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Comment by deytempo | Hacker News Reader

This has to do with mitochondrial metabolic processes being the most efficient to break down smaller quantities of sugar. There are mitochondrial mechanisms to break down a lot at once that are turned on in the presence of more sugar but they just aren’t as finely tuned and thus generate free radicals which can cause cellular problems. There really wasn’t a point throughout evolutionary history where there was a prolonged abundance of sugar available to the degree it is today. Because of that, the mechanisms to break down a lot of carbohydrates/sugars at the same time just did not evolve to be as operationally efficient. Free radicals can cause DNA/RNA disruptions and also damage other processes. Source: father is a dedicated microbiologist

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Interesting to know about free radical creation when mitochondria are overwhelmed. I’m sure there’s a lot more factors involved in aging however, not the least of which would be senescent cells. Telomeres only allow cells to divide ~50 times before they’re unable to replicate further.

Unable or won't?

Before they start eating their own instructions. Every chromosome will become a Y chromosome some time in the future if we do not invent the necessary means.

Unfortunately free radical aging theories are not enough. It's a tiny piece of a picture, because effectively immortal organisms still use the same mechanisms. And it's not for some magic scavenging either.

Even telomere bound is not enough.

It's likely a set of advanced repair and local homeostasis so that feels still execute the complex maturing program correctly.

Too many senescent or damaged cells might just break the conditions... And mitochondria and cells have excellent mechanisms of dealing with reactive species they make, but sometimes chemicals leak in.

I'd be more concerned with infections and resulting damage at this point, plus toxic damage. Including endogenous like glycation.

Ask your father about drug induced mitochondrial dysfunction. I had ciprofloxacin 4 years ago and my exercise tolerance swiftly dropped in the months afterward. Research tells me this is due to mtdna depletion and dna damage and I just want to know how to get better. I now have stage 1 diastolic dysfunction and a plethora of seemingly unrelated problems, coming from none before.

It's probably not fixable if it's really that. Even if mtDNA is fine the mitochondria have their own mechanism for senescence based on other damage, just like cells. It does not even have to be caused by radicals.

Why wouldn't it be fixable?

And would there be a way you think to test if that's really the case?

I have talked with some people who had like severe reactions to the drug who managed to get some kind of mitochondria testing and it would say stuff like "30% of the active sites are blocked on the mitochondria"

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