This was published in Nature Aging, not Nature. Nature (the company) has 100+ journals, I dont think any of them are as selective as Nature (the journal). That doesn't make this a bad article or a poorly reviewed one, but I wouldnt equate it with an article published in Nature.
I feel like I see some strongly-worded headline about anti-aging of some sort here every two weeks.
Imagine opening up your floorboards, and there's a bunch of rats underneath, chatting about baseball.
The reporting is typically... not as great. At the very least, the headlines are typically extremely over-stated.
The logic i see here is that, having excessive level of iron storage protein, may be it makes sense to cut somewhat back on one of the best sources of hem iron - i.e. red meat.
He addresses the specific reasons that the mouse results don't translate, but the interesting part to me is that the scientific community seems to be behind the amyloid hypothesis while the media likes to run with any story that refutes it.
Most deaths seem to be cardiovascular, heart disease, stroke, then followed by cancer.
Oh, that's just derived from old theology.
Genesis 6:3, 'Then the LORD said, “My Spirit will not contend with humans forever, for they are mortal; their days will be a hundred and twenty years.”'
This kinda got spread throughout the zeitgeist long ago as a "maximal lifespan", but the reality is that only 3 in 10,000 even make it to 100. There's no hard cutoff, but functionally essentially no one gets to 110.
Scientifically, there's no hard reason we couldn't increase our lifespans indefinitely, but we've got a lot of work to do before we'll be able to get a reasonable number of people up to 125.
2. The most common causes of death for wild mice are predation, diseases, and starvation. Theoretically immortal mice have no chance in the real world if not very well-adapted to these conditions.
[1] https://biologyinsights.com/the-mice-mating-process-and-thei...
Fascinating, really.
Just off the top of my head, I think the longest they ever got a mouse to live in a study was the C-60 study where they wanted to test whether it was toxic and the mouse lived almost twice their normal lifespan. This paper has been cited over 300 times, so it's not like people haven't taken notice of it. There are a few supplement companies selling c-60 olive oil too:
https://www.sciencedirect.com/science/article/abs/pii/S01429... "Here we show that oral administration of C60 dissolved in olive oil (0.8 mg/ml) at reiterated doses (1.7 mg/kg of body weight) to rats not only does not entail chronic toxicity but it almost doubles their lifespan"
Study reveals blood sugar control is a key factor in slowing brain aging 150 points by gnabgib 9 months ago - https://news.ycombinator.com/item?id=42049418
Study Reveals Immune Driver of Brain Aging 232 points by oedmarap on Jan 22, 2021 - https://news.ycombinator.com/item?id=25871347
Brain aging shows nonlinear transitions, suggesting a midlife "critical window" 276 points by derbOac 79 days ago - https://news.ycombinator.com/item?id=44175905
High blood sugar increases the amount of iron your body stores, and FTL1 is a mechanism used to store iron in your body. Thus, a contributor to cognitive decline might be a protein that your body makes too much of when your blood sugar is high.
I wonder if they could run tests on regular blood donors as well for those with iron sensitivity and not.
stevenjgarner•4h ago
Could lowering FTL1 restore synaptic connectivity and memory in old mice represent a master switch in brain aging, or just one of many parallel mechanisms? If FTL1 is sufficient to induce both structural and functional brain aging in mice, what does that imply about the hierarchy of molecular drivers in neurodegeneration
[1] https://www.nature.com/articles/s43587-025-00940-z
Ygg2•4h ago
stevenjgarner•4h ago
1. Field Maturation
We’ve moved from “aging is inevitable” → “aging can be slowed” → “specific mechanisms can be reversed in vivo.” That shift means:
- Tools (CRISPR, single-cell omics, proteomics) are now precise enough to pinpoint single culprits.
- Researchers are designing interventions that don’t just extend lifespan, but restore youthful function in cognition, muscle, or immunity.
2. Convergence on a Core Set of Mechanisms
Different labs, different pathways (NAD+, senolytics, plasma dilution, now FTL1), but similar outcomes: old mice regaining youthful traits. This convergence hints aging may not be a diffuse “wear and tear” process, but the result of a relatively small number of upstream regulators.
3. Proof-of-Concept Momentum
Even if each specific intervention fails to translate, the fact that so many are succeeding at all in mice makes it harder to dismiss rejuvenation as fringe. The signal: aging can be manipulated, not just observed.
4. Cultural Shift in Geroscience
Funders, journals, and institutions are increasingly willing to spotlight “reversal” claims, where a decade ago the same results might have been relegated to smaller journals. The fact we’re seeing more of these studies may reflect both real progress and changed editorial appetite.
the trend suggests aging is experimentally tractable and reversible in model organisms. That doesn’t mean translation to humans is imminent, but it reframes aging from “inevitable decline” to “complex but solvable engineering problem.”
throw310822•3h ago
About this: it seems to me that the idea itself of "wear and tear" is just silly. It's a metaphor taken from the realm of mechanical objects that have no regeneration abilities. Any living being is continuously repairing localised damages back to a pristine state, while aging is diffuse and organic. This suggests that any "wear and tear" can only be at the cellular level- but still it can't be a biological necessity given the wildly different lifespans of organisms- from a few days to centuries.
bitwize•2h ago
jjk166•2h ago
throw310822•40m ago
glenstein•1h ago
I find them to be an unfortunate mix dismissiveness and principled restraint, that veers to much into the Onions Learned Sage territory.
dgfitz•4h ago
greenavocado•3h ago