You seem to be cherry-picking quotes. From the same paper:
aging – despite remarkable variation in the duration of life among different species – might be a fundamental and inevitable property of cellular life.
Aging clearly exists, and is (almost) universal. But the fact that organisms have a certain property is only weak evidence that property was selected for. As I commented here, the other possible explanations are that immortal varieties either never arise in the first place, and so can’t be selected; or else are always linked to some tradeoff or disadvantage which is selected against. And both options seem quite plausible and I believe have been demonstrated in specific cases.
The mechanism discussed in the article is (from memory, having read about the linked article once) roughly as follows. A cell accumulates damage over time (‘ages’). When it divides, it can split damage between both child cells, making them both somewhat younger. Or it can place most of the damaged organelles in one child cell, producing a young and an old cell. This is a tradeoff that (unsurprisingly) is resolved differently by different cells at different times.
But the fundamental idea is that aging is damage accumulating over time. That’s what the quote about “a fundamental and inevitable property of cellular life” refers to. There isn’t a gene or behavior ‘for’ aging, and therefore there isn’t an available mutation that doesn’t age because it doesn’t have that gene, and so evolution can’t select it.
Contrary to Lander’s view that “evolution has installed many many mechanisms to ensure that organisms die and make room for the next generation”.
Complex animals nonetheless have a method of producing young cells in their offspring—which capability is obviously a requirement for gene survival. That we don’t have the same sort of capability to refresh the cells in our own mature bodies is either an accident[1], or the costs/risks[2] of it aren’t worth it for our own benefit, or (per Lander, I guess) is counterproductive to your genes compared to short aging-enforced reproductive generations.
(your argument is good and I agree with it)
[1] (more complex design simply hasn’t been reached yet, or it’s impractical for adults, requiring a womb, etc.)
[2] I have no idea what risks would be present in a world where we replenish ourselves with young cells, but I can imagine at least novel types of bad growth and rejuvenation, aside from the normal cancers
I quoted the paper in support of my view (and in opposition to Lander’s). Then you said I cherry-picked that quote and here was another quote from the same paper that said something different. But I’m saying, no look, that other quote isn’t different, it doesn’t contradict what I’m saying at all.
So how am I exhibiting motivated cognition? Is it just because I initially picked the quote that best supports my case? The quote I didn’t pick didn’t contradict my case...
How could a distinguished professor of biology, a leader of the HGP and advisor to the US President, get something so elementary wrong, when even a biology undergrad dropout like myself notices this seems wrong?
before your second edit. LWers have a strong anti-deathism bias, at least anti-deathism for humans (chickens might be another matter entirely), and your hasty conclusion was an indication of it, as confirmed by your quote selection.
Your second comment appears to be factually wrong:
There isn’t a gene or behavior ‘for’ aging, and therefore there isn’t an available mutation that doesn’t age because it doesn’t have that gene, and so evolution can’t select it.
There are definitely are genes which affect aging, so there is something to select for.
I agree that when Lander says
I don’t think immortality is technically possible—evolution has installed many many mechanisms to ensure that organisms die and make room for the next generation. I bet it is going to be very hard to completely overcome all these mechanisms.
he shows a deathism bias, since he probably does not have the data to support his statement. A more charitable reading would be that prevention of aging is hard and requires a lot of genetic changes, something evolution never needed to bother with, so researchers have their work cut out for them.
How could a distinguished professor of biology, a leader of the HGP and advisor to the US President, get something so elementary wrong, when even a biology undergrad dropout like myself notices this seems wrong?
That sentence should be read with a ‘but’ at the beginning. I was saying that I couldn’t believe he would make such a basic mistake. I thought I must be missing something. That’s why I posted here instead of dismissing the whole thing as him being wrong.
I recognize I’m emotionally biased against deathism and thereby against people who appear to be pro-deathism. But I did make an effort to find out the actual truth.
