3

WHY WE AGE

Ageing is not a mechanism to prevent overpopulation. The history of Ireland shows that this is simply a common misconception. Ageing is a side effect of the evolutionary programme for life, whose goal is for our DNA to be passed on to our children. When we are 50, and our children are grown up and able to have children of their own, our work is done. Our body is allowed to age and can be ‘thrown away’. Known as the ‘disposable soma theory’, this idea is based on the assumption that a person’s development follows economic principles. When resources are scarce, two options are available: to invest in one’s children or to invest in one’s own body. Since each can only be done at the expense of the other, having lots of children means reducing one’s own life expectancy. This has been demonstrated in experiments with fruit flies, and in research among the British nobility.

By 2015, there were over 7 billion people living on planet Earth, and the population was rising by about 200,000 a day. Many people are extremely worried that, if this number continues to increase, a time will come when we can no longer produce enough food to ensure that everyone on the planet will have at least enough to eat to survive. Unbridled population growth could jeopardise the future existence of the human species. How can we keep the size of the population in check? We often hear the reasoning that such a thing as ageing exists so that people will die in time, thus preventing the population from growing too quickly. The ageing mechanism is said to be determined by our genetic makeup for that very purpose, thereby preventing our species from dying out.

Of course, it is not only humans who face the risk of overpopulation and extinction, but all species. Apart from ageing, other mechanisms are said to exist to limit the number of individuals of a species. Take, for example, an island where the population of lemmings has grown too large, and food shortages threaten to cause massive mortality. The mass suicide of some of the lemmings, by leaping off a cliff into the sea, is then said to prevent a species-threatening shortage of food. This is often quoted as a further example of a genetically programmed mechanism to limit the population of individuals within a species. Although such selfless behaviour on the part of lemmings appears logical, these animals do not, in reality, sacrifice themselves for the general good. The 1958 Disney documentary film, White Wilderness, showing this behaviour appears to have been staged. Similarly, the reasoning that there is a genetically determined ageing programme in order to curb the growth of human populations is also incorrect. In the following section I will use the example of the history of Ireland to show that the relationships between overpopulation and scarcity of resources, self-sacrifice, and ageing should be interpreted in an entirely different way.

AGEING IS NOT NECESSARY

Thomas Malthus (1766–1884) was a British demographer, economist, and clergyman. He is best known for his gloomy theories of demographics — the study of the size and structure of populations. In 1798, he published a pamphlet entitled An Essay on the Principle of Population in which he predicted that the global population would increase to such an extent that food production would no longer be able to keep up. The tipping point at which there would be a shortage of food is known as the ‘Malthusian ceiling’: the maximum possible size of the population in relation to the yield from available land. Once the ceiling was reached, famine would inevitably occur — the ‘Malthusian catastrophe’. Mass mortality would restore the balance between the human population and agricultural production.

Malthus’s work was extremely influential at the time it was published. Charles Darwin wrote that the essay was crucial to the development of his theory of natural selection.

As an economist, Malthus was witness to the start of the Industrial Revolution in England. This must have been a thrilling time, when entrepreneurs were able to realise large-scale projects that would previously have been considered impossible. But, as a man of the church, Malthus must also have been struck by the human misery that this process of industrialisation brought with it. The swift pace of industrial development created a huge demand for labour, prompting a massive wave of migration from the countryside to the towns. The number of city-dwellers increased rapidly, as did the inhumane conditions resulting from this swift rise in the urban population. Child labour, poverty, and alcohol abuse were rife. In addition, the depopulation of rural areas caused a severe drop in agricultural production, and it became necessary to import food from Ireland to provide ‘fuel’ for the English cities, the engines of economic development. But the population was growing at an explosive rate in Ireland, too, and agricultural yields were too small at that time to feed both the Irish and English populations. These developments led Malthus to reason that sooner or later everyone on Earth would be faced with great poverty and famine. For this reason, he called for an interventionist population policy to limit the number of children born, beginning with the poor. After all, they were the ones who had insufficient means to bring up their offspring and secure their future.

