Has ageing also been selected, and is it adaptive in that it helps reproduction? There have been suggestions that ageing was selected in order to reduce the number of adults so they did not compete with each other and so reduce reproduction in the group, but there is evidence to show that this is wrong.
It is essential to distinguish changes with time as an organism develops, and later grows, from the process of ageing. Ageing is not similar to the other biological changes that we go through with time as we develop in the embryo, and then grow older and mature after birth. An embryo gets older from the time it is fertilised, and the most obvious change with age after birth is growth itself, which is part of our genetically controlled developmental programme. We continue to grow for some 16 years. Puberty begins around 11 years and is the period of transition from childhood to adolescence, marked by the development of secondary sexual characteristics, accelerated growth, behavioural changes, and eventual attainment of reproductive capacity. Puberty changes occur as a consequence of the activation of a complex system that leads to an increase in frequency and amplitude of the hormones which stimulate the growth of sexual organs. This system is active in the early infancy periods, but becomes relatively quiescent during childhood, and puberty is marked by its reactivation leading to sexual maturity.
A remarkable case of failure to grow is Brooke Greenberg, a girl from Maryland who at 17 years old remained physically and cognitively similar to a toddler, despite her increasing age. She was about 30 inches tall, weighed about 16 pounds and had an estimated mental age of 9 months to 1 year. Brooke’s doctors termed her condition Syndrome X.
Another major change with age is that each of us will have two successive sets of teeth. The baby teeth begin to erupt at the age of around six months. Usually by 2 years old most of a child’s baby teeth will be in place. Some children get their teeth early, others later. Then typically by the age of 12, all of a child’s baby teeth will have fallen out and been sequentially replaced by a second set of teeth.
All these changes with age are quite different from ageing with its negative effects, and have been selected in evolution as part of our development programme to help with reproduction. So why do we have the negative effects of ageing? Was ageing selected and programmed into our development?
The blame must fall heavily on evolution. To repeat, evolution is only interested in reproduction and not in health once we have reproduced. Ageing, as we shall see, is due to the accumulation of damage in our cells with time. Ageing is not part of our developmental programme and there are no normal genes that promote ageing, though as we shall see there are changes in genes which can cause premature ageing. On the contrary, evolution has sensibly selected cell activities that prevent the damage in cells due to ageing, but which are usually only active until reproduction is greatly reduced. No animals die of old age, but they die because of predators and illnesses, including those which are age-related. The effect of evolution can be seen by comparing two-year-old mice with baby elephants at the same age. The mice are already old. Evolution has selected mechanisms to prevent the elephant ageing before it has offspring, and for some elephants old age is only evident from worn-out tusks. Evolution has generated great diversity in lifespan. For example, rats live for 7 years, and squirrels for 12.
As mentioned earlier, August Weismann, the great German theorist and experimental biologist of the nineteenth century, was one of the first biologists to use evolutionary arguments to explain ageing. His initial idea was that there exists a specific death-mechanism designed by natural selection to eliminate the old, and therefore worn-out, members of a population. The purpose of this programmed death of the old is to clean up the living space and to free up resources for younger generations: ‘… there is no reason to expect life to be prolonged beyond the reproductive period; so the end of this period is usually more or less coincident with death.’ Weismann probably came to this idea while reading the following notes of one of Darwin’s contemporaries and a co-discoverer of natural selection, Alfred Russel Wallace, which he later cited in his essay ‘The Duration of Life’:
…when one or more individuals have provided a sufficient number of successors they themselves, as consumers of nourishment in a constantly increasing degree, are an injury to those successors. Natural selection therefore weeds them out, and in many cases favours such races as die almost immediately after they have left successors.
But the theory is wrong, as almost all animals in the wild die before they get old. Death in the natural environment is not caused by ageing but is due to many other factors, particularly predators. Some animals like elephants do age in the wild, but such cases are rare. Wild mice die in the field at about 10 months, while in the laboratory they can live for several years. A number of animals have lifespans longer than might have been expected—for example flying birds live three times longer than land-living animals. Robins can live for 14 years but the albatross 50 years. This is because flying enabled them to escape predators and find new food sites, so early reproduction was no longer necessary. Why some reptiles like crocodiles and turtles have long lives is not clear.
The illnesses associated with ageing have a significant negative impact on human mortality. Weissman later rejected his theory, and then wisely proposed that ageing was the result of resources being given to the germ line rather than the body. If deleterious ageing occurred in germ cells, eggs or sperm, the species would die out—how right he was.
Theories concerning the ageing process emerged which are not based on it being adaptive, and thus not due to pressures of natural selection. The first was the ‘mutation accumulation’ theory, first proposed by the great scientist Peter Medawar in 1952, and referred to earlier, which proposes that mutations in the DNA of genes which lead to detrimental age-related changes in cells could accumulate over successive generations, if their serious negative effects were only expressed well after the age of peak reproductive success. These mutations are chance events. Life tables for humans show that the lowest likelihood of death in human females comes at about the age of 14, which in primitive societies would likely be an age of peak reproduction. Evolution has ensured that the peak of reproduction is when animals are young. Women lose their eggs at a more or less constant rate until they are 35, when the rate increases twofold.
Deleterious mutations expressed later in life are relatively neutral to selection because their bearers have already reproduced, and so have transmitted their genes to the next generation. As few individuals would actually reach those ages, such mutations would escape negative selective pressure—evolution would neglect them. The theory also predicts that if there are fewer external hazards for an animal, ageing will be slowed down, as is the case for animals like the albatross. According to this theory, ageing is a non-adaptive trait because natural selection is negligent of events that occur in a few long-lived animals that provide little additional contribution to offspring numbers.
Genes can be beneficial in early life, and then damaging later on. In other words, genes showing favourable effects on fitness at young ages, and deleterious ones at old age, could explain the ageing process. Such genes will be maintained in the population due to their positive effect on reproduction at young ages despite their negative effects at older post-reproductive ages, and those effects in later life will look exactly like the ageing process.
Mutation accumulation theory thus suggests that from an evolutionary perspective, ageing is an inevitable result of the declining force of natural selection with age. For example, a mutant gene that kills young children will be strongly selected against and so will not be passed to the next generation, while a lethal mutation with effects confined to people over the age of 80 will experience no selection because it has no effect on reproduction, and people with this mutation will have already passed it to their offspring by that age. Over successive generations, late-acting deleterious mutations will accumulate, leading to an increase in mortality rates late in life, which is just what we see and experience.