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Did Eating Too Many Sardines Increase Homocysteine?

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Can This New Enzyme Reverse Aging?

This is rather technical.


Researchers at Revel Pharmaceuticals and Calico Life Sciences have engineered CMLase, an enzyme that removes carboxymethyl-lysine (CML) — a glycation product long considered permanent damage on our longest-lived proteins. In this video I explain the details behind this discovery and what it means for the aging field.

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official website — https://www.thesheekeyscienceshow.com/

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through PayPal — https://paypal.me/sheekeyscience?coun… through Patreon — / thesheekeyscienceshow TIMESTAMPS 0:00 – Intro: what CML is and why it seemed irreversible 2:25 – How they made the enzyme 6:20 – Human tissue data 7:40 – My thoughts and limitations Paper: Trabosh et al., Nature Communications, 2026 — https://doi.org/10.1038/s41467-026-75… note that The Sheekey Science Show is distinct from Eleanor Sheekey’s teaching and research roles. The information provided in this show is not medical advice, nor should it be taken or applied as a replacement for medical advice. The Sheekey Science Show and guests assume no liability for the application of the information discussed. Icons in intro; “https://www.freepik.com/free-photos-v…“Background vector created by freepik — www.freepik.com.
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TIMESTAMPS

Synergistic senolyticregenerative therapy significantly extends healthspan and lifespan Translational Medicine

Current barriers to achieving radical life extension include the inability to use syngeneic, youthful mesenchymal stem cells (MSCs) and the anti-regenerative effects of senescence-associated secretory phenotype (SASP) factors. We aim to overcome this by a combination approach in which senescent cell burden is reduced utilizing SenoVax™ a dendritic cell based senolytic immunotherapy combined with syngeneic pluripotent stem cell derived MSC.

We induced hepatic injury and accelerated aging using two established murine models: carbon tetrachloride (CCl₄) mediated liver injury and doxorubicin induced systemic senescence. Animals were treated with control, SenoVax, pMSCs or the combination. Outcomes included biochemical and histologic indices of liver injury, circulating and tissue biomarkers of senescence (IL-11, YKL-40, IL-6, IL-23 R) and regeneration (Klotho, FGF-2, neo-VEGF, GDF-11).

Both CCl₄ and doxorubicin induced a robust senescent phenotype characterized by increased pro-inflammatory and pro-fibrotic mediators and downregulation of regenerative biomarkers. Combined senolytic and pMSC therapy outperformed mono therapies and produced clear synergistic benefits, including significant biochemical improvement of liver failure parameters, reversal of accelerated aging features, and restoration of regenerative signaling pathways. Senolytic monotherapy yielded partial improvements, while pMSCs alone showed limited activity in the presence of a high senescent-cell burden.

Jaron Lanier: The Singularity Is A Religion for Geeks

Fifteen years ago, I sat down with the father of virtual reality, and he told me the Singularity was a religion for geeks.

I disagreed with him. To his face.

Jaron Lanier was no technophobe. He built the tech. He just refused to worship it. In 2011, that made him an outlier. Everyone in my orbit was mapping exponential curves and setting dates for digital immortality.

Now look at the culture around #AI.

We have prophets and prophecies, heretics and true believers, people who genuinely expect a machine god to arrive and solve death, meaning, and the economy on our behalf. Lanier saw the shape of that faith before most of us would admit it was a faith at all.

I still think he was wrong about parts of it. I also think he was early on the part that matters most: technology is the How. It was never going to answer the Why or the What. That is the work a religion does, and for a lot of brilliant people the #Singularity quietly became exactly that.

Helping cells find their perfect match

Researchers including those from the University of Tokyo found a way to optimize how cells bind to small packages they release called extracellular vesicles. By coating the vesicles with metal ions, they made cells and their corresponding vesicles stick together more strongly than they would naturally. This reduced the time needed for cells to capture their own vesicles, even in mixtures containing billions of other vesicles. The team demonstrated an application of this by improving two kinds of blood tests for cancer cells, and it could have downstream applications in drug delivery, rejuvenation and more.

Anyone afflicted with cancer will often face a long and difficult journey. The early stages of any medical intervention will necessarily include a biopsy, tissue sample collection, such as a liquid biopsy which uses a blood sample. These aren’t perfect, but medical researchers are trying to improve them, with one such method being how to amplify the signals indicating cancer cells. This should be possible as all cells release tiny telltale particles known as extracellular vesicles. Professor Keisuke Goda from the Department of Chemistry at the University of Tokyo and his team members found a way to engineer extracellular vesicles in a way never seen before which could improve liquid biopsies and aid in some other medical and research applications in drug delivery, rejuvenation and more.