Even during his own lifetime, Malthus saw that his predictions were not always true. The potato had been imported to Europe from South America by Spanish explorers. It proved to be an extraordinarily good source of food — rich in vitamins, and high in calories. But the potato was not cultivated on any great scale, perhaps because the plant’s stalks and berries are poisonous. This changed around the year 1800, when potatoes began to be cultivated on a massive scale in Ireland. The success of this newly introduced crop staved off the Malthusian catastrophe.

Despite the non-appearance of the catastrophe in Ireland, it remains the case that there is indeed a relationship between environmental conditions, the amount of food available, mortality, and population growth. Malthus was not completely wrong. Ten years after his death, in the period from 1845 to 1849, almost all potato crops failed due to the ‘blight’, a fungal infection whose spread was accelerated by the practice of monoculture and the damp climate in Ireland. Once more, food shortages occurred, and this time they did indeed lead to great starvation and death. During the Irish Famine (1845–1850), an estimated one million Irish people died, and a similar number emigrated. The population fell by a quarter. Malthus turned out to have been right in predicting that the ‘land’ — the amount of food produced — can impose a check on population size. However, the Irish population was ravished not only by hunger, but also by disease. At that time, a person’s chance of dying from infectious diseases was large, especially among the poor, who were not well nourished. Typhus, cholera, and many other epidemics caused huge waves of deaths, and the young were hit hardest. Poverty, starvation, and infectious diseases formed an inextricable trinity of misery that claimed a large number of human lives.

The assumption that there is a mechanism for ageing stored in our genetic code in order to check population growth is not warranted. On the contrary, when we see that harsh conditions have caused mass mortality many times among the hundreds of thousands of generations that have reproduced, we recognise that no such genetic mechanism has been necessary to keep the number of people on the planet in check. And the same reasoning applies to all species in the animal and plant worlds.

The question should really be posed the other way round: how have humans managed to avoid extinction throughout the millions of years of their evolution? A simple answer is: because we invest as much as we possibly can in the next generation. If we were ever unable to keep enough offspring alive, especially when the circumstances around us (suddenly) become unfavourable, then we humans, or any other species in the same situation, would rapidly disappear from the face of the Earth. The past, both recent and distant, abounds with examples. Dinosaurs died out 65 million years ago as a result of climate change. Around the year 900 AD, the Maya culture in Mexico almost completely disappeared, probably because of prolonged drought. In today’s world, we interfere with the habitats of plants and animals, and then worry about the decline in biodiversity.

How can we explain the fact that individual members of a species continue to invest adequately in their offspring? In his 1876 autobiography, Charles Darwin wrote:

In October 1838, that is, fifteen months after I had begun my systematic enquiry, I happened to read for amusement Malthus on Population, and being well prepared to appreciate the struggle for existence which everywhere goes on from long-continued observation of the habits of animals and plants, it at once struck me that under these circumstances favourable variations would tend to be preserved, and unfavourable ones to be destroyed. The results of this would be the formation of a new species. Here, then, I had at last got a theory by which to work.

This oft-quoted passage shows how important Malthus’s ideas were for Darwin’s theory of natural selection. Darwin noted that humans and animals are able to produce far more offspring than the resources in the environment can support. Their reproductive programme is geared solely towards producing offspring. At the same time, an overabundance of offspring leads to competition between those children. Since genetic variation means that brothers and sisters differ slightly from one another, some siblings have a better chance of survival than others. These survivors are the ones who will pass on the reproductive programme to their offspring. In this way, the mechanism for reproduction and survival persists through the generations.

