Patent granted! Super proud of the team’s invention of the first truly safe age-reversal technology - for healing injuries, treating diseases, and hopefully extending human lifespan @Y_Ryan_Lu

Less than 7 hours of sleep is associated with ~14% higher mortality Too much (8–9 hours) can raise it up to 34% The sweet spot for most people is ~7–8 hours

ITOA states DNA breaks (and other stresses) create epigenetic noise that contributes to a loss of gene expression/cell identity & this leads to aging (exdifferentiation). These changes are reversible via mechanisms currently unknown

Exciting new paper on aging: 1. CRISPR-mediated DNA breaks cause heritable epigenetic changes 2. Changes occur genome-wide, not just at breaks 3. Natural DNA breaks also disrupt the epigenome Strongly supports The Information Theory of Aging (ITOA) https://t.co/Vw4veR0JV3

New Review: Biological or epigenetic age is accelerated by severe stressors such as pregnancy, followed by only partial recovery https://t.co/Hsbl1pw6sH

Sitting >3 h/day may account for ~3.8% of all deaths worldwide—over 400,000 deaths/year. Micro-movements matter (Rezende et al., Am J Prev Med 2016)

Good news: you don’t need 12,000 steps. In 15 cohorts, the most active people had 40–53% lower mortality, with benefits plateauing at 6–10k steps (Paluch et al., Lancet Public Health 2022)

Will be watching closely

New paper: A peptide analog called NN501 just drove substantial weight loss in high-fat diet mice with modest decreases in appetite. Could this be the future: burn off weight by engaging receptors in the brain rather than GLP-1RAs? @Cell_Metabolism

The original article is here:

Slowing and reversing epigenetic drift can be achieved using epigenetic reprogramming, soon to be tested in humans in 2026

Here is the Oct 2025 Cell paper from the Belmonte Lab demonstrating Mesenchymal Drift

Here is the ITOA Hypothesis in @NatureAging, first presented in a cell paper (2008) and refined in Lifespan: Why We Age and Why We Don't Have To (2019)

An increased level of mesenchymal drift is associated with disease progression and a higher mortality risk

Epigenetic drift is observed across numerous aging human tissues and in various age-related conditions, including lung, liver, and kidney fibrosis, heart failure, and neurodegenerative diseases

Cells gain mesenchymal characteristics such as increased motility, reorganization of the cytoskeleton, and deposition of extracellular matrix components, which can lead to tissue stiffening and fibrosis.

Non-mesenchymal cells e.g. skin epithelial cells, blood vessel endothelial cells, blood vessels, and lymphatic tissue take on the gene expression patterns of mesenchymal cells that make up bone, muscle and fat

Mesenchymal drift (MD) is a recent concept in biology, describing the progressive, widespread acquisition of features typical of mesenchymal cells by cells that should maintain their specialized, non-mesenchymal identity. This phenomenon is considered a hallmark of aging

New article: The Information Theory of Aging (ITOA) states that epigenetic drift is a cause of aging, with cells taking up new identities. New review says slowing a process called "mesenchymal drift" has emerged as is a new strategy for rejuvenation

The commentary by my friend, Prof. Yousin Suh & Dr. Zev Williams

The original mouse paper by my colleague at @harvardmed Dr. Vadim Gladyshev https://t.co/ldSqU9TwTS