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 👏

True

Daily prompt journaling…

He’s right

🚨: Whenever you feel sad, remember that there are tiny kinesin proteins doing their best to make you happy.

“Los Angeles utility workers are making over $700,000 a YEAR.” Spencer Pratt pulled LADWP payroll records — 100 employees clearing over $500,000, some topping $700,000. An $11 billion department with the SAME political appointees. This is institutionalized FRAUD.

Watch Starship's twelfth flight test x.com/i/broadcasts/1pKkOykQR…

Three years of research. One award-winning documentary. Independently financed so that science is the star. Coming to Apple TV in 60 countries on May 26th. Show your support and pre-order it today. Link in bio. @NirBarzilaiMD @prof_horvath @Naveen_Jain_CEO @TarynSouthern @drjuliea @BuckInstitute @EinsteinMed

Advances in precision geriatrics. GrimAge methylation clock works in centenarians. Striking new preprint from the Henne Holstege lab (Yaran Zhang et al., 100-plus Study) in n=247 cognitively healthy Dutch centenarians: GrimAge predicts mortality at extreme old age (HR ≈ 1.6 per SD increase). New to me that GrimAge still discriminates past 100. Mechanism: GrimAge tracks the age-related myeloid shift in peripheral blood (monocyte/lymphocyte ratio r = 0.47). Consistent with declining adaptive immunity and expanding innate compartment. But the myeloid shift doesn't fully explain the signal. After adjusting for MLR and RBC, GrimAge still predicts mortality (HR = 1.27). GrimAge is reading something beyond immune-aging. Interestingly, GrimAge is uncorrelated with cognitive assessment (MMSE r = −0.04) and plasma NfL (r = 0.12), i.e. independent of brain aging. While MMSE predicts short-term mortality (1–3 years), GrimAge predicts longer-term mortality (>3 years). Combining them improves mortality prediction. Zhang et al (2026) Peripheral Epigenetic Aging Predicts Survival in Cognitively Healthy Centenarians Independent of Brain Aging-Related Biomarkers medrxiv.org/content/10.64898…

This woman just made ultramarathon history in 56-hour, 250-mile run in Arizona. Rachel Entrekin won the Cocodona 250 outright in a 56-hour, 250 mile effort, beating the entire men’s field, setting a new course record, and marking a landmark moment in ultrarunning history.

Nithya Raman’s city council approved a homeless NPO scam that bought a crooked developer $27M for an $11M property. And they still support it! Where did the money go??

I’m sorry I am now a broken record but oh my God I did not have Spencer Pratt, exposing Karen Bass’s entire communist, revolution history during the race for mayor in Los Angeles. I mean the best part about this is everything he’s saying is completely 100% true. So if you don’t know who Karen Bass is, you should watch this video and ask yourself why are there so many Democrat politicians training in Cuba before being elected into powerful positions in American public office?

Karen Bass is an incredible liar.

The incredible DNA Repair System DNA - and Life - cannot exist without it. It requires 6-7 sub-systems working together a massive complex network of 130–200 unique proteins. Simpler versions don't work. Only Intelligence designs systems like this.

Footage of a Single Brain Cell Growing and Looking for a Connection

Microscopic life inside a small forest pond