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Elevate Your Performance

⚫ A digital twin of Aubrey de Grey. ⚫ More good partial reprogramming news. ⚫ Nudging old bodies toward youth. ⚫ Reprogramming with small molecules. ⚫ Young turns old, old turns young. ⚫ Is semaglutide a longevity drug? ⚫ Bonafide damage repair. ⚫ Game of the year. ⚫ Good news for metal fans. ⚫ For some of us cryonics works just fine. ⚫ A new longevity think tank. ⚫ Your funeral in 4k. ⚫ Calling aging a disease. ⚫ Making a case for metformin in 2025. ⚫ Inside New Limit. ⚫ Let’s replace Putin, Xi and our failing bodies.

New to LEVITY? Start here! Want to know more about who’s behind LEVITY? Check out this page. 🙏🏼 Not subscribed to the LEVITY podcast on Youtube yet? Do it here. 🎧 More of a listener? The podcast is also available on Spotify, Apple Podcasts and other places.

Since this is a mega round-up, your email provider will probably clip it. I recommend reading online instead - it avoids the cut-off and looks much better.

I’m also changing how I publish. Longer pieces will now go out as separate posts: some free, some for Premium subscribers. Don’t worry - whatever the format, I’ll always link them in upcoming newsletters so you won’t miss a thing.

Round-ups like this one will appear every other week. And even though I’m pulling out the bigger stuff, there’s still plenty to dig into here. Use the table of contents above to quickly reach what interests you the most.

Finally: we’ve just released a new LEVITY episode with Matt Kaeberlein. Check it out here.

As always: Life is good. Death is bad.

/Peter

What’s happening in the longevity landscape

It’s very ambitious and completely novel. Picture (if you can) an Aubrey de Grey-inspired AI co-scientist strapped to a blockchain funding layer. Born out of decentralized science (DeSci) circles, the plan is to fund longevity moonshots that stall in grant committees and pharma pipelines. Oh, and it talks back on X when you tag it.

It’s called Aubrai, developed by Swizz startup Bio Protocol, a company that recently raised $6.9M to “enable distributed groups of researchers, patients and crypto users to create and grow AI-driven research networks that automate scientific tasks and monetize biotech discoveries.”

Paul Kohlhaas, founder and CEO of Bio Protocol, says in a press release that science today is locked in “institutional black boxes”. “[It’s] cut off from the very researchers who birth it and the communities primed to accelerate it.”

Bio Protocol sees Aubrai as a the first of many so-called BioAgents, and it has been developed in partnership with another DeSci player, VitaDAO*, and Aubrey de Grey’s Longevity Escape Velocity Foundation (LEVF).

* For more on VitaDAO, check out the LEVITY episode with Laurence Ion.

In fact, Aubrai is deeply integrated with LEVF’s huge lifespan study, Robust Mouse Rejuvenation 2, ingesting de Grey’s lab data and community insights.

“Having the agent at our disposal has been transformative for our planning pipeline. It identified points of consideration we had not yet encountered through literature, and it was proactive in suggesting ways to circumvent foreseen limitations”, Aubrey de Grey told CoinDesk.

A week after going live the associated $AUBRAI token - used to steer funding and governance decisions - had risen 150x in value from $269K to $40M, while Aubrai had generated over a thousand scientific hypotheses minted on-chain.

In the second half of this decade, partial reprogramming will quite literally stand trial: in early 2026, human patients are set to receive the therapy for the first time.

Until then, evidence from the lab continues to build. At this year’s ARDD conference in Copenhagen, Life Biosciences - the company behind that upcoming trial - reported improved liver health across multiple disease markers in mice.

“This news is strong evidence that the original vision to develop therapies that reversal of aging to prevent and cure diseases of aging and injuries isn’t just a fanciful idea”, wrote David Sinclair, Life Bio’s co-founder, wrote on X.

As I like to say, where there’s FOXO3, there’s longevity. In a new study published in Cell, researchers engineered human progenitor cells so that this celebrated gene regulator stays permanently switched on.

Led by Juan Carlos Izpisua Belmonte, with aging-clock pioneer Steve Horvath on board, the team infused the edited cells into elderly macaques every two weeks for nearly a year. The results? Better memory, sturdier bones, and tissues across the body showing molecular patterns more typical of youth. No tumours were seen during the study period.

But the real story may not lie in the cells themselves. These human grafts probably didn’t stick around. Instead, while alive, they shed exosomes - microscopic parcels of proteins and RNAs - that drifted through the bloodstream and nudged monkey cells into younger behaviour. And here FOXO3 matters again: with the gene regulator locked in the “on” position, the cells seem to fill those parcels with anti-inflammatory and stress-resistance factors, broadcasting the traits that link FOXO3 to longevity in the first place.

Then again, many of the beneficial effects could be down to reduced levels of chronic inflammation. Quieter inflammation alone can ripple through bone, brain and immune systems, making animals look healthier than they are.

In any case we’re looking at a “systems-level” tweak: signals reached several tissues all at once. But aging, of course, is a lot more complicated than that. On the inside of cells, DNA errors and misfolded proteins build up. On the outside, the cellular environment fills with toxic signaling. This therapy seems to target the outside noise rather than repair the inner damage.