Around the year 1800, when the environmental conditions were relatively favourable, the average life expectancy in Ireland fluctuated around the 40-year mark. That is a minimum life-expectancy value for the human species, because if it sinks to below 40, the population will begin to shrink. Put more precisely: the chance of dying is then so high that a couple has insufficient time to raise at least two children to adulthood. During the time of the Irish crop failures, life expectancy dropped well below 40 years. More than half of newborns failed to reach the age of five, killed by a combination of cold, infectious disease, and famine. But even if they survived childhood, people in Ireland were not guaranteed a long life. Only the nobility could escape the bleak Malthusian scenario. They always had enough food and shelter; they could flee epidemics of infectious diseases, and that meant they lived longer. Their average life expectancy stood at around 60 years, even at that time.

Thanks to technological innovation and the mechanisation of agriculture, food production has increased continuously — something Malthus could never have imagined possible — and more people today are living longer lives than ever before. Also, the interventionist population policy expounded by Malthus to keep the number of children in check has had little effect in practice, insofar as it has been put into practice at all. The number of people living on the planet has continued to rise. The reason for this is not only that children are still being born in great numbers and staying alive, but also that we are living ever-longer lives. If, as is the case, the number of people on the Earth is continuing to rise, we must conclude that the purpose of the ageing process is not to keep population growth in check.

THE ‘DISPOSABLE SOMA’

If ageing is not a mechanism to prevent overpopulation, and if some species, such as hydras, do not age, why must we ‘suffer’ the ageing process? Why do our bodies and our minds become infirm, and why must these infirmities, as well as illness, eventually kill us?

There is one part of us that does not seem to age: our DNA, which contains the genetic code of our lives. Copies of our DNA are preserved in our progeny, and in this way, that code is protected from degeneration. So the question of why we age can be put more precisely: why do our bodies and minds decline as the years go by, while our genetic code remains intact?

The English gerontologist Tom Kirkwood came up with an answer to this question in the form of his ‘disposable soma theory’ (soma is the Greek word for ‘body’). Individual members of a species, including humans, are selected for fertility — the ability to produce offspring. Those offspring will carry a copy of the parent individual’s DNA. Obviously, those individuals who die young will not contribute to the next generation. The same is true of infertile individuals, irrespective of how long they live. So, when a childless couple dies, a branch of the family dies with them. In England, for instance, childlessness was common among the nobility. Over the centuries, much has been written about ‘extinct peerages’ — noble family lines that have died out. Through natural selection, species — including humans — have adapted their way of living to their environment to allow them survive long enough to reproduce. Once its children have been born and raised to adulthood, an individual’s body becomes ‘disposable’, since the continuation of its DNA has then been guaranteed. In other words, ageing is ‘allowed’ to occur. From an evolutionary point of view, after 50 years of faithful work, our bodies can be left to run down and decay: our DNA sloughs its old skin like a snake.

The disposable soma theory is based on the idea that the development, growth, and survival of individuals follows fundamental economic principles: the scarce resources that are available must be distributed optimally among several biological processes. To put it simply, there are two options: either individuals invest in fertility and reproduction, or they invest in maintaining their own body. One kind of investment always comes at the expense of the other. There is no doubt that investing in both body and mind are necessary and expedient. If a congenital abnormality, a physical defect, or risky behaviour means that an individual fails to reach adulthood and produce offspring, or if individuals fail to provide for their offspring, then, from an evolutionary point of view, all is lost. This is why humans have a body that will last about 50 years or so, depending on individual genetic predisposition, in order to engage in sex, reproduction, and care of their young.

The question is whether there is an evolutionary advantage to possessing a body and mind that remain functional for longer than 50 years. There is nothing ‘wrong’ with living beyond 50, unless investing in an above-average body comes at the expense of the investment necessary for reproduction. In the latter case, the individual may well live longer than average, but will produce fewer offspring. And natural selection will not allow those two characteristics to exist side by side: after all, the fitness programme that steers us is not geared towards longevity, but towards creating the next generation. The production of many offspring is what is maximised by natural selection. It is logical, but also contentious, to infer that investing more in maintaining our own bodies, allowing us to continue looking good and feeling healthy well beyond the age of 50, does not serve any evolutionary purpose. By then, the continuation of your DNA through your children is already guaranteed.

