In accepting an evolutionary argument for ageing, there may be a temptation to believe that ageing is all in our genes. Thus, if it was not for those darn genes with late-acting deleterious effects that are not purged from the population, or genes which give us a right royal hangover after the excesses of the reproductive party, then perhaps we would live indefinitely. We have come full circle from wear-and-tear, but we wish to stress that without damage, the gene-based view would also be far too one-sided. Certain damsel-flies have lower rates of reproduction later in life because their wings tatter, while certain bacteria may decline in their rate of reproduction because of cellular damage—we may ask why damselfly wings are not made of sturdier stuff, or why bacteria cannot sort out their problems, but at the heart of ageing comes the damage.
Consider, for example, the observation that various strains of fruit flies selected for extended lifespan also exhibit an increased resistance to oxidative stress, through the enhanced activity of antioxidant enzymes.53 Do we age due to ROS, or a lack of further selection to do anything about it? In a way, both assertions may be right—gerontolo-gists and evolutionary biologists have simply been tackling the problem from different perspectives. The former mechanism provides one reason why things go wrong in cells, and the latter helps explain some of the variability in species responses.
Was this article helpful?