👍 No excuses now😧
Peter Adams🇪🇺🇺🇳 tweet mediaPeter Adams🇪🇺🇺🇳 tweet mediaPeter Adams🇪🇺🇺🇳 tweet mediaPeter Adams🇪🇺🇺🇳 tweet media
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Joseph Younis, MD
Joseph Younis, MD@YounisJoseph·
If this guy has to remind us one more time that he’s an MD PhD… just change your name to Emdee Peeaychdi it’s easier for all of us
Nick Norwitz MD PhD@nicknorwitz

Peter Misses the Plot: a Swift Debunking 👇 It’s come to my attention that @PeterAttiaMD has come out with an attempted debunk to The Cholesterol Code documentary and, more broadly, the research on lean mass hyper-responders. I won’t mince words: It’s embarrassing. It’s simultaneously arrogant, deeply misinformed, and, as I read it, a transparent avoidance of the facts at hand. It’s posturing, not insight. And I’m prepared to back that up. First, Peter attempts to discredit the documentary, the research on lean mass hyper-responders, and the Lipid Energy Model, on superficial grounds: credentials and authority. He almost exclusively referring to the work as a product of the Citizen Science Foundation (CSF), i.e., @realDaveFeldman: the 'uncredentialed' outsider. He conspicuously avoids discussing the broader teams involved, many of whom carry credentials that would easily meet the standards typically valued in more traditional, credential-focused settings (and exceed his own). Even setting aside myself, an MD-PhD, there is: Dr. Adrian Soto-Mota, MD-PhD, ith the Lundquist team, there are others who have co-authored work in this space, including Anatol Kontush, Ronald Krauss, William Cromwell, and, notably, Peter’s own former head of research, Bob Kaplan. Go figure. Might have been a fact fact for Peter to include: "My former head of research was a coauthor on the Lipid Energy Model paper I'm inadequately trying to debunk." And that’s the short list. I’ll also point out that when I was writing an editorial on lean mass hyper-responders, I reached out to Peter, and he declined to contribute, citing that it was not his area of expertise. He instead referred me to Ronald Krauss at “the expert,” who has now collaborated with us on a couple of projects. So even at a superficial level, what we’re seeing here is avoidance, posturing, and frank hypocrisy. Peter further attempts to cast doubt on lean mass hyper-responders by questioning the existence of the phenotype, which is, frankly, comical. It exists. It is defined by three clear cut points, and people meeting those criteria unquestionably exist. It is also a dynamic and reproducible phenomenon, as demonstrated by multiple experiments, case series, and even meta-analyses of randomized controlled trials that we have published. Peter forgot to talk about those data. No surprise there. Peter also demonstrates a misunderstanding of the Lipid Energy Model, for example by incorrectly suggesting a contradiction between the model and the low triglycerides observed in lean mass hyper-responders. And, more broadly, he reveals a lack of familiarity with the practical realities and constraints of clinical study design. If we are going to lean on authority, then it is fair to ask about experience. To my knowledge, Peter has not conducted clinical trials, and frankly, that gap shows here. At a deeper level, I don’t think Peter understands this physiology or this domain. And behavior like this, particularly when presented under the banner of scientific critique, is exactly the kind of thing that fuels “broader distrust in institutions and experts.” This is a textbook case of the pot calling the kettle black. I could go on, but I think the core point is clear. If further discourse is needed, Peter and his colleagues, including Tom Dayspring, have had ample opportunity to engage, collaborate, and discuss these ideas directly. If they choose not to, that speaks for itself. In the meantime, we’re not going anywhere. And no amount of pedantic posturing is going to change the trajectory of the data. Oh, and two more things… i. For those tempted to fall back on the overly simplistic take that “they’re saying high LDL is good” and “fear mongering about pharma,” or similar caricatures, you’ve entirely missed the plot. And, I have something coming this week. Again, if you interpret it as a pivot, you’ve missed the point entirely, as Peter has. ii. Finally, Peter’s central criticism seems to be that the documentary and our research suggest that even very high LDL cholesterol may not always indicate cardiovascular risk. Well, yes. The alternative is to argue that in all circumstances, at all times, very high LDL necessarily drives cardiovascular disease. This isn’t about discrediting, with a blanket statement, any role of ApoB or LDL in cardiovascular disease. This is about asking important questions at the frontier of science, because the status quo has been wholly inadequate in addressing the problem at hand. That's obvious. At least to some extent, we have been barking up the wrong tree. Anyone with a modicum of perspective can see that. And anyone with genuine curiosity would be willing to engage with the nuance, rather than lecture, avoid, and misrepresent, as Peter is doing here. Lastly: See the Cholesterol Code Documentary. It's on Amazon. And judge for yourself.