The biological ageing mechanism can be compared to the mechanics of an old jalopy juddering to a halt on the road. Timely inspections of the engine by a mechanic, regular tuning and adjustments, and replacement of damaged parts could have prevented the breakdown. But preventive maintenance is costly; the necessary time and money are not always available, and so it is often carried out inadequately. Our bodies, too, require preventive maintenance, and that is a complex business. In every cell of the body, damage to the DNA must continuously be identified and repaired to make sure that the genetic code it contains remains unaltered. After all, our DNA is the blueprint for the functioning of all our cells, tissues, and organs. To achieve this, an ingenious biological mechanism has developed: large knots of cooperating proteins ride like trains over the rails of the DNA molecules, identifying damage and repairing it on the spot as they go. This process requires a lot of investment. But it prevents permanent damage to a cell’s DNA, which can lead the cell to produce the wrong proteins, or to go ‘off the rails’ and cause cancer.

The proteins that make up cells, tissue, and organs may themselves be damaged over the course of time. These proteins are complex, folded structures whose functions depend on the way they are folded. To assist in the correct folding of these proteins, cells are equipped with other, specialised proteins called ‘chaperones’, which initiate and guide the folding process. Sometimes, proteins spontaneously unfold, or become damaged in some other way, lose their functionality, and have to be replaced. Some proteins, such as those in the lenses of our eyes, or in our brains, are unique; they cannot be replaced, but they can be repaired. Chaperones can help some proteins to re-fold back into the correct shape. But, just like repairing damage to DNA, this process also requires a great deal of investment, and so not all proteins are repaired or replaced at any cost. The proteins in the lenses in our eyes, for example, are originally fully transparent, but the older we get, the more they congeal like those in the white of an egg, becoming increasingly opaque. The result is cataracts. More resilient lenses are evolutionarily superfluous; humans only need keen eyesight for the duration of two generations. This is the reason people who require cataract operations are rarely younger than 50 years of age.

The disposable soma theory offers an explanation for why ageing is part of our lives, but also for why life expectancy differs so greatly from species to species. Mice develop in a very brief time into sexually mature adults, gestate their young for a short time, and give birth to a large number of offspring per litter. These investments in producing the next generation come at the expense of investing in maintaining their own bodies. Under natural circumstances in the wild, the average lifespan of a mouse is just a few months. In their natural environment, predation, cold, or lack of food means they are not blessed with a long life. That is why you seldom see an old mouse in the wild; they are all youngsters. They do age when kept as pets, or held in optimum conditions in a laboratory. When they reach old age, mice go grey, lose muscle strength and mobility, develop cancer, and die after a maximum lifespan of three years.

Changes in the environment can exert a great influence on the length of time it takes individuals to develop to sexual maturity, and on the structure and length of individuals’ lives. The evidence for this abounds. When circumstances are unfavourable and the chance of dying is high, the evolutionary pressure to produce more offspring increases. More progeny are needed. There is then selection in favour of those individuals that are able to reproduce at an early age, even to the detriment of their own ability to survive for a long time. We see this in mice. Like all other short-lived mammals, they have acquired characteristics that allow them to make the maximum possible investment in fertility at a young age.

The advent of trawlers — large ships that fish by dragging, or trawling, a funnel-shaped net behind them — brought about a drastic change in the circumstances in which cod live. Trawlers have become ever more powerful, the nets have become bigger, and their meshes smaller, all in the pursuit of landing ever greater catches. This new kind of fishing means that cod have much less chance of surviving in the sea if they are older, and therefore bigger. Only small, young fish can slip through the trawlers’ nets. This has led to a significant drop in the average age of cod living in the sea. Before the advent of trawler fishing, it was mainly the large cod that spawned, as they did so late in life. Now it is the small, young fish that maintain the species’ population. Fishery biologists have discovered that cod are reaching sexual maturity at a much younger age and smaller body size than before. The cod has evolved through this (non-natural) selection towards earlier development, and has thus adapted as a species to its changing environment.

