There are several other more sophisticated non-evolutionary (or at least not directly evolutionary) explanations of ageing very similar to wear-and-tear, but in these cases the damage is associated with an intrinsic breakdown of the genetic machinery, rather than an accumulation of chemical or physical damage. Paralleling the decline in fission rates in single-celled organisms, it is now recognized that cells within a multicel-lular body can only go through a limited number of cell divisions before ceasing active division. In the case of human cells, for example, the maximum limit is in the order of 50-60 divisions. This restriction is known (in honour of its discoverer Leonard Hayflick) as the Hayflick limit.48,49 What causes these Hayflick limits? Accumulation of deleterious mutations within cells may play some roles50 as well as changes in the quantity and distribution of chemicals ('epigenetic factors') which bind to DNA to influence gene expression, but a widely discussed candidate is the gradual shortening of 'telomeres'. Telomeres are, put simply, disposable buffers located at the ends of chromosomes. They comprise repeating DNA sequences and act as caps, protecting strands of DNA from recombining after replication51,52 (think of them as similar to the end of a zip fastener). With each cell division, a small amount of DNA is necessarily lost in replication at each chromosome end, resulting in ever-shorter telomeres and altered telomere structure. A key consequence of this shortening may be ineffective buffers and eventual replicative senescence. Intriguingly, cancer cells are different and potentially immortal in that many types can bypass replicative senescence by expressing greater quantities of special enzymes involved in the restoration of telomeres, called telomerases.53
Collect together cells with Hayflick limits and you potentially have a cellular explanation for the ageing of the whole organism. Indeed, it has been calculated that the Hayflick limit would allow a developing human foetus to grow and develop through repeated cell divisions just about long enough to complete development before senescence sets in.49 There is even some evidence that cells from short-lived species reach their Hayflick limits earlier than those of long-lived species.49 Similarly, several very long-lived animals, such as the American lobster and the rainbow trout, show high levels of telomerase in their cells.28 Telomeres shorten more slowly in longer-lived birds, and in Leach's storm petrels (a long-lived seabird) they may even lengthen.54 But are we describing a cause or an effect? Hayflick limits are highly variable both among cell types of the same species and among species. It therefore seems likely that the maximum number of cell divisions is tailored to fit the lifespan of the organism, and not the other way around.48,49 Of course, we still have to explain why cells cannot be given carte blanche to replicate indefinitely until the organism dies, but as we see from cancers, unlimited growth is not always a good thing.55 Furthermore, the limits on cell division cannot provide the whole explanation for senescence since many invertebrates, such as adult insects, show little cell division in their bodies56 yet (as we have seen in the case of antler flies) they still senesce. Finally, telomerase-deficient mice do not tend to show higher rates of ageing57; therefore, even if telomeres are primarily responsible for Hayflick limits, then telomeres cannot provide the complete explanation for ageing.
Just as the number of cell divisions may be tailored to fit the lifespan of an individual, another clue to the fact that senescence is shaped by natural selection comes when we consider what parts of a multicellular body tend to deteriorate and when. In vertebrates, circulatory system, nervous system, skin, and muscles all tend to give out more or less simultaneously. Of course this might arise because a single factor links them all (rather like multiple parts of a car malfunctioning when the battery goes58), but evidence indicates that the synchrony is much more likely to have arisen because different parts age independently and at similar rates. The relative lack of success of transplantation of old organs into young individuals supports this latter contention (similarly a gearbox from an old car will not be 'born again' when placed in a young car). As Richard Dawkins suggests,59 from an evolutionary perspective, there is little value in having a long-lived expensive Rolls Royce engine in a short-lived cheap chassis, and the deterioration patterns of animals' bodies largely support this interpretation.
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