It seems to me that the better argument is more along the lines of “bodies put a lot of effort into policing competition among their constituent parts” and “bodies put a lot of effort into repelling invaders.” It is actually amazing that multicellular organisms overcome the prisoners’ dilemma type situations, and there are lots of mechanisms that work on that problem, and amazing that pathogens don’t kill more of us than they already do.
And when those mechanisms fail, the problems are just as dire as one would expect. Consider something like Tasmanian Devil Facial Tumor Disease, a communicable cancer which killed roughly half of all Tasmanian devils (and, more importantly, would kill every devil in a high-density environment). Consider that about 4% of all humans were killed by influenza in 1918-1920. So it’s no surprise that the surviving life we see around us today is life that puts a bunch of effort into preventing runaway cell growth and runaway pathogen growth.
What will cells of my body win by defecting and how can they defect?
Consider something like Aubrey de Grey’s “survival of the slowest” theory of mitochondrial mutation. The “point” of mitochondria is to do work involving ATP that slowly degrades them, they eventually die, and are replaced by new mitochondria. But it’s possible for several different mutations to make a mitochondrion much slower at doing its job—which is bad news for the cell, since it has access to less energy, but good news for that individual mitochondrion, because less pollution builds up and it survives longer.
But because it survives longer, it’s proportionally more likely to split to replace any other mitochrondion that works itself to death. And so eventually every mitochondrion in the cell becomes a descendant of the mutant malfunctioning mitochondrion and the cell becomes less functional.
(I believe, if things are working correctly the cell realizes that it is now a literal communist cell, and self-destructs, and is replaced by another cell with functional mitochondria. If you didn’t have this process, many more cells would be non-functional. But I’m not a biologist and I’m not certain about this bit.)
but good news for that individual mitochondrion, because less pollution builds up and it survives longer.
Recall that we are talking about evolution. Taking the Selfish Gene approach, it’s all about genes making copies of themselves. Only the germ-line cells matter, the rest of the cells in your body are irrelevant to evolution except for their assistance to sperm and eggs. The somatic cells never survive past the current generation, they do not replicate across generations.
Your mitochondrion might well live longer, but it still won’t make it to the next generation. The only way for it to propagate itself is to propagate its DNA and that involves being as helpful to the host as possible, even at the cost of “personal sacrifice”. Greedy mitochondrions, just as greedy somatic cells, will just be washed out by evolution. They do not win.
I’m well aware. If you don’t think that evolution describes the changes in the population of mitochondria in a cell, then I think you’re taking an overly narrow view of evolution!
Your mitochondrion might well live longer, but it still won’t make it to the next generation.
I happen to be male; none of my mitochondria will make it to the next human generation anyway. (You… did know that mitochondrial lines have different DNA than their human hosts, right?)
But for the relevant population—mitochondria within a single cell—these mutants do actually win and take over the population of the cell, because they’re reproductively favored over the previous strain. And if we go up a level to cells, if that cell divides, both of its descendants will have those new mitochondria along for the ride. (At this level, those cells are reproductively disfavored, and thus we wouldn’t expect this to spread.)
That is, evolution on the lower level does work against evolution on the upper level, because the incentives of the two systems are misaligned. Since the lower level has much faster generations, you’ll get many more cycles of evolution on the lower level, and thus we would naively expect the lower level to dominate. If a bacterial infection can go through a thousand generations, why can’t it evolve past the defenses of a host going through a single generation? If the cell population of a tumor can go through a thousand generations, why can’t it evolve past the defenses of a host going through a single generation?
The answer is twofold: 1) it can, and when it does that typically leads to the death of the host, and 2) because it can, the host puts in a lot of effort to make that not happen. (You can use evolution on the upper level to explain why these mechanisms exist, but not how they operate. That is, you can make statements like “I expect there to be an immune system” and some broad properties of it but may have difficulty predicting how those properties are achieved.)
(That is, the lower level gets both the forces leading to ‘disorder’ from the perspective of the upper system, and corrective forces leading to order. This can lead to spectacular booms and busts in ways that you don’t see with normal selective gradients.)
If you don’t think that evolution describes the changes in the population of mitochondria in a cell, then I think you’re taking an overly narrow view of evolution!
That may well be so, but still in the context of this discussion I don’t think that it’s useful to describe the changes in the population of mitochondria in an evolutionary framework (your lower level, that is).
happen to be male; none of my mitochondria will make it to the next human generation anyway.
Unless you have a sister :-) Yes, I know that mDNA is special.
The answer is twofold:
There is also the third option: symbiosis. If you managed to get your hooks into a nice and juicy host, it might be wise to set up house instead of doing the slash-and-burn.