Humans and elephants are far less exposed in their natural environments to dangers that could threaten their existence than cod are, and so their lives can last much longer. They can afford to invest in the maintenance and repair of their own bodies. Indeed, such investments are necessary to enable them to produce sufficient offspring, despite requiring many years to develop to sexual maturity, and long gestation periods for their unborn young. If we compare the lifetimes of mice, humans, elephants, and all other mammals, we see that their average life expectancy is inversely proportional to the number of offspring they produce. That is: the more offspring, the shorter the life. The lifespans of different species can vary from short and sharp to long and languid. But natural selection has given each species the length of life that fits the environment it lives in. Nowhere in the animal world do we find the combination of a perfectly maintained body and many offspring. This is in accordance with Tom Kirkwood’s disposable soma theory, and the distribution of scarce resources.

Some species’ lifecycle seems extremely strange, but can be better understood if we bear the disposable soma theory in mind. Salmon live most of their lives at sea. When they have built up enough fat reserves for migration and spawning, they enter rivers and begin to swim upstream. Once in the freshwater environment, they undergo a metamorphosis. Their colour changes, and the males develop a hook — called a kype — on their lower jaw. The spawning period lasts for about two weeks, and is so intense that most salmon do not survive it. In a very short space of time, they put all means available into their fertility and reproduction, at the cost of their own survival. As the season ends, the spawning grounds are strewn with dead salmon. Fewer than 5 per cent of adult salmon will eventually make it back to the ocean, where they return to their salt-water form and continue to grow. Their progeny will follow in their wake. And one day, they, too, will swim upstream and repeat the cycle.

But that is not even the most extreme example. After successful mating, the female praying mantis devours her partner. In this way, the male provides food for the female, to the benefit of both their offspring.

THE COST OF SEX

In the pursuit of experimental evidence for the disposable soma theory, much research has been done on fruit flies. These insects have been used for many years in a huge range of biological investigations, and have provided scientists with a wealth of knowledge. They live only a few weeks, which is an important prerequisite for studies into animals’ lifespans. Another, not unimportant, advantage is that they are cheap to raise in large numbers in the lab. However, scientists face a fundamental problem when carrying out their ageing experiments: when they identify a fruit fly that has reached a great age, it will, of course, be biologically old, less fertile, and on the verge of death. But it is precisely these animals the researchers want to use for their (crossbreeding) experiments.

During his doctoral research, Bas Zwaan, an inspired Dutch professor of genetics, came up with an elegant solution to this problem. He made use of the phenomenon that fruit flies live longer when the temperature is low, and shorter when it is high. He divided each new generation of flies randomly into two groups. One group was exposed to a high-temperature environment, allowing the scientist to establish quickly which of the otherwise indistinguishable individuals were naturally long-lived. Once he had found out in this way which families were long-lived and which were short-lived, he took their siblings, which had been kept in cooler conditions and so were still alive, to use in his experiments. And his results were remarkable. It turned out that repeatedly selecting the longest-lived flies for reproduction led to a significant increase in average lifespan within just a few generations. Bas Zwaan’s selection programme for longevity in fruit flies was comparable to, and just as effective as, the ancient selective breeding activities of dairy farmers in Friesland, leading to the famous high-milk-producing qualities of today’s Friesian cows.

At the same time, Bas Zwaan also studied the flies’ capacity to produce eggs. Remember, he had selected neither for nor against this characteristic. He found that the long-lived flies produced fewer eggs during their lifetimes. And the opposite also turned out to be the case: fruit flies that produced a lot of eggs lived significantly shorter lives. These biological experimental results are in accordance with the disposable soma theory: investments in living longer come at the expense of investments in the number of progeny produced.

