Hm, the evidence summarized there is quite weak, especially when we compare programmed ageing to something like a damage model of ageing, under which about half of the items are just as likely.
So I’ll try and follow up on the claims that actually look useful: programmed ageing (or more accurately, death) in “semelparous” organisms (“Semelparous organisms are animals and plants whose life histories are organized around a single burst of reproduction.” Source here, I’m basically just reading this.).
Anyhow, there does seem to be more to it than the wikipedia article would suggest, but I think the “all ageing is programmed ageing” claim is still just obviously wrong. To supply a potentially novel counterargument to a claim from the book I cited, chromosomes having telomeres, and thus “built-in” ageing, is actually very weak evidence that ageing is an adaptation, because chromosomes with telomeres just do so many other things. This same claim of adaptedness is apparently a problem in lots of evolutionary psychology, where a study finds that something is genetically determined and then goes “and therefore it’s an adaptation.”
I don’t personally buy programmed aging (as the explanation of most organisms’ aging), but I think this is a situation more like interpretations of quantum mechanics: no theory is entirely satisfactory, and this theory I am skeptical of (Copenhagen, or programmed aging) is not so obviously wrong that I should dismiss it as irrationality.
Hm. I admit that in the historical picture, it makes a lot of sense. There’s no fundamental reason why things have to die of old age, and the first microscopic “damage model” of ageing cited turned out to not fit the facts. And in a certain gene-driven viewpoint, it makes total sense that if you want the body to do something new as it ages, you need additional genes to make it do the new stuff.
But we get to take advantage of modern knowledge about how microscopic damage accumulates (see e.g. Aubrey de Grey’s stuff) to go beyond genes a bit, and when you see stuff like the metabolic rate and lifespan being really close to inversely correlated (the seed of the idea dates back to the 1930s, but I think the connection between metabolic rate and lifespan may be more recent), it’s good confirmation.
So, I guess what I’m actually confident about is that a damage model of ageing is correct for most animals, and that we’re not like octopuses or annual flowering plants. But that doesn’t actually mean that our ageing can’t be an adaptation—it would just mean that rather than dying at some specific time, the human body plan ages on some time scale that made sense for some long-gone ancestor, e.g. an early multicellular animal. This does have a slight falsifiability problem, though—either we simply never stumbled upon and spread the genes that would fix our damage, or we did stumble upon those genes, but didn’t spread them because ageing is good for us. Both leave essentially identical fossils and genomes behind.
One piece of evidence may be mutations that would have changed the time scale of ageing without granting immortality—it certainly seems unlikely that all these different species are still best served by dying with the proportionality to metabolic rate set down by our ancestor.
Hm, the evidence summarized there is quite weak, especially when we compare programmed ageing to something like a damage model of ageing, under which about half of the items are just as likely.
So I’ll try and follow up on the claims that actually look useful: programmed ageing (or more accurately, death) in “semelparous” organisms (“Semelparous organisms are animals and plants whose life histories are organized around a single burst of reproduction.” Source here, I’m basically just reading this.).
Anyhow, there does seem to be more to it than the wikipedia article would suggest, but I think the “all ageing is programmed ageing” claim is still just obviously wrong. To supply a potentially novel counterargument to a claim from the book I cited, chromosomes having telomeres, and thus “built-in” ageing, is actually very weak evidence that ageing is an adaptation, because chromosomes with telomeres just do so many other things. This same claim of adaptedness is apparently a problem in lots of evolutionary psychology, where a study finds that something is genetically determined and then goes “and therefore it’s an adaptation.”
I don’t personally buy programmed aging (as the explanation of most organisms’ aging), but I think this is a situation more like interpretations of quantum mechanics: no theory is entirely satisfactory, and this theory I am skeptical of (Copenhagen, or programmed aging) is not so obviously wrong that I should dismiss it as irrationality.
Hm. I admit that in the historical picture, it makes a lot of sense. There’s no fundamental reason why things have to die of old age, and the first microscopic “damage model” of ageing cited turned out to not fit the facts. And in a certain gene-driven viewpoint, it makes total sense that if you want the body to do something new as it ages, you need additional genes to make it do the new stuff.
But we get to take advantage of modern knowledge about how microscopic damage accumulates (see e.g. Aubrey de Grey’s stuff) to go beyond genes a bit, and when you see stuff like the metabolic rate and lifespan being really close to inversely correlated (the seed of the idea dates back to the 1930s, but I think the connection between metabolic rate and lifespan may be more recent), it’s good confirmation.
So, I guess what I’m actually confident about is that a damage model of ageing is correct for most animals, and that we’re not like octopuses or annual flowering plants. But that doesn’t actually mean that our ageing can’t be an adaptation—it would just mean that rather than dying at some specific time, the human body plan ages on some time scale that made sense for some long-gone ancestor, e.g. an early multicellular animal. This does have a slight falsifiability problem, though—either we simply never stumbled upon and spread the genes that would fix our damage, or we did stumble upon those genes, but didn’t spread them because ageing is good for us. Both leave essentially identical fossils and genomes behind.
One piece of evidence may be mutations that would have changed the time scale of ageing without granting immortality—it certainly seems unlikely that all these different species are still best served by dying with the proportionality to metabolic rate set down by our ancestor.