The Biological Basis of Aging and Death

Abstract

A Means to an End: The Biological Basis of Aging and Death William Clark Oxford University Press A Means to an End: The Biological Basis of Aging and Death by William Clark deals with senescence, the process by which our vulnerability to disease and death increases steadily with age. One chapter discusses the evolutionary basis for differences in lifespan. We may be tempted to say that naturally living organisms wear out, as do machines, and we should not be surprised when tissues grow old and fail to function. However, this process for similar tissues occurs at quite different rates. At the microscopic and biochemical level, the cellular processes in a mouse and a human are quite similar. Yet the maximum lifespan of a mouse is only 3.5 years while for a human it is 122 years. Clearly, the tissues of some species are engineered to function longer than those of other animals. Why do different species have such different lifespans? Clark points out that part of it seems related to the age of reproduction. Animals whose function declines before reproduction would be out reproduced by animals whose bodies lasted longer. What has prevented human bodies from evolving to last longer is that most of us have finished rearing our young by the time really serious deterioration has set in (say age 65). While we would like to live longer, living into retirement age contributes little to the number of descendants we leave. Thus, if the price of this living longer is fewer children born at younger ages, there is likely to be selection against the genes for body maintenance. While Clark argues that we have genes for senescence (as well as genes that retard it), he never is quite clear on why those that delay senescence (and hence have a longer reproductive life) do not out reproduce those experiencing earlier senescence. The missing detail is that delaying senescence probably has costs (possibly from diverting energy to cell maintenance and repair). Individuals that divert resources from bodily maintenance can use these resources to avoid being eaten, to fight parasites, or to find mates. The individuals that leave the most descendants accept a shorter lifetime in exchange for other benefits that contribute to leaving descendants. Arking (1998) provides a better discussion of theories of aging. That an organism's length of life can evolve in response to selection for early or late reproduction has been shown in several experiments. When each succeeding generation of fruit flies was grown from eggs laid late in the life of the fly, the lifespan of fruit flies was increased. In Trinidad, it was found that guppies from the lower pools reproduced earlier and had a shorter lifespan than those from the upper pools. In the lower (further down the river) pools the main predator ate guppies of reproductive age. In the upper pools the main predator ate immature guppies. In the later case, once a guppy had survived to reproductive age it would leave more offspring if its body survived longer. Thus, the guppies had evolved to live longer. When breeding stock from the pools where lifetime was short were introduced into pools where the predators neglected the older fish, the guppies evolved towards an older lifespan. Finally, when predators that went after the older fish were introduced into the pools with the originally short lived upper pool stock, these guppies evolved shorter lifespans. Thus, it appears that in these two species at least, and probably in other species, including humans, the gene pool contains genes for a longer life span. In human populations (races) evolving in different circumstances, lifespans could be different. Miller (1994) has argued that in climates where male provisioning of the young is necessary for children to survive, selection for a long life has been stronger than in tropical areas. The evolutionary mechanism that produces the correlation between lifespan and age of reproduction could also operate within humans. …