The underlying mechanism in the issue of whether body or brood is prioritised has also been described as ‘the cost of sex’. The British biologist Linda Partridge decided to try to get to the bottom of this mechanism. One of her experiments involved studying survival rates among male fruit flies that she had divided into two groups: one group that had sex, and another that did not. She found that the mortality rate among males that were presented with females to mate with every day was five times higher than that among males that were not allowed to mate. This increased risk of dying disappeared again as soon as the males were denied contact with females. Under the microscope, it could be seen that the sexually active males had suffered considerable damage, including to their wings, during the act of mating. Since fruit flies have only a very limited capacity for repair, sex usually leads to lasting damage, a loss of functionality, and thus increased mortality. Such complications related to mating are known as the ‘direct cost of sex’.

There are also ‘indirect’ costs of sex. They are not linked to the act of mating itself, but to the ability to be sexually active and to produce offspring. In other words, this is the price that has to be paid for the ability to make several versions of the same species. Most species have two sexes — male and female — each of which has just one kind of gamete, or reproductive cell. But hermaphroditism — the state of having both genders — also exists in the animal world. Solitary hermaphrodites can reproduce independently, without the need to mate with other individuals from the same species.

We get a first indication of the indirect cost of sex when we look at sexless species such as the hydra. It reproduces by means of budding from one of its ‘totipotent’ stem cells, which are distributed throughout its whole body. No sex of any kind is involved in this method of reproduction. These are the same stem cells that can be used to repair all types of tissue damage. In this way, the little polyp can reproduce by cloning itself, while managing to avoid the ageing process by means of its excellent regenerative abilities.

Not all that long ago, it was discovered in the lab that some hydras undergo a sexual transformation. This happens when conditions become less favourable. Hydras see such a change as a threat to their survival. The asexual animals react by becoming hermaphrodite hydras. The evolutionary logic of this is that sexual reproduction will give a hermaphroditic hydra more chance than asexual cloning of producing successful offspring in a changing environment. But there is a high price to be paid for this sexual transformation. Unlike their asexual counterparts, hermaphrodite hydras’ statistical chance of dying does increase as they get older. Hermaphrodite hydras do age!

Stem-cell researchers have found out why such hydras are susceptible to ageing. In all mammals, the reproductive cells originate in what biologists call the germ line — in the ovaries or testicles — which is made up of ‘unipotent’ stem cells. These are stem cells that only have the ability to develop into reproductive cells, or gametes. So, the stem cells in the germ line are fundamentally different from their ‘totipotent’ counterparts that can develop into any kind of bodily tissue and which can be used by a hydra, for example, to clone itself. When a hydra becomes a hermaphrodite, it still possesses stem cells, as in the germ line, but they no longer have the ‘totipotent’ ability that those of an asexual hydra have. The conclusion is obvious: such a sexual transformation comes at the expense of a hydra’s regenerative powers. Or, to put it another way: a hermaphrodite hydra’s body becomes ‘disposable’.

ARISTOCRATIC FRUIT FLIES

In 1998, I had the opportunity to work with Tom Kirkwood for a year in Manchester. His disposable soma theory inspired me to think about how and why we humans age. Once I had completely understood the evolutionary concepts involved in the theory, I was faced with the inevitable question: Does the disposable soma theory apply to humans, too? Until then, the only evidence gathered on the theory was from fruit flies.

In Leiden, studying under Professor Jan Vandenbroucke, I had been trained in the observational method for the scientific study of humans — called the epidemiological method. Most research biologist use experiments: working in the lab, they deliberately introduce a change in the genetic material of their test animals, or in their environment, and then study the effects of that change. However, for various reasons, most such laboratory experiments cannot be carried out on humans. Jan Vandenbroucke taught me that spontaneous events in human populations can resemble the kind of deliberate interventions made by experimental biologists in their labs, although, of course, those changes were not intended for any particular purpose. By closely studying these events — pseudo-experiments — in human populations, a lot can be learned about the causes underlying illness and health. For example, patients suffering from age-related blindness often turn out to be carriers of genetic variations in the body’s immune defences against infections. This knowledge has helped to define the role of immune defences in causing damage to the retina.