Your second comment appears to be factually wrong:
There isn’t a gene or behavior ‘for’ aging, and therefore there isn’t an available mutation that doesn’t age because it doesn’t have that gene, and so evolution can’t select it.
There are definitely are genes which affect aging, so there is something to select for.
You’re right; there are definitely genes which affect aging and longevity and can be selected. And I expect that if they have no other effect, then the selection prefers those variants which confer longevity. It’s only when they are tied to tradeoffs or other effects caused by the same genes, that the selected variant may not be the longest-lived.
You seem to be cherry-picking quotes. From the same paper:
Aging clearly exists, and is (almost) universal. But the fact that organisms have a certain property is only weak evidence that property was selected for. As I commented here, the other possible explanations are that immortal varieties either never arise in the first place, and so can’t be selected; or else are always linked to some tradeoff or disadvantage which is selected against. And both options seem quite plausible and I believe have been demonstrated in specific cases.
The mechanism discussed in the article is (from memory, having read about the linked article once) roughly as follows. A cell accumulates damage over time (‘ages’). When it divides, it can split damage between both child cells, making them both somewhat younger. Or it can place most of the damaged organelles in one child cell, producing a young and an old cell. This is a tradeoff that (unsurprisingly) is resolved differently by different cells at different times.
But the fundamental idea is that aging is damage accumulating over time. That’s what the quote about “a fundamental and inevitable property of cellular life” refers to. There isn’t a gene or behavior ‘for’ aging, and therefore there isn’t an available mutation that doesn’t age because it doesn’t have that gene, and so evolution can’t select it.
Contrary to Lander’s view that “evolution has installed many many mechanisms to ensure that organisms die and make room for the next generation”.
Complex animals nonetheless have a method of producing young cells in their offspring—which capability is obviously a requirement for gene survival. That we don’t have the same sort of capability to refresh the cells in our own mature bodies is either an accident[1], or the costs/risks[2] of it aren’t worth it for our own benefit, or (per Lander, I guess) is counterproductive to your genes compared to short aging-enforced reproductive generations.
(your argument is good and I agree with it)
[1] (more complex design simply hasn’t been reached yet, or it’s impractical for adults, requiring a womb, etc.)
[2] I have no idea what risks would be present in a world where we replenish ourselves with young cells, but I can imagine at least novel types of bad growth and rejuvenation, aside from the normal cancers
My comment was about the tell tale signs of motivated cognition by the OP, not about the substance of the topic.
I don’t understand.
I quoted the paper in support of my view (and in opposition to Lander’s). Then you said I cherry-picked that quote and here was another quote from the same paper that said something different. But I’m saying, no look, that other quote isn’t different, it doesn’t contradict what I’m saying at all.
So how am I exhibiting motivated cognition? Is it just because I initially picked the quote that best supports my case? The quote I didn’t pick didn’t contradict my case...
Originally I was reacting to
before your second edit. LWers have a strong anti-deathism bias, at least anti-deathism for humans (chickens might be another matter entirely), and your hasty conclusion was an indication of it, as confirmed by your quote selection.
Your second comment appears to be factually wrong:
There are definitely are genes which affect aging, so there is something to select for.
I agree that when Lander says
he shows a deathism bias, since he probably does not have the data to support his statement. A more charitable reading would be that prevention of aging is hard and requires a lot of genetic changes, something evolution never needed to bother with, so researchers have their work cut out for them.
When I wrote,
That sentence should be read with a ‘but’ at the beginning. I was saying that I couldn’t believe he would make such a basic mistake. I thought I must be missing something. That’s why I posted here instead of dismissing the whole thing as him being wrong.
I recognize I’m emotionally biased against deathism and thereby against people who appear to be pro-deathism. But I did make an effort to find out the actual truth.
You’re right; there are definitely genes which affect aging and longevity and can be selected. And I expect that if they have no other effect, then the selection prefers those variants which confer longevity. It’s only when they are tied to tradeoffs or other effects caused by the same genes, that the selected variant may not be the longest-lived.