Antagonistic Pleiotropy
Medawar's theory was further developed by George C. Williams in 1957, who noted that senescence may be causing many deaths, even if animals are not 'dying of old age.' In the earliest stages of senescence, an animal may lose a bit of its speed, and then predators will seize it first, while younger animals flee successfully. Or its immune system may decline, and it becomes the first to die of a new infection. Nature is such a competitive place, said Williams, (turning Medawar's argument back at him), that even a little bit of senescence can be fatal; hence natural selection does indeed care; ageing isn't cost-free.
Williams's objection has turned out to be valid: Modern studies of demography in natural environments demonstrate that senescence does indeed make a substantial contribution to the death rate in nature. These observations cast doubt on Medawar's theory. Another problem with Medawar's theory became apparent in the late 1990s, when genomic analysis became widely available. It turns out that the genes that cause ageing are not random mutations; rather, these genes form tight-knit families that have been around as long as eukaryotic life. Baker's yeast, worms, fruit flies, and mice all share some of the same ageing genes.
Williams (1957) proposed his own theory, called antagonistic pleiotropy. Pleiotropy means one gene that has two or more effects on the phenotype. In antagonistic pleiotropy, one of these effects is beneficial and another is detrimental. In essence this refers to genes that offer benefits early in life, but exact a cost later on. If evolution is a race to have the most offspring the fastest, then enhanced early fertility could be selected even if it came with a price tag that included decline and death later on. Because ageing was a side effect of necessary functions, Williams considered any alteration of the ageing process to be "impossible."
Antagonistic pleiotropy is a prevailing theory today, but this is largely by default, and not because the theory has been well verified. In fact, experimental biologists have looked for the genes that cause ageing, and since about 1990 the technology has been available to find them efficiently. Of the many ageing genes that have been reported, some seem to enhance fertility early in life, or to carry other benefits. But there are other ageing genes for which no such corresponding benefit has been identified. This is not what Williams predicted. This may be thought of as partial validation of the theory, but logically it cuts to the core premise: that genetic trade-offs are the root cause of ageing.
Another difficulty with antagonistic pleiotropy and other theories that suppose that ageing is an adverse side effect of some beneficial function is that the linkage between adverse and beneficial effects would need to be rigid in the sense that the evolution process would not be able to evolve a way to accomplish the benefit without incurring the adverse effect even over a very long time span. Such a rigid relationship has not been experimentally demonstrated and, in general, evolution is obviously able to independently and individually adjust myriad organism characteristics.
In breeding experiments, Michael R. Rose selected fruit flies for long life span. Based on antagonistic pleiotropy, Rose expected that this would surely reduce their fertility. His team found that they were able to breed flies that lived more than twice as long as the flies they started with, but to their surprise, the long-lived, inbred flies actually laid more eggs than the short-lived flies. This was another setback for pleiotropy theory, though Rose maintains it may be an experimental artifact.
Read more about this topic: Evolution Of Ageing