There are a number of theoretical debates about aging. One is the question of whether we are "programmed to die". Those who believe this think that at a point creatures get to a stage where the organism at a cellular level starts processes which deliberately set out to end the life of the multicellular organism. Another potentially contradictory view is simply that creatures accumulate damage up the point at which they can no longer survive.
It is possible, however, to look at different species and see how their lifespan operates. What is clear is that different species age in different ways. Some species don't age in the same way as others. It is worth having a look at how species vary and to what extent that explains the relationship between evolution and lifespan.
Firstly, it is clear that there are species where the adult commits some form of suicide after mating. Octopuses and Pacific Salmon
There are, however, also species which have negligible senescence. For example Bechstein's Bats, Naked Mole Rats and Bigmouth Buffalo Fish
Hive Creatures (eg NMR) such as Bees and Ants have distinctive phenotypes for the Queen.
However, the BBF and BB are creatures where the population is limited by external circumstances. In terms of BBF it is the predation of the young and BB it is environmental catastrophies.
A particularly interesting species is Hydra oligactis. This species lives in two different ways depending on the temperature. At 22 degrees centigrade it replicates by asexual budding, but if you cool it to 10 degrees it starts replicating sexually, but also aging and then dying after 60 days.
What I think is clear from the above is that evolution can and does select both to extend normal lifespan and to reduce it.
Thinking practically if grandparents compete for resources with their grandchildren then the species is likely to run out of resources.
We then have the question as to what the role of aging is in terms of development. My own personal view is that aging is simply a continuation of the development process using the cytosolic acetyl-CoA levels to determine mRNA splicing and gene expression options. However, there is a broader view which is similar called hyperfunction.
There is then the cellular reprogramming camp who believe that there is somewhere that we have not yet found that there is a backup copy of the development program which can be reset. (I think this is wrong as I think the development programme is primarily driven by metabolism and we know where all the molecules are).
There is also a programmed theory of aging in that at a point creatures robustly set out to die. That can be seen in the Pacific Salmon (above) and Octopuses, but I don't think that is true about most mammals.
On the other hand I do think that our average lifespan is programmed by our genes and other things we inherit life from (such as the cellular membrane). Our genes establish the balance between damage to mitochondrial DNA and repair of that DNA. This dynamic equilibrium affects how quickly we age and as consequence our average lifespan. I accept that it would be reasonable to say there that this is a form of programming. However, I do not myself describe it as "programmed aging" in the sense that applies to Pacific Salmon and Octopuses.
I wrote about recent mtDNA research here.
It is possible, however, to look at different species and see how their lifespan operates. What is clear is that different species age in different ways. Some species don't age in the same way as others. It is worth having a look at how species vary and to what extent that explains the relationship between evolution and lifespan.
Firstly, it is clear that there are species where the adult commits some form of suicide after mating. Octopuses and Pacific Salmon
There are, however, also species which have negligible senescence. For example Bechstein's Bats, Naked Mole Rats and Bigmouth Buffalo Fish
Hive Creatures (eg NMR) such as Bees and Ants have distinctive phenotypes for the Queen.
However, the BBF and BB are creatures where the population is limited by external circumstances. In terms of BBF it is the predation of the young and BB it is environmental catastrophies.
A particularly interesting species is Hydra oligactis. This species lives in two different ways depending on the temperature. At 22 degrees centigrade it replicates by asexual budding, but if you cool it to 10 degrees it starts replicating sexually, but also aging and then dying after 60 days.
What I think is clear from the above is that evolution can and does select both to extend normal lifespan and to reduce it.
Thinking practically if grandparents compete for resources with their grandchildren then the species is likely to run out of resources.
We then have the question as to what the role of aging is in terms of development. My own personal view is that aging is simply a continuation of the development process using the cytosolic acetyl-CoA levels to determine mRNA splicing and gene expression options. However, there is a broader view which is similar called hyperfunction.
There is then the cellular reprogramming camp who believe that there is somewhere that we have not yet found that there is a backup copy of the development program which can be reset. (I think this is wrong as I think the development programme is primarily driven by metabolism and we know where all the molecules are).
There is also a programmed theory of aging in that at a point creatures robustly set out to die. That can be seen in the Pacific Salmon (above) and Octopuses, but I don't think that is true about most mammals.
On the other hand I do think that our average lifespan is programmed by our genes and other things we inherit life from (such as the cellular membrane). Our genes establish the balance between damage to mitochondrial DNA and repair of that DNA. This dynamic equilibrium affects how quickly we age and as consequence our average lifespan. I accept that it would be reasonable to say there that this is a form of programming. However, I do not myself describe it as "programmed aging" in the sense that applies to Pacific Salmon and Octopuses.
I wrote about recent mtDNA research here.
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