“Each extracellular vesicle is only about a thousandth the width of a human hair and carries a tiny sample of material from the cell that made it like a little molecular ‘message in a bottle.’ Cancer cells release these packages too but finding them in blood is like searching for a few specific grains of sand on a beach,” said Assistant Professor Tianben Ding from the Department of Chemistry. “So, we developed a simple way to make both the packages and the cancer cells much easier to find. By coating the packages with tiny amounts of lanthanide metals, we made matching packages and cells stick together over 25 times more strongly. This provides a versatile platform that can improve how engineered extracellular vesicles interact with their target cells, enabling applications ranging from cancer detection to targeted drug delivery and rejuvenation.”

Scientists found three gene variants that may change when Alzheimer’s begins

One of the strongest findings involved a variant in CCNG1, which was associated with an earlier age of dementia onset. Carriers of the risk allele developed dementia roughly a decade earlier than those without it.

The same variant was also linked to higher levels of TDP-43, a protein implicated in several neurodegenerative diseases, and signs of accelerated brain aging on MRI scans.

The researchers also found that a variant in RHOJ was associated with biological markers of more severe Alzheimer’s disease. Individuals carrying the risk allele had higher levels of total tau and phosphorylated tau 181 in cerebrospinal fluid and a lower Aβ42/Aβ40 ratio—changes commonly associated with Alzheimer’s pathology.

Age-Reversing Stem Cell Treatment Succeeds in Human Trial | Dr Koji Tanabe

Discover how original Yamanaka co-author Dr. Koji Tanabe uses automated iPSC cassettes and autologous stem cell secretomes to reverse cellular aging and repair damaged joints.

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In this landmark episode of Modern Healthspan, we sit down with Dr. Koji Tanabe, founder and CEO of iPS, Inc. and co-author of the historic 2007 Nobel Prize-winning paper on human-induced pluripotent stem cells (iPSCs). Dr. Tanabe shares how twenty years of technological advancement have raised iPSC reprogramming efficiency from under 1% to over 80%, while cutting manufacturing costs through automated cleanroom cassettes. We discuss practical longevity applications available today, including autologous stem cell banking from a simple blood draw, secretome extract therapies for joint and skin rejuvenation, and Japan’s approval of iPSC-derived heart tissue. Finally, Dr. Tanabe offers a critical scientific perspective on in vivo partial reprogramming, detailing the cellular identity loss and tumor risks associated with OSK gene delivery. Watch now to learn where stem cell age reversal truly stands today.

📚 Chapters.
00:00 — How the 2007 Yamanaka Breakthrough Reverses Cell Age.
09:58 — Cellular Reprogramming in Nature (Salamanders & Limbs)
15:01 — From 1% to 90%: Scaling Transfection Efficiency.
19:57 — Mass Production: Automated Cassettes for Stem Cells.
24:57 — Slashed Costs: Disrupting the $10M Treatment Price Tag.
29:58 — Retrovirus Danger: Preventing Toxic Contamination.
35:01 — Japan’s Law: Safety Testing & Rejuvenation Services.
39:58 — Next-Gen Immune Therapy: iPSCs vs Cancer & Aging.
44:59 — The In-Vivo Reprogramming Risk: Why It Fails.
49:59 — Infinite Cellular Supply: Pluripotency’s Power.
54:57 — Beyond Reprogramming: Solving the Extracellular Matrix.

Medical Disclaimer:

Senescent cell heterogeneity in brain aging and neurodegenerative disease

This review by Graves et al. synthesizes emerging evidence that senescent brain cells are heterogeneous, dynamic, and context dependent, highlighting determinants of diverse programs and emphasizing integration of single-cell-and spatial-omics with mouse studies to facilitate mechanistic insights and possible therapeutics.

Inside the World’s First Age Reversal Trial | Lifespan with Dr. David Sinclair — S2, Ep. 4

At Lifespan, our mission is to help you and your loved ones live your longest, healthiest lives while supporting medical research into breakthroughs to improve all lives.

We’re building the world’s largest longevity community: Join us at https://lifespan.com.

Follow us on YouTube, Apple, and Spotify for new Lifespan episodes every 2 weeks.

In this episode of Lifespan, Dr. David Sinclair, A.O., Ph.D. – Professor of Genetics at Harvard Medical School and pioneer in longevity research – explores the science of eye aging, vision loss, and emerging strategies to preserve vision throughout life.

Dr. Sinclair shares an inside update on ER-100, including his team’s successful restoration of vision in non-human primates and the launch of the world’s first FDA-cleared age reversal human clinical trial. This Phase 1 clinical trial will evaluate the safety of epigenetic cellular restoration as a therapy.

Additionally, drawing on decades of research, Dr. Sinclair explains why the eyes may offer one of the earliest windows into biological aging, how everyday factors such as sleep position, alcohol consumption, and intraocular pressure influence long-term eye health, and what the latest evidence reveals about nutrition, supplements, and the connection between the eyes and the brain.

Why the Next 10 Years May Add 50 to Your Lifespan | Dr. Derya Unutmaz

The next 10 years may add decades to human lifespan by compressing the time it takes to understand, treat, and prevent disease. In this episode, Dr. Derya Unutmaz explains why accelerating AI could transform drug discovery, shorten clinical trials, and push cancer treatment toward increasingly personalized interventions. He also reframes AI not as an existential threat, but as a medical enabler that doctors may soon be ethically obligated to use.