And we should remember the study’s limitations: small groups and no lifespan or long-term outcomes.

Two more items in the partial reprogramming news department:

One: The Ocampo Lab have shown that cellular rejuvenation can be triggered with chemicals alone, bypassing the need for Yamanaka transcription factors. A short-term treatment with small molecules reversed genomic instability, restored youthful chromatin marks, and reduced oxidative stress in human cells. When tested in C. elegans, the treatment extended both lifespan and healthspan, hinting at a future where rejuvenation could be achieved with drugs rather than gene therapy.

Two: Another study - again featuring Juan Carlos Izpisua Belmonte - introduces the concept of “mesenchymal drift”. It’s a gradual slide where aging cells let go of their specialist roles and shift toward a generic, scar-forming (wound-healing) state. This drift shows up across multiple tissues and tracks with worse survival in idiopathic pulmonary fibrosis. Partial reprogramming, however, can push cells back toward their original identity. According to the authors this might “offer a framework for developing interventions to reverse age-related diseases”.

To solve aging, we’ll need to keep the brain in working order. Perfect muscles and spotless arteries won’t matter much if memory fades and personality dissolves. That’s one reason many scientists are excited by a new Calico-led study - it hints at how we might preserve our minds. Another reason is the ingenuity of the experiments themselves.

The researchers started with a deceptively simple question: are brain immune cells -microglia - old because of their own internal wear and tear, or because the aged brain environment pushes them into decline? To find out, they set up what you might call a postcode test. Old microglia were relocated into young brains, and young ones into old.

The results are fascinating. Old cells transplanted into a youthful neighbourhood quickly shed their decrepit identity, while young cells moved into aged surroundings began to look just as run-down. In other words, microglial “age” is less about the cell’s birth certificate and more about its address.

Digging deeper, the team found that aging brains send out interferons - immune distress signals - that flip on a control switch called STAT1 inside microglia. With STAT1 active, the cells take on an aged profile. When the researchers turned STAT1 off, the microglia stayed youthful, even in an old brain. And the constant “alarm” seems to come from a handful of NK immune cells, stirring up trouble where none exists.

For a field often mired in descriptive atlases and correlations, this is refreshingly causal: a clean experiment, a tractable pathway, and a plausible upstream driver. If we want healthy bodies and healthy minds, this paper suggests that keeping the brain’s neighbourhood peaceful may matter just as much as fixing the neurons themselves.

There was plenty of fanfare. Alex Zhavoronkov, ARDD co-organiser, called it “a watershed moment.” Longbio industry outlet Longevity Technology even declared: “Geroscience has been waiting for its champagne moment; in Copenhagen, the corks finally popped.”

I’m less inclined to celebrate.

What actually happened at this year’s ARDD in Copenhagen was that two pharma executives said the word longevity. Eli Lilly’s Andrew Adams asked whether GLP-1s might be “the world’s first longevity drugs.” And Lotte Bjerre Knudsen - pivotal behind the development of Ozempic - headlined her talk: “Semaglutide as a proven longevity medicine.”

That’s catnip for the folks at ARDD, succinctly summed up by Longevity Technology:

But here’s the thing: branding semaglutide as a “longevity drug” is certainly a stretch. GLP-1s seems to have systemic effects - beyond diabetes and weight loss they improve cardiovascular outcomes, maybe tamp down inflammation and there are som early promising Alzheimer’s data. It’s plausible they nudge the trajectory of aging, but there’s no convincing human evidence that they rejuvenate tissues or reverse biological age.

That said, slowing aging is still worth something. A lot, even. Incremental interventions buy us time. If GLP-1s keep more people alive and healthy long enough to reach the era of true rejuvenation therapies, they matter.

The risk, though, is that pharma treats “longevity” as a marketing slogan and nothing more. The hope is that this is just the opening move toward deeper interventions. Until I see which way it goes, the champagne stays on ice.

Every now and then the repair paradigm that Aubrey de Grey has long championed shows itself in unusually sharp focus. Cyclarity is one such case. Instead of lowering cholesterol or damping inflammation upstream, their approach is to target the toxic junk itself - 7-ketocholesterol, a by-product that gums up immune cells and drives atherosclerosis. Their engineered cyclodextrin, UDP-003, is built to pull this molecule out of foam cells and restore their ability to clean up arteries. That’s damage repair in the strict SENS sense: identify a concrete lesion, remove it, and let biology recover.

The latest preclinical data suggest this works as intended, and first-in-human studies are now underway. If UDP-003 can show real plaque regression and event reduction in people, it would stand as one of the clearest demonstrations yet that repairing damage - not just adjusting risk factors - can be a viable strategy for combating cardiovascular aging. That the company is led by Matthew “Oki” O’Connor, former VP of Research at the SENS Research Foundation, makes the lineage plain.

