Lifeboat Foundation: Safeguarding Humanity
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Category: life extension – Page 2

Think of the Hume Band as your personal longevity sherpa

Most wearables tell you what you did.
The Hume Band tells you whether it’s helping or hurting you.
What I like is the idea of metabolic momentum — seeing whether your daily habits are accelerating or slowing your pace of aging, based on sleep, stress, and activity over time.
It’s very “longevity-optimized” thinking: push when it’s smart, recover when it’s not, and let the data guide sustainable decisions without blood tests or guesswork.

SAVE 20% on HUME BAND with this link and USE CODE: LSN20
https://humehealth.com/pages/hume-band?bg_ref=o89scHYZhn&utm…o89scHYZhn

A group of researchers compared the DNA of Italian centenarians with prehistoric genomes… and what they discovered left them stunned: the secret to living to 100 could lie in genes from 14,000 years ago

Italian centenarians share DNA links to Ice Age hunter gatherers, hinting that ancient genes may support extreme longevity.

Scientists Have Discovered a Protein That Reverses Brain Aging in The Lab

Our brains age along with the rest of our bodies, and as they do, they produce fewer new brain cells. Now, researchers have found a key mechanism through which the typical age-related decline in neuron production might be slowed.

In later life, the neural stem cells (NSCs) that turn into fully fledged neurons become more dormant – almost as if they’re going into retirement after a long lifetime of service. As that happens, cognitive decline creeps in.

A major reason why NSC activity fades with age is the wear and tear on telomeres, the protective caps on the ends of DNA. Telomeres fray a little more each time a cell divides, and over time, this impairs cells’ ability to grow and divide, leading to increasing cell death.

Anti-Aging Breakthrough: Regenerate Your Liver

NewLimit just announced something that could be a major step toward real anti-aging medicine:
their first therapy is designed to regenerate the liver potentially making it 10–20 years younger.
Human trials are still ahead, but they’re already working on similar approaches for the immune system and vascular system.
Cartilage. Teeth. Liver.
Regeneration is moving from science fiction to clinical reality.
And it raises a bigger question:
medicine today often requires lifelong dosing like GLP-1 weight loss drugs (Ozempic, Wegovy).
What if the future is different?
What if one shot could actually repair the system instead of managing it forever?

How Epigenetic Reprogramming Makes Cells Act Young Again

Aging doesn’t rewrite your DNA, it scrambles how your cells read it.

This clip explains epigenetic drift and how Life Biosciences’ therapy, ER100, uses Yamanaka factors to restore youthful epigenetic patterns in aged cells. By resetting the chemical marks that control gene expression, cells can behave as if they’re young again without changing the underlying DNA.

It’s the same biological process that happens early in embryonic development, applied in a controlled way to adult cells.

Brave New Biology: Intelligence Trumps DNA — with Dr. Michael Levin and Dr. John Vervaeke

Dr. Michael Levin is a professor in the Department of Biology at Tufts University and an associate faculty member at the Wyss Institute at Harvard. He directs the Allen Discovery Center at Tufts, where his team integrates biophysics, computational modeling, and behavioral science to study how cellular collectives make decisions during embryogenesis, regeneration, and cancer.

Levin’s research centers on diverse forms of intelligence and unconventional embodied minds, bridging conceptual theory, experimental biology, and translational work aimed at regenerative medicine. His lab also pioneers efforts in artificial intelligence and the bioengineering of novel living machines.