Since this started connected to economics, there are probably parallels with roving bandits and stationary bandits.
It seems to me that the better argument is more along the lines of “bodies put a lot of effort into policing competition among their constituent parts” and “bodies put a lot of effort into repelling invaders.” It is actually amazing that multicellular organisms overcome the prisoners’ dilemma type situations, and there are lots of mechanisms that work on that problem, and amazing that pathogens don’t kill more of us than they already do.
And when those mechanisms fail, the problems are just as dire as one would expect. Consider something like Tasmanian Devil Facial Tumor Disease, a communicable cancer which killed roughly half of all Tasmanian devils (and, more importantly, would kill every devil in a high-density environment). Consider that about 4% of all humans were killed by influenza in 1918-1920. So it’s no surprise that the surviving life we see around us today is life that puts a bunch of effort into preventing runaway cell growth and runaway pathogen growth.
I just don’t see those “prisoners’ dilemma type situations”. Can you illustrate? What will cells of my body win by defecting and how can they defect?
Cancer is not successful competition, it’s breakage.
That’s anthropics for you :-)
Consider something like Aubrey de Grey’s “survival of the slowest” theory of mitochondrial mutation. The “point” of mitochondria is to do work involving ATP that slowly degrades them, they eventually die, and are replaced by new mitochondria. But it’s possible for several different mutations to make a mitochondrion much slower at doing its job—which is bad news for the cell, since it has access to less energy, but good news for that individual mitochondrion, because less pollution builds up and it survives longer.
But because it survives longer, it’s proportionally more likely to split to replace any other mitochrondion that works itself to death. And so eventually every mitochondrion in the cell becomes a descendant of the mutant malfunctioning mitochondrion and the cell becomes less functional.
(I believe, if things are working correctly the cell realizes that it is now a literal communist cell, and self-destructs, and is replaced by another cell with functional mitochondria. If you didn’t have this process, many more cells would be non-functional. But I’m not a biologist and I’m not certain about this bit.)
Recall that we are talking about evolution. Taking the Selfish Gene approach, it’s all about genes making copies of themselves. Only the germ-line cells matter, the rest of the cells in your body are irrelevant to evolution except for their assistance to sperm and eggs. The somatic cells never survive past the current generation, they do not replicate across generations.
Your mitochondrion might well live longer, but it still won’t make it to the next generation. The only way for it to propagate itself is to propagate its DNA and that involves being as helpful to the host as possible, even at the cost of “personal sacrifice”. Greedy mitochondrions, just as greedy somatic cells, will just be washed out by evolution. They do not win.
I’m well aware. If you don’t think that evolution describes the changes in the population of mitochondria in a cell, then I think you’re taking an overly narrow view of evolution!
I happen to be male; none of my mitochondria will make it to the next human generation anyway. (You… did know that mitochondrial lines have different DNA than their human hosts, right?)
But for the relevant population—mitochondria within a single cell—these mutants do actually win and take over the population of the cell, because they’re reproductively favored over the previous strain. And if we go up a level to cells, if that cell divides, both of its descendants will have those new mitochondria along for the ride. (At this level, those cells are reproductively disfavored, and thus we wouldn’t expect this to spread.)
That is, evolution on the lower level does work against evolution on the upper level, because the incentives of the two systems are misaligned. Since the lower level has much faster generations, you’ll get many more cycles of evolution on the lower level, and thus we would naively expect the lower level to dominate. If a bacterial infection can go through a thousand generations, why can’t it evolve past the defenses of a host going through a single generation? If the cell population of a tumor can go through a thousand generations, why can’t it evolve past the defenses of a host going through a single generation?
The answer is twofold: 1) it can, and when it does that typically leads to the death of the host, and 2) because it can, the host puts in a lot of effort to make that not happen. (You can use evolution on the upper level to explain why these mechanisms exist, but not how they operate. That is, you can make statements like “I expect there to be an immune system” and some broad properties of it but may have difficulty predicting how those properties are achieved.)
(That is, the lower level gets both the forces leading to ‘disorder’ from the perspective of the upper system, and corrective forces leading to order. This can lead to spectacular booms and busts in ways that you don’t see with normal selective gradients.)
That may well be so, but still in the context of this discussion I don’t think that it’s useful to describe the changes in the population of mitochondria in an evolutionary framework (your lower level, that is).
Unless you have a sister :-) Yes, I know that mDNA is special.
There is also the third option: symbiosis. If you managed to get your hooks into a nice and juicy host, it might be wise to set up house instead of doing the slash-and-burn.
Since this started connected to economics, there are probably parallels with roving bandits and stationary bandits.