Professor researching why we age & how to reverse it. Author & host of Lifespan. Mission: Extend healthy life for all. Views are entirely his own. @joinlifespan
Harvard
Joined March 2012
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lifespan.com/blogs/magazine/…
David Sinclair retweeted
Could your high-protein diet be working against longevity? Protein helps protect muscle, but eating more isn’t always better for long-term health. Learn about the trade-offs between protein, muscle and lifespan lifespan.com/blogs/magazine/…
Surprised @TheLancet published such unscientific polemic. This on the heels of the new ER-100 results reminds me of when @NYT predicted powered flight could take a million yrs, just 69 days before the Wright brothers flew.
“Several renowned experts told me” is what people write when they lack evidence. Expect more articles from the establishment as we make progress. People often fear what they don’t understand.
ICYMI:
“There are two delusions driving the world of longevity: the first is that ageing in humans is as malleable, or plastic, as it is in roundworms, fruit flies, and mice. The human body, the product of millions of years of evolution, is not, as our tech overlords believe, a programmable dataset. Several renowned biogerontologists told me that a significant biotech mediated expansion of human lifespan is unlikely in the foreseeable future: the longevity industry is a goldrush without gold. The second delusion is that longevity is primarily a scientific, or medical, concern. It is not.” 🙈
"The longevity industry exists to exploit humanity, not to save it." - Seamus O'Mahony writes @TheLancet
Or, as he puts it, "the longevity industry is a goldrush without gold."
Talk about throwing out the baby with the bathwater!
Of course, the field is drowning in hype and commercial interests pushing unproven interventions. But that doesn't detract from the fact that slowing human aging - even if slightly - would have enormous health and medical benefits.
Manipulating human aging may prove harder than many in the field currently promise. But aging is no doubt malleable, so let's not lose sight of the field's long-term transformative potential.
The challenge is to tell hype from science, not to dismiss the science because of the hype.
David Sinclair retweeted
Peptides are everywhere, but “peptide therapy” can mean anything from an FDA-approved medicine to an untested vial labeled “For Research Use Only.” What do we actually know about the compounds people are injecting? lifespan.com/blogs/magazine/…
Long-term NMN treatment increases lifespan and healthspan in mice in a sex dependent manner
biorxiv.org/content/10.1101/…
Woohoo
Proud to be named one of @Fortune’s Best Workplaces in BioPharma 2026! This recognition reflects the people behind our mission and the collaborative culture driving our work to advance epigenetic restoration to reverse diseases of aging. View the list here:bit.ly/4hKrfgd
Yup
Next step: Longevity and Rejuvenation. We are almost there.
Researchers in Bonn turned blood cells from an 80-year-old into neural stem cells with a molecular age below 20. More than 60 years younger by epigenetic clocks, which estimate age from chemical marks on DNA.
The team directly reprogrammed blood precursor cells into neural stem cells, skipping the usual pluripotent stem cell stage. The rejuvenation unfolded gradually and could be tracked for over 100 days.
Never thought to squeeze a cell
Squeezing a fibroblast nucleus for a moment opens chromatin at mappable loci. Yang Song and Song Li at UCLA aimed CRISPRa guides at exactly those spots. Fibroblast to neuron conversion went from under 3% to about 40%, with no virus. In aged mouse fibroblasts, the same mechanically enhanced Oct4 activation lowered DNA methylation age on the mouse skin clock, close to the level of cells from young animals. But global methylation also drops. so how much of this is rejuvenation rather than dilution is the open question. Title: Mechano-epigenetic enhancement of CRISPR activation of target genes fo… sciencedirect.com/science/ar…
David Sinclair retweeted
Bowhead whales can live for >200 years - longer than any other known mammal on earth! 🐳
Enjoy more science cartoons in Lifespan Magazine: lifespan.com/magazine
🤖 Made with AI
Big congratulations to Dr. Christoph Gorgulla @StJude, a Lifespan Foundation Laureate, with a check for $100K to study AI-mediated drug design using quantum
Thank you to subscribers of LS Magazine, who help support the Lifespan Foundation & research like Christoph's 🙏
So true - the Information theory of aging in 2008:
NAD+ ➡️ sirtuins ➡️ histone modification ➡️ epigenetic stability ➡️ cellular identity ➡️ slower aging
cell.com/cell/fulltext/S0092…
NAD boosting and epigenetic restoration are two levers aimed at the same aging biology. David Sinclair (Harvard Medical School) at #ARDD2026. Photos: agingpharma.org/photos2026
It’s confusing. Some studies examine sildenafil (Viagra), others tadalafil (Cialis). So many new studies are indicating surprisingly positive effects on various organs & even immune cells fighting cancer. How about a new Lifespan episode called “What’s not to love?”
There is no convincing evidence that low dose Cialis associated with altered lens proteins or causes cataracts. There are potential side-effects to discuss with a physician, like a potentially slightly higher occurrence of a “stroke in the eye” (NAION), as with GLP-1RAs
David Sinclair retweeted
People are living longer than ever. But could the average lifespan really jump by another 10 years? Lifespan Magazine 📚️ lifespan.com/blogs/magazine/…
Today it was great meeting with the team to chart the future
The story of this technology is amazing. Happy to be able to share it, and big kudos to @davidasinclair lab in originating it!
NEW PAPER: In rats, the NAD booster NMN effectively alleviates polycystic ovary disease, a common cause of infertility, by increasing SIRT2 activity, suggesting NMN as a possible therapeutic
Highlights from authors:
1. NMN effectively ameliorates metabolic and endocrine disorders in PCOS
2. NMN activates granulosa cell glycolysis via SIRT2-mediated LDHA deacetylation
3. LDHA then converts pyruvate to lactate
3. K119 is a critical functional acetylation site of LDHA.
4. Targeting the SIRT2/LDHA-K119 axis improves follicular development in PCOS