I suggested to Tom Kirkwood that we should use the epidemiological method to test his disposable soma theory. His initial reaction was negative. What spontaneous events among humans could be compared to Bas Zwaan’s crossbreeding experiments with flies? Unlike in an experiment in the lab, where flies that have been specially selected for longevity are forced to have sex, human beings usually have sex voluntarily and fairly randomly. However, the principle that sexual reproduction jumbles up the genetic material of a male and a female is the same for humans as it is for flies. For that reason, the children produced by a couple can be seen as the results of a genetic experiment carried out by the mother and father — even if that was not, of course, the motivation of the parents for having those children.

Kirkwood eventually came round to my way of thinking. Using the guiding principle of Bas Zwaan’s experiments, Tom Kirkwood and I began searching for sets of parents in which he, she, or both had reached advanced old age, in order to investigate whether the children of that union lived longer than average, and had fewer children than average themselves. As always in scientific research, there was an element of luck involved. In that year, 1998, advertisements appeared in the British newspapers for a genealogical CD containing every aristocratic title, and a list of those who held them. From time immemorial, the British nobility has kept precise family history records — who married whom, how many children they had, and how long they lived. This CD made those archives available, even to ‘commoners’, with the click of a mouse. Anyone could check whether they were descended from a noble family.

That CD presented us researchers with a golden opportunity. It offered a chance to study the descendants of thousands of married couples as if in a natural experiment. The fact that they were all aristocrats also solved another tricky problem. Differences between socio-economic classes can seriously disrupt observational studies. Members of the upper class have a lower mortality rate, live longer, and have fewer children, on average. A superficial examination of the data can lead to a false conclusion: that class can explain why some people live longer and have fewer children than others. However, since these British aristocratic families have always belonged to the upper class through the centuries, and people from lower socio-economic classes were not included in the archives, this problem did not occur.

Once Kirkwood and I had sorted the thousands of aristocratic lives into groups, we noticed that married noblewomen who died young had had fewer offspring than those who lived longer. That’s logical, of course, because a longer lifetime means more opportunity to bring children into the world. But, a long life after the menopause clearly does not have that advantage, since a woman’s natural fertility is then at an end. Remarkably, it appeared that noblewomen who reached the age of 80 and above were more often childless or had given birth to just one living child. It makes no sense to suppose that these women had deliberately decided early in life to remain childless or to have few children so that they could live to be very old. On the contrary, succession was of paramount importance in British aristocratic families, and so we can reasonably assume that these women’s childlessness was not by choice. In line with the disposable soma theory, and in accordance with the fruit-fly experiments of Bas Zwaan, we were able to conclude that a long human life and a large number of children usually do not go together.

After Kirkwood and I published a scientific paper describing our findings, the British press — always on the lookout for a juicy story — ran the headline ‘British Aristocracy Mate Like Fruit Flies’.

One remarkable realisation that came out of our study of the British aristocracy was that in modern times there no longer appeared to be a relation between age at death and number of children — I return to this point in Chapter 5 — as if there were no longer any ‘costs of sex’ in our modern society. In part, that is, in fact, the case. Death in childbirth, let alone death as a direct consequence of having sex, are now extremely rare. Most sexually transmitted diseases can now be cured. However, the question remains whether having more or less sex makes you live longer or die sooner. It is often claimed that sex is good for your health. However, this is based on the fact that healthy people remain sexually active into old age, while those who report less sexual activity tend to be frail and sick. But is it not probable that people who are sick and infirm have less sex for that very reason, rather than the other way round? Sex in old age has an emotional value, and is important in relationships. It is unlikely that it makes you either live longer or die sooner.

Sexual reproduction forms an integral part of the lives of humans and other (mammalian) animals. This evolutionary development has led us to invest in our offspring at the expense of ourselves. This provides a logical explanation for the reason people age. In the chapters that follow, I further explore the way in which sex is partially responsible for causing us to age.