The Evolutionary Causes of Aging and Death
Why aren’t we Immortal?
One of the core ideas of the Principia Cybernetica ethics is that “cybernetic” immortality is an essential long-term goal we (or evolution) should strive for. However, when assuming that immortality is “good” in an evolutionary sense, we must justify why we are not immortal as yet, being the products of evolution.
A useful way to look at this problem is Dawkins’s “Selfish Gene” picture of evolution, where the fundamental unit to be maintained by natural selection is not the individual, nor the group or the species, but the gene. Individuals are merely disposable vehicles for the replicating information contained in the genes. As long as the genes survive (that is, are replicated in offspring before the individual dies), the survival or death of the individual is not very important. This leads to the “disposable soma” (disposable body) theory of aging, which we will summarize below.
Though some theories assume that aging (and hence death) are preprogrammed in the genes, thus implying some kind of evolutionary necessity of individual mortality, more recent theories explain aging without such special assumptions. The main idea is that every evolutionary adaptation has a cost: using genes for one specific activity or function implies that resources (matter, energy, time, neguentropy) are wasted, which thus can no longer be invested in another function. In practice there is always a trade-off, and it is impossible to simultaneously maximize two different functions (e.g. reproduction and survival).
For a gene, the main criterion that must be fulfilled or maximized in order to be naturally selected, is that its vehicle (individual organism) should survive long enough to be able to produce (numerous) offspring. Now, one might argue that the longer the organism lives, the more offspring it can produce, and the more copies of its genes will be made. Hence, the genes of organisms that do not age, and thus live longer, would be naturally selected. However, mortality depends on at least two different factors: (internal) aging, and (external) perturbations (accidents, diseases, predation, starvation, …). Though a gene can make its vehicle or carrier stronger, smarter and more resistant, it can never completely eliminate all possible perturbations causing death.
On the other hand, we might imagine genes stopping the process of aging. There are enough examples of self-repair mechanisms in cells and organisms to suggest that this is possible. Moreover, the fact that genes themselves are immortal should be sufficient to counter any arguments based on uncontrollable deterioration because of the second law of thermodynamics. Indeed, it is well-known that primitive organisms (e.g. bacteria, algae, protozoids, …) are in a sense immortal. That is, when they reproduce (by mere splitting of cells) there is no difference between “parent” and “offspring”: both splitted cells continue to survive, and undergo further splits, without any apparent aging or senescence. Our own process of reproduction (meiosis) is merely a more complicated version of this, in which just a few cells (sex-cells or germ-line cells) can indefinitely reproduce, while the other cells die after a while. Even the increase of thermodynamic entropy can be counteracted indefinitely in an open system with a constant input of neguentropy. So there is no a priori reason why living systems would not be able to indefinitely maintain and repair their structural organization.
But the question is whether it is worthwhile for a gene to invest lots of resources in counteracting the effects of aging. The factor of death because of external perturbations could be measured as some kind of average probability for an individual to be killed in a given lapse of time due to external causes. This would make it possible to compute an average life expectancy, not taking into account internal aging. The normal life expectancy for primitive people living in a natural environment (unlike our own highly protective environment) seems to be about 20-30 years.
Now, if you are likely to die around the age of 25 by external causes, there is little advantage in spending a lot of resources on combating the effects of aging, so that you might theoretically live for 1000 years. That is why we might expect that in the trade-off between early reproduction and long-time survival the genes would tend towards the former pole, making sure that sufficient off-spring is generated by the age of 25, rather than trying to extend the maximal age beyond 120 years (the apparent maximum for humans).
This implies that if our present environment, where the probability of being killed by predators, starvation or diseases before reaching old