Get weekly, protocol-driven research breakdowns from Dr. Rhonda Patrick to advance healthspan, longevity, brain health, and resilience: https://www.foundmyfitness.com/newsle… 00:00:00 Introduction 00:02:16 Why the next 10 years may add 50 to your lifespan 00:06:25 How AI is transforming drug discovery 00:11:55 Could digital twins shorten clinical trials? 00:14:31 Can AI predict drug safety and efficacy? 00:18:46 Have we already reached AGI? 00:24:28 Why AI may be medicine’s greatest force multiplier 00:30:41 Can AI replicate a scientist’s biological intuition? 00:37:22 Is it malpractice for doctors not to use AI? 00:43:24 What happens when AI monitors disease in real time? 00:46:58 Which AI models should doctors trust? 00:52:34 Claude vs. GPT—does the model matter for diagnosis? 00:56:04 Generalist vs. specialized AI—which works better in medicine? 00:59:30 Why cancer is so hard to cure 01:03:24 Could cancer be curable within a decade? 01:07:35 Can AI design cancer treatments on demand? 01:09:37 How AI could curb overtreatment and side effects 01:12:33 Predicting cancer years before it forms—is it possible? 01:18:55 Why biology could go exponential with AI 01:24:04 Why aging may be easier to prevent than reverse 01:29:56 Can the body be engineered to resist aging? 01:35:13 Can AI model how gene therapy will behave? 01:39:17 What people who reach 110+ reveal about Human 2.0 01:41:27 From Dolly to Yamanaka factors—the case for cellular age reversal 01:46:02 Why full-body rejuvenation is an engineering problem 01:53:49 What happens when AI reasons longer about biology? 01:56:31 The biosecurity dilemma of powerful AI 02:01:17 What should we actually measure to track aging? 02:07:40 How old immune cells distort aging clocks 02:10:28 Why reversing brain aging is uniquely difficult 02:16:55 The ultimate prompt for extending lifespan 02:18:56 What data does a true digital twin need? 02:23:38 How to build a mini digital twin today 02:28:32 How to give AI a long-term memory of your data 02:31:39 Why personal baselines matter for AI advice Derya Unutmaz, M.D. X: https://twitter.com/DeryaTR_ EPISODE LINKS Show notes & transcript: https://www.foundmyfitness.com/episod… PODCAST INFO Apple Podcasts: https://podcasts.apple.com/us/podcast… Spotify: https://open.spotify.com/episode/4BPh… SUPPORT MY MISSION Access more than 130 episodes of my premium podcast (The Aliquot) when you become a FoundMyFitness Premium Member: https://www.foundmyfitness.com/crowds… #ai.

CHAPTERS:
00:00:00 Introduction.
00:02:16 Why the next 10 years may add 50 to your lifespan.
00:06:25 How AI is transforming drug discovery.
00:11:55 Could digital twins shorten clinical trials?
00:14:31 Can AI predict drug safety and efficacy?
00:18:46 Have we already reached AGI?
00:24:28 Why AI may be medicine’s greatest force multiplier.
00:30:41 Can AI replicate a scientist’s biological intuition?
00:37:22 Is it malpractice for doctors not to use AI?
00:43:24 What happens when AI monitors disease in real time?
00:46:58 Which AI models should doctors trust?
00:52:34 Claude vs. GPT—does the model matter for diagnosis?
00:56:04 Generalist vs. specialized AI—which works better in medicine?
00:59:30 Why cancer is so hard to cure.
01:03:24 Could cancer be curable within a decade?
01:07:35 Can AI design cancer treatments on demand?
01:09:37 How AI could curb overtreatment and side effects.
01:12:33 Predicting cancer years before it forms—is it possible?
01:18:55 Why biology could go exponential with AI
01:24:04 Why aging may be easier to prevent than reverse.
01:29:56 Can the body be engineered to resist aging?
01:35:13 Can AI model how gene therapy will behave?
01:39:17 What people who reach 110+ reveal about Human 2.0
01:41:27 From Dolly to Yamanaka factors—the case for cellular age reversal.
01:46:02 Why full-body rejuvenation is an engineering problem.
01:53:49 What happens when AI reasons longer about biology?
01:56:31 The biosecurity dilemma of powerful AI
02:01:17 What should we actually measure to track aging?
02:07:40 How old immune cells distort aging clocks.
02:10:28 Why reversing brain aging is uniquely difficult.
02:16:55 The ultimate prompt for extending lifespan.
02:18:56 What data does a true digital twin need?
02:23:38 How to build a mini digital twin today.
02:28:32 How to give AI a long-term memory of your data.
02:31:39 Why personal baselines matter for AI advice.

Derya Unutmaz, M.D.
X: https://twitter.com/DeryaTR_

EPISODE LINKS
Show notes & transcript: https://www.foundmyfitness.com/episod

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