The consensus view on the evolution of aging is that it is a consequence of a race to the bottom in terms of competition for early life reproductive success. The result is mechanisms and systems that aid early fitness at the cost of later dysfunction – and consequent aging and death. This is known as the antagonistic pleiotropy hypothesis. So we exist, do pretty well at the outset of life, but are equipped with a biochemistry that is incapable of repairing itself well enough for the long term. Some metabolic byproducts cannot be broken down, and accumulate to cause issues. The adaptive immune system must store information, and eventually runs out of capacity. And so on.
There are other minority viewpoints on the evolution of aging, numerous varieties of the programmed aging hypothesis. In this view, degenerative aging is directly selected rather than a side-effect. It is in some way advantageous to fitness. Looking at today’s research materials, the variety of programmed aging hypothesis that springs to mind is the one invoking group selection: aging exists to control the population so that ecosystem collapse is avoided. Speaking generally, group selection is not well regarded, and not thought a valid mechanism of evolution. But are there circumstances in which researchers believe that group selection could be involved in the evolution of aging? The example here is a collection of organisms that are all clones of one another – such as microbes, or some lower animals such as nematodes.
Some worms programmed to die early for sake of colony
Evolutionary theorists originally believed that ageing evolved to reduce the population in order to increase food availability for the young, but scientists have since shown this cannot be true for most animal species as longer-lived non-altruists would usually be favoured by natural selection. However, certain organisms possess what appear to be self-destruct programmes, preventing them from living beyond a certain age. For example, in the tiny roundworm C. elegans, mutations to particular genes can massively increase their lifespan (from two to three weeks under laboratory conditions, to close to 20 weeks), presumably by switching off the life-shortening programme.
Researchers investigated the specifics of the C. elegans life cycle to understand why programmed death may work for them, by devising computer models of a C. elegans colony growing on a limited food supply. They tested whether a shorter lifespan would increase the reproductive capacity of colonies, by generating the equivalent of colony seeds (a dispersal form of worm called a dauer). They found that shorter lifespan, as well as shorter reproductive span and reduced adult feeding rate, increased the reproductive success of the colony.
“Our findings are consistent with the old theory that ageing is beneficial in one way, as they show how increasing food availability for your relatives by dying early can be a winning strategy, which we call consumer sacrifice. But adaptive death can only evolve under certain special conditions where populations of closely related individuals don’t mix with non-relatives. So this is not predicted to apply to humans, but it seems to happen a lot in colonial microorganisms.”
Shorter life and reduced fecundity can increase colony fitness in virtual Caenorhabditis elegans
In the nematode Caenorhabditis elegans, loss of function of many genes leads to increases in lifespan, sometimes of a very large magnitude. Could this reflect the occurrence of programmed death that, like apoptosis of cells, promotes fitness? The notion that programmed death evolves as a mechanism to remove worn out, old individuals in order to increase food availability for kin is not supported by classic evolutionary theory for most species. However, it may apply in organisms with colonies of closely related individuals such as C. elegans in which largely clonal populations subsist on spatially limited food patches.
Here, we ask whether food competition between nonreproductive adults and their clonal progeny could favor programmed death by using an in silico model of C. elegans. Colony fitness was estimated as yield of dauer larva propagules from a limited food patch. Simulations showed that not only shorter lifespan but also shorter reproductive span and reduced adult feeding rate can increase colony fitness, potentially by reducing futile food consumption. Early adult death was particularly beneficial when adult food consumption rate was high. These results imply that programmed, adaptive death could promote colony fitness in C. elegans through a consumer sacrifice mechanism. Thus, C. elegans lifespan may be limited not by aging in the usual sense but rather by apoptosis-like programmed death.