Ronald A. Primas,MD,FACP,FACPM @Primas

A patient pointed me to this today. Honored to be included and grateful for the kind mention. It's encouraging to see #longevity medicine receiving thoughtful recognition as the field continues to evolve. spannr.com/articles/longe…

@SecKennedy @POTUS @SecRollins Reach out to @GaiaHerbs . They have an incredible regenerative program that us very very innovative. Great regenerative model.

I had the incredible pleasure of being on the Thresh Architects Podcast and having a wonderful conversation with Zach. All things LIGHT! We covered it ALL!! Go give this episode a listen, it was one of my favorite podcasts I’ve been on! The Invisible Light Disease That's Plaguing Our Homes | Jonathan Jarecki youtu.be/AFb_VKtq_zw?is…

@agingdoc1 Love this!

@NYPDPC @NYPDnews We thank him for his service🙏🏽

Well done @JamesPeyer ! Congrats to you and the team!

Nir Barzilai @NirBarzilaiMD

a week ago

After years of big pharma's attempt to target AMPK as an exercise mimetic, this one couples it's actions together in a very promising way!

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This is consistent with a perspective I've shared with patients for many years: if we can slow the biological processes of aging, we may simultaneously reduce risk across multiple age-related diseases, including cancer.

David Sinclair @davidasinclair

a week ago

Paper indicates cancer rates are increasing because our lifestyles are accelerating biological aging. Another reason aging is worth tackling

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@GadSaad Congratulations

@Jonathanjarecki Cant wait.

@agingdoc1 Can't wait to hear it my friend

I'm excited to share the very first episode of Longevity for Dogs, the new podcast from the Dog Aging Institute @dogaginginst . youtube.com/watch?v=6-v594… For our inaugural episode, I sat down with my longtime collaborators and friends, Kate Creevy and @DPromislow , to tell the story of how the @DogAgingProject began, why we believe aging biology can transform veterinary medicine, and what we've learned from studying more than 50,000 companion dogs. We discuss: • Why aging itself is the biggest risk factor for most chronic diseases in dogs • The scientific rationale for targeting the biology of aging rather than individual diseases • The origins of the Dog Aging Project and the challenges of launching a nationwide longitudinal study • The development of the TRIAD rapamycin clinical trial • What we've learned from following tens of thousands of dogs over time • Why healthspan—not just lifespan—is the goal • The vision behind the Dog Aging Institute and where the field is headed next This work has always been grounded in open science, collaboration, and a shared commitment to improving the lives of companion dogs and the people who love them. If you're interested in aging biology, veterinary medicine, or simply want your dog to enjoy more healthy years, I hope you'll check it out. And if you're already part of the Dog Aging Project community—thank you. None of this would be possible without you. 🐕❤️

Julian is one of the best longevity podcasters out there, and Adam and Nathan are heading one of the most powerful longevity organisations. Have a listen!

Julian Issa @juliankissa

3 weeks ago

Our vitalist / longevity special with @realNathanCheng and @adamgries is out now on The Beyond Tomorrow Podcast

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150 million Americans struggle with poor sleep. Current insomnia treatments fail more than 70% of patients. ARPA-H launched REST to move sleep medicine beyond tracking and into treatment. We are looking for leading teams across sleep, neuroscience, biosensing, AI, engineering, and neuromodulation ready to take on one of the biggest drivers of health. Sleep medicine needs a wake-up call. Register for Proposers’ Day. arpa-h.gov/explore-fundin…

Getting to the root of age-related diseases. By studying a rare accelerated aging genetic disorder, gain-of-function mutations of DNMT3A were found to be causal. DNA hyper-methylation was then linked to stem cells dysfunction and multiple age-related diseases (blood, bone, metabolic). Work in mice and humans. @NatureGenet nature.com/articles/s4158…

NEW PREPRINT: Scientists may have found direct evidence that aging is driven by the loss of cellular information, not just the accumulation of damage For decades we've focused on what aging cells accumulate. This paper focuses on what they lose: Information. Using a new technology called SeqTag, researchers measured gene expression, chromatin accessibility, and histone modifications in the same aging cells. What they found was striking: the regulatory systems that tell cells who they are become increasingly out of sync with age. The authors call this "molecular asynchrony." As cells age, chromatin structure, histone marks, and gene expression begin drifting apart. Regulatory entropy rises. Repressive chromatin erodes. Cells become less certain of their identity and more likely to drift toward alternative fates. This is what the Information Theory of Aging (ITOA) states: that aging occurs when cells lose epigenetic information, the instructions that tell the genome how to maintain youthful function. DNA may remain largely unchanged, but the system that reads it gradually loses fidelity. What's remarkable is that this paper doesn't just describe this phenomenon. It quantifies it. The authors measure increasing regulatory entropy, loss of H3K27me3-mediated repression, erosion of heterochromatin, weakening lineage fidelity, and increased cell-fate drift during aging. In progenitor cells, the barriers that normally preserve cellular identity become progressively weaker with age. Mechanistically, the study argues that aging is associated with increasing molecular asynchrony between chromatin accessibility, H3K27ac/H3K27me3 remodeling, and transcriptional state. This decoupling is accompanied by increased regulatory entropy, loss of repressive chromatin architecture, and weakening of lineage constraints. Genes affected are those involved in chromatin organization, DNA damage, and Wnt signaling, consistent with ITOA. Importantly, the authors provide quantitative evidence that age-related heterochromatin erosion lowers the energetic barriers that maintain cell identity, offering a potential mechanistic link between epigenetic information loss, cell-fate drift, and late-life disease susceptibility 👏

@davidasinclair Well done my friend!!! Congrats to you and the team!!!

@TulsiGabbard Glad to hear the surgery was successful. Recovery is often the hardest part, but it sounds like Abraham is on the right path. Wishing him strength, comfort, and a full recovery. Keeping you both in my thoughts and prayers.

Well said. While we gather this Memorial Day weekend with family and friends, enjoying BBQs, laughter, and the freedoms we often take for granted, let us pause to remember the brave men and women who made the ultimate sacrifice so that we may live free. Their courage, duty, and selflessness are the foundation upon which this nation stands, and we remain forever indebted to them. May we never forget those who gave everything in defense of freedom and the values we hold dear. May they all rest in peace. The more you sweat in peace, the less you bleed in war.

Glycine is a powerful sleep enhancer. 3g of glycine before bed: ⬩Increases subjective sleep quality ⬩Decreases time to fall asleep ⬩Increases cognitive performance the next day ⬩Makes falling asleep easier ⬩Lessened daytime sleepiness in part due to glycine's ability to help regulate the circadian rhythm in the brain via the NMDA receptor in the SCN.

Dalton (Analyze & Optimize) @Outdoctrination

a year ago

Glycine is a powerful sleep enhancer. 3g of glycine before bed: ⬩Increases subjective sleep quality ⬩Decreases time to fall asleep ⬩Increases cognitive performance the next day ⬩Makes falling asleep easier ⬩Lessened daytime sleepiness in part due to glycine's ability to

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