Remember Aubrai, discussed a few miles above? That was moving an AI agent on-chain. But decentralized science (DeSci) comes in many flavors. Pump.Science looks more like a game: every proposed longevity regimen becomes a token, and when enough people buy in, a new “level” unlocks. First stage: worms. Clear that, and it ascends to flies. Hit the higher cap and you graduate to mice. Once triggered, automated labs like Ora’s Wormbot run the assays, and dashboards on Pump.Science update with survival curves and health metrics as the data come in.

Swedish researcher Krister Kauppi, familiar to LEVITY readers from earlier newsletters, has been one of the first to climb all three levels. Through his Rapamycin Longevity Lab he launched rapamycin-based combinations that were funded for worm and fly tests in minutes - and have now also secured the threshold for mouse experiments. Had this been a video game, we would have called it GOTY - game of the year.

Lithium is back in the spotlight. A new Nature paper reports that people with Alzheimer’s or mild cognitive impairment have reduced lithium levels in their brains.

Some supplement makers greeted the news with a quick “told you so”, while others noted that higher lithium levels in drinking water have been linked to longer life expectancy.

Imagine this: two embryos are created through IVF from the same parents. One becomes a baby girl, born in 1994. The other - her biological brother - isn’t born until 2025, to parents who were toddlers back when his sister arrived. You might need an emoji right about now. 🤯

And this isn’t a thought experiment - it really happened. The second embryo had been cryopreserved for decades before being adopted by a couple in Ohio.

As aging biologist João Pedro de Magalhães put it on X: “A reminder that there are people alive now who were once frozen for decades, even if admittedly when they were very very small”.

We’ve talked quite a bit about decentralized science in this newsletter. Another, more traditional route, is of course to fund longevity science through government and philanthropy. That’s where Andrew Steele - author of Ageless - is putting his energy. He is co-founder of The Longevity Initiative, a new independent UK think tank and educational organisation dedicated to advancing aging-biology research, pushing for longevity medicines, and helping public policy catch up.

This is what Steele told Lifespan last year:

What to read, watch, and think about this week

"Iphone cameras are getting better and better every year. Meanwhile, my body is getting worse and worse. And nobody cares. They’re doing their best to take exceptionally good photos from my funeral".

Yeah, if you’re aligned with LEVITY in your views, chances are you are going to like Vanya Usovich’s 65-minute stand-up special built around deadpan riffs on death and immortality.

I’ve followed this field for more than a decade. Early on, I took a hard line: aging is a disease, full stop. It was (and still is) a useful provocation against fatalism. But, as Karl Pfleger points out in an excellent opinion piece for Longevity.Technology, it can’t be the whole strategy.

Pfleger’s point - and I think he’s right - is that the endless “is aging a disease?” debate is a dead end for regulatory progress. Drug development runs on indications and endpoints, not metaphysics. If we want trials that move fast and read out clearly, we should, according to Pfleger, break “aging” into testable sub-processes (senescent burden, proteostasis, stem-cell function, etc.), validate biomarkers and surrogate endpoints for each, and let companies win approvals step by step.*

* By the way, I think ARPA-H’s Prospr program - which I covered here - is a promising way forward.

Where I diverge is not on the science or the trial design, but on the culture. The label does matter outside the FDA. Most people still think aging is a background constant - inevitable, untouchable, barely worth arguing about until it’s already too late. That belief system has consequences: it shapes political will, philanthropy, how clinicians talk to patients, and whether the public even asks for prevention rather than late-stage rescue. Here, the rhetoric ”aging is a disease,” or at least “aging is malleable and should be treated” - isn’t academic; it’s a norm-shifting device. It primes society to expect intervention and to reject the quietism that kills investment and slows trials.

First it was telomeres, then senolytics stole the spotlight, and now partial reprogramming dominates the conversation. In geroscience, the hype cycle moves fast.

Metformin, once the poster child for longevity drugs, has seen its star fade. The much-anticipated TAME trial remains in limbo, and recent studies have cast doubt on metformin’s credentials as a true gerotherapeutic.

But in a new interview with Lifespan, the world’s leading metformin advocate, Nir Barzilai, comes out swinging. He argues that the evidence for metformin is stronger than ever - and he makes a surprisingly convincing case. It’s a delightful no-holds-barred read.

If you follow LEVITY you’re probably quite familiar with partial reprogramming (there’s been several news items on the field in this very newsletter). Even so, it’s not very often we get this close to the science as in this Core Memory video report from New Limits’ lab.

What I’ve been up to lately

Ny Teknik, the newspaper I work for, has been nominated for Magazine of the Year by Sveriges Tidskrifter. ”With credibility and deep expertise in a closely followed field, the magazine stands out. Ny Teknik is the news leader in its domain, and the site is a natural hub for the tech industry,” the jury writes in its citation.

I was also part of the inaugural episode of the podcast Vetenskapligt Talat to talk about longevity and aging. The brilliant Sara Hägg is a guest as well. Check it out (if you understand Swedish)!

The upside: longevity finally made global headlines. The downside: the discussion that followed the hot-mic exchange between Winnie the Pooh and Darth Putin never got deeper than a puddle. Then, again, it’s not every day that The Guardian publishes an article on the replacement strategy.

Psilocybin never runs out of ways to make you see things in a different perspective. A new paper now reframes it from mind-expander to potential life-extender.