Loss of epigenetic information can drive aging in mice
hms.harvard.edu
hms.harvard.edu
https://khn.org/news/a-fountain-of-youth-pill-sure-if-youre-...
https://www.nutraingredients-usa.com/Article/2022/11/15/FDA-...
“ This is the first study showing that we can have precise control of the biological age of a complex animal; that we can drive it forwards and backwards at will”
And the paper doesn’t show that at all. The paper does not show them reversing the aging of anything.
He’s also helped pioneer and make credible the entire field of aging research to reform people’s idea of how to look at aging.
Don’t be so cynical dude.
Where did he ever say that resveratol was the fountain of youth? Interviews I've seen with him seem more reasonable then I always hear people make him out to be.
NMN does have some promising results based on recent studies- what do you mean he pushed hard? Where did he actually do that?
NAD+ “is the closest we’ve gotten to a fountain of youth.”
Both quoted in an excellent article on Sinclair:
https://www.bostonmagazine.com/health/2019/10/29/david-sincl...
You should see what Huberman often shills and he's a prestigious professor as well.
Would also add that until recently - and by his own hand - Jordan Peterson was a professor at first Harvard, then the University of Toronto.
https://hubermanlab.com/developing-a-rational-approach-to-su...
Joking, are we?
https://www.nia.nih.gov/research/dab/interventions-testing-p...
His commentary on new papers in ageing is pretty good, in my opinion.
He has a good coverage of NIA ITP trials as well: https://duckduckgo.com/?q=site%3Afightaging.org+NIA&ia=web
While it's probably the most important cause of aging, reversing it may be not enough.
Also currently there's no way to prevent cancer cells from being created.
,,Simply titrating the amount of Yamanaka factors that we express, whether by using mRNA, or by having inducible promoters or whatever… these things will stop the mouse or the human from getting teratomas, but I don’t think they’re going to stop them from getting regular cancers, simply because the body of even people your age or my age is already chock-full of cells that have spontaneously accumulated most of the mutations needed to become cancerous.''
Let’s face it—-aging is wonderfully complex.
It uses 1000 mice, so it costs a lot, but finally there's enough money and data to start the mouse rejuvenation project.
See: https://www.nia.nih.gov/research/dab/interventions-testing-p...
We published initial genetic results from the first 3500 animals in Science this Sept (2022).
I think one of the difference in goals is that interventions testing program repurposes approved drugs, while robust mouse rejuvenation is experimenting with unapproved drugs that have potential to both make mice live longer and translate into humans (thereby having a higher chance of rejuvenating mice)
Both are great and important projects, I'm just hoping that they fight together instead of against eachother.
And sure, keep the brother 10 months old forever, but that takes a long time.
It doesn't prove much if they invented a way to wreck mice' bodies in a pre-designed, controlled way, and then un-wreck them in a way specially tailored to undo that exact kind of damage.
Sure, right scientist MUST make test on control group, which is neutral. This is classics of right science.
How many other teams could we get working on projects in this field, were it not for funders preferring less risky but far less valuable studies?
And more generally: I think a lot that’s wrong with this world stems from the fact that humans are risk averse. This served us well in evolutionary times, when failure often meant death. But in modern societies it causes a lot of problems.
Wow.
But no, I'm getting my hopes up. And I didn't start today.
Sure. But that's only half of it. What's promising is when, afterwards, you give that person a gene therapy which reverses the aging-adjacent damage.
Which is a long way of saying, yes, I agree with you; the methylation metric may be total bunk. But there isn't anything else (IIRC) that we can all agree to measure instead. That's why the Harvard article emphasized that they were using a metric for aging they'd developed in-house. I just want to read the paper before passing judgement, and right now sci hub doesn't have it.
The experiment was to test whether vitamin D supplements could attenuate behavioral problems associated with fetal alcohol syndrome. Our lab used a rat model of FAS. When the post doc told me about her experiment idea, I (as an undergrad at the time) told her it was interesting but couldn't be performed in a rat model because vitamin D was poison to rats. It calcifies their skin because they cant break D down like humans can. My warning was ignored, and the experiment was conducted anyway. She found that vitamin D treatment mitigated hyperactivity associated with FAS, and presented this finding at conferences. Well no shit this treatment would reduce activity in rats. If my skin was calcified I wouldn't want to move either.
So… do more backups?
really needs to be a Tag or something doesn't it...
The "in mice" hot take is used to dismiss any new finding without actually contributing anything to the conversation.
I appreciate if you're trying to be helpful, and hope you'll interpret this unsolicited feedback generously in the constructive spirit it is offered: I didn't find the callout helpful or useful.
https://hn.algolia.com/?dateRange=all&page=0&prefix=true&que...
I know it sucks when your submission was the earlier, overlooked one. We should eventually have some sort of karma-sharing to take care of this. In the meantime, it at least evens out in the long run, since the reason is randomness.
https://hn.algolia.com/?dateRange=all&page=0&prefix=true&que...
Aging is simply the continuation of the development process that starts with conception. It also has to be coordinated across the entire organism somehow so that all tissues and organs age at the same rate, like they do in reality. "There's something in the bloodstream that tells the organism how old it is so it could then act its age" the only plausible explanation for the results of heterochronic parabiosis and other related experiments.
How could you possibly justify this claim?
This oversimplifies the research. There is strong evidence for programmed death. That doesn't mean there isn't also damage accumulation.
But it’s possible that the changes are indeed random or probabilistic and that they simply build on each other over time in a way that merely resembles coordinated aging.
What??
But cells are highly specialized. For example, you only grow nails on the tips of your fingers and toes.
This is due to what your pulled quote characterizes as organizational effects. The level of activity [protein production] of a given stretch of DNA varies wildly from cell to cell. Structural features are attached to the DNA that make it more or less likely to be expressed. What it would produce if it were expressed ("the code itself") doesn't change.
For this analogy, you can think of your genome like BusyBox: a single unified executable that will do wildly different things depending on how you call it.
On the other hand, there is a satisfying romance to it all. That a cell is borne and joins into the system ready to grow into anything. It makes our 'self' feel like a co-operative experiment.
I'm not an expert, but I'd imagine the main reason (at least our) cells all contain genetic code for the whole organism, is largely because stem cells contain genetic code for the whole organism. If stem cells didn't have genetic code for say, both heart cells and lung cells, then it couldn't turn into those types of cells. And since all cells, stem from stem cells... then they also end up with the genetic code for the whole organism.
Additionally, DNA is regularly used for creating proteins a cell needs for various purposes. Having extra genetic material than necessary, probably provides some benefits in terms of robustness. Like imaginably when a cell is exposed to a toxic substance, and has genetic code (recipe) for a protein that can neutralize it. Maybe 99% of the time it never needs that genetic code, nor is unnecessary to the cells particular function, but having it around can be beneficial in those rare circumstances.
So is it wasteful and bad? Perhaps, but it likely also comes with some positive tradeoffs.
That generally doesn't happen; a single-cell fertilized egg will grow into the whole organism, but the more usual birth of cells, from the division of an older already-specialized cell, preserves the older cell's existing epigenetic markings.
> Is it not wasteful for each of our cells to contain genetic code for the whole of the organism?
Depends on your point of view. From an evolutionary perspective, DNA is the part of you that replicates and so having more copies of it is its own reward.