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Comment by fintechie | Hacker News Reader

Take this with a pinch of salt. We've managed to cure a myriad of diseases in mice.. eg balding. 99.9% of the time things don't translate to the human body.

For now just follow common sense: exercise regularly, low stress and a (mostly) mediterranean diet.

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The problem isn't that the drug results don't translate from mice to humans. The problem is that after testing the drug successfully in mice, they follow that with testing the marketing campaign with the mice. The mice never buy the drug, so they decide to drop it as unprofitable and move on to another drug.

I think the issue isn’t about mice demand, it’s more that mice have notoriously awful insurance coverage.

They also have a live fast, die young risk taking culture that isn’t big on health awareness. I mean, they come into my kitchen at night even though I am actively trying to murder them.

"Live fast, die young, bad mice do it well..."

Really 99.9%?

The thing is that even if this is is true we can explore things like TOR which mice definitely have and it definitely adds to the list of evidence that inhibiting TOR extends lifespan

I would bet a dollar inhibiting TOR via protein restriction turns out to be one of those things thats good for mice but bad for humans. Whatever aging gains you get are probably over-ridden by earlier onset of sarcopenia. Too many studies show how having muscle and strength is key to aging well, something mice in a cage don't have to worry about. Agree though that 99.9 is probably high.

It shows it’s biologically possible for mammalian cardiac cells to (a) do the job of the heart while (b) being regenerated. That’s not clinically relevant for humans. But it’s scientifically relevant for researchers (and those interested in the science of it).

Agreed on the common sense stuff but disagree about the difficulty to translate this to practice. Depends if you need it from Big Pharma or if you’re biohacking.

The authors highlight a multi step pathway and one of the steps is accumulation of alpha-ketoglutarate which is a common ketone we all already have tons of, and it increases from fasting. Seems like their research indicates there’s a second system hiding behind the first and it only turns on when you have ketones and can’t burn fat. That’s like the logical converse or contrapositive or something to fasted state. This is analogous to diabetic ketoacidosis but seems to have a healthy impact, which is surprising.

TLDR: if you think about it, fatty acid oxidation pathways are some of the easiest to target (even with zero drugs…just stop eating for a few days)

I think the point is that there's no reason as of yet to think this same thing happens in humans. Rats and humans are very very different. Humans may have developed a stress response or any other myriad of things that cause the results to be dissimilar.

Seems to me if mice ever develop advanced intelligence they will either hate us for the experiments or be grateful to have the medical knowldge to extend their lifespans and cure every one of their disease under the sun. Maybe both?

This wasn’t heart regeneration in ordinary mice, though - it was in genetically modified mice.

So if you want your heart to regenerate using this technology, you need to go back in time and edit your genes before you were born.

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