Read more about Dr. Michael Levin’s work: https://drmichaellevin.org/
X: https://twitter.com/drmichaellevin.
YouTube: ‪@drmichaellevin‬

John Vervaeke’s YouTube channel: ‪@johnvervaeke‬

📖 Let’s take our stories back. Check out our latest book in the Tales for Now and Ever series, Rapunzel and the Evil Witch: https://rapunzelbook.com/

Join Fr. Stephen De Young in his Jubilees and the Nephilim course, now streaming live on The Symbolic World: https://www.thesymbolicworld.com/cour… 00:00 — Coming up 01:14 — Intro music 01:40 — Introduction 02:23 — What Michael does 06:19 — Example experiments 07:51 — Memories outside the brain 12:46 — Terminology: memory 13:59 — Communicate to biological cells 15:54 — Limitations? 17:39 — Platonic patterns 34:06 — Incarnation and constraints 39:26 — Causes 49:28 — New beings in new spaces 52:25 — What the Enlightenment dismissed 55:32 — Molecular medicine 57:36 — Subtle bodies 01:00:45 — Ethics 01:03:37 — Medical and meaning applications 01:11:42 — Frightening 01:14:31 — Against the status quo 01:19:03 — Should we dabble in this technology? 💻 Website and blog: http://www.thesymbolicworld.com 🔗 Linktree: https://linktr.ee/jonathanpageau 🔒 BECOME A PATRON: https://thesymbolicworld.com/subscribe Our website designers: https://www.resonancehq.io/ My intro was arranged and recorded by Matthew Wilkinson: https://matthewwilkinson.net/

Continue reading “Brave New Biology: Intelligence Trumps DNA — with Dr. Michael Levin and Dr. John Vervaeke” | >

Plasma Proteome Profiling of Centenarian Across Switzerland Reveals Key Youth‐Associated Proteins

The full list of differentially expressed proteins was compared to the list of aging biomarkers in blood determined by the TAME working group (Justice et al. 2018), see full list of APs in Table S2d. Of the seven aging biomarkers selected by TAME as gold standard, five proteins (CST3, GDF15, IL6, NPPB, TNF) were available and significantly differentially expressed when comparing healthy controls with centenarians or with geriatric patients; two proteins (CRP, IGF1) were unavailable from the Olink panels (Cardiometabolic I and Inflammation I).

On the expanded list of blood-based biomarkers (74 total) selected by TAME, when comparing healthy controls with centenarians, 47 biomarkers were not available in both panels (63.5%). Of the available markers, 23 were significantly differentially expressed in centenarians (85.2%) and 4 were not significantly differentially expressed in centenarians (14.8%). When comparing healthy controls with geriatric patients, 47 biomarkers were not available in both panels (63.5%); 25 were significantly differentially expressed in the geriatric group (92.6%), and only 2 were not significantly differentially expressed in hospitalized geriatric patients (7.4%). Only 2 proteins (SERPINE1, SOD1) among the 25 proteins available in the SWISS100 dataset demonstrated different results in both comparisons (Healthy2Cent and Healthy2Geriatric). Thus, both the short and expanded list of blood-based biomarkers proposed by TAME as APs are highly reproducible in the SWISS100 study based on proximity extension assay. Table S2d contains the complete list of DEPs in blood with age that overlap between both studies.

DNA-protein cross-links promote cGAS-STING–driven premature aging and embryonic lethality

Unrepaired DNA-protein crosslinks—highly toxic tangles of protein and DNA—cause a process that leads to premature aging and embryonic lethality in mice.

The findings in Science reveal a previously unrecognized link between defective DNA repair and immune-driven inflammatory disease.

DNA-protein cross-links (DPCs) are highly toxic DNA lesions that block replication and transcription, but their impact on organismal physiology is unclear. We identified a role for the metalloprotease SPRTN in preventing DPC-driven immunity and its pathological consequences. Loss of SPRTN activity during replication and mitosis lead to unresolved DNA damage, chromosome segregation errors, micronuclei formation, and cytosolic DNA release that activates the cyclic GMP-AMP synthase (cGAS)–stimulator of interferon genes (STING) pathway. In a Sprtn knock-in mouse model of Ruijs-Aalfs progeria syndrome, chronic cGas-Sting signaling caused embryonic lethality through inflammation and innate immune responses. Surviving mice displayed aging phenotypes beginning in embryogenesis, which persisted into adulthood.

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