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Jamie Timmons
Jamie Timmons@metapredict·
@AdamsBioAging @agingroy When tested for efficacy in large long term RCT, exercise has been disappointing. Never tested alone, it failed in LookAhead to touch any CV endpoint. In HF-Action it failed. Failed in cognition/dementia Warwick RCT. Short term physical prehab/rehab it's more promising.
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Avi Roy
Avi Roy@agingroy·
Your doctor measures cholesterol. They don't measure the molecule that drives most of the remaining risk for heart disease. It's called IL-6. It fuels chronic inflammation. For the first time, drugs targeting it are in massive trials. 7 programs. 4 biological targets. 22,000+ patients enrolled. The injectable IL-6 blockers: → Ziltivekimab (@novonordisk) drops hsCRP by 90%. Three Phase 3 trials running (ZEUS, ARTEMIS, HERMES), 22,000 patients. Results 2026-2027. → Pacibekitug (@Novartis, $1.4B Tourmaline acquisition) cuts hsCRP 85% with one shot every 3 months. The oral pills: → VTX3232 (@EliLillyandCo, $1.2B Ventyx acquisition) is an NLRP3 inhibitor. Reduced hsCRP ~80% in the first week. Combined with semaglutide, it beat GLP-1 drugs alone on inflammation and Lp(a). → MRT-8102 (@MonteRosaTx) degrades NEK7, upstream of the whole cascade. 85% hsCRP reduction. Crosses the blood-brain barrier, dropping brain inflammation 75% in two patients. → Dapansutrile: another NLRP3 inhibitor, Phase 2/3 for gout, diabetes, and post-MI inflammation. The wildcards: → PPV-06 isn't a drug. It's a vaccine that trains your immune system to make its own anti-IL6 antibodies. Phase 2 launching 2026. → Colchicine: already approved, $0.30/day. Proven to reduce heart attacks (COLCOT, LoDoCo2). Most cardiologists still don't prescribe it. The genetic proof: Mendelian randomization (Nature Cardiovascular Research, 2025) shows people born with lower IL-6 have fewer heart attacks, fewer strokes, less diabetes. No increase in infections. Your DNA running a lifelong clinical trial. The next risk factor your doctor will test isn't cholesterol. It's inflammation.
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Jamie Timmons
Jamie Timmons@metapredict·
@agingroy You are completely correct. For two decades the largest science con I'm aware of, has brainwashed an entire generation of scientists working in exercise, metabolism & health. The originators of the defective & oft fabricated data, remain front & centre cell.com/cell-metabolis…
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Alexander M. Wolf
Alexander M. Wolf@AlexanderMWolf7·
@AdamsBioAging @UCSDHealth @MolinaLab1 For me too, but even reversal of some actual function would be much more assuring than the reversal of a marker. After all, hair dye doesn't reverse aging, but reverses a marker of aging.
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Peter Adams🇪🇺🇺🇳
Peter Adams🇪🇺🇺🇳@AdamsBioAging·
Would be nice to have some functional measures to go with the clock data, but even so - seems like an exciting human study. Nice to see it coming from San Diego @UCSDHealth @MolinaLab1 Michael Corley and colleagues
Aging Science News@AgingBiology

An FDA-Approved Tenofovir Alafenamide-Based Antiretroviral Therapy Reduces Biological Age in Healthy Adults: First Human Proof-of-Concept for Retrotransposon-Targeted Gerotherapeutics medrxiv.org/content/10.648…

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David J Glass MD
David J Glass MD@davidjglassMD·
Spare Parts, the play I wrote, was reviewed in the journal Science. I think I'm probably one of the few people to have had papers published in Science, and two plays reviewed there. ;-) science.org/doi/10.1126/sc…
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Peter Lidsky
Peter Lidsky@LidskyPeter·
Do you think we have evidence that the primary cause of aging lies in epigenetics? I don't think we have evidence. We have evidence that epigenetics changes, but it likely changes in all other pathologies, and thus, the phenotype is not specific to aging. We don't think we should treat epigenetic changes in the context of diabetes or infections, we found better ways to go there.
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Peter Adams🇪🇺🇺🇳
Peter Adams🇪🇺🇺🇳@AdamsBioAging·
This is an excellent conceptualisation of epigenetics of aging. Takes a complicated topic and distills it down. Good to see histone H3.3 featured. For our latest contribution on histone H3.3 and aging see here biorxiv.org/content/10.648… @NatureAging
Lifespan@JoinLifespan

This review is one of the most important syntheses in years. It doesn’t just catalog things. It proposes a unifying framework. ie. aging is a breakdown of epigenetic fidelity, the ability of cells to maintain correct gene expression over time...

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Peter Adams🇪🇺🇺🇳
Peter Adams🇪🇺🇺🇳@AdamsBioAging·
@LidskyPeter @NatureAging Great question, Peter. I don’t think that epigenetics sits on top of a hierarchy of aging mechanisms, nor that epigenetic reprogramming is a cure for aging any time soon (specific pathologies maybe, as @davidasinclair is testing in humans).
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Peter Adams🇪🇺🇺🇳 retweetledi
Aging Science News
Aging Science News@AgingBiology·
p16High-expressing immune cells control disease tolerance as a defense and health span-extending strategy cell.com/immunity/fullt…
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Zane Koch
Zane Koch@zanehkoch·
for a while i've had a slight fear that the bluetooth from my airpods could be frying my brain this weekend i pulled the raw data from a $30m government study of 1,679 mice blasted with cell phone radiation and reanalyzed it what i found was...not what I expected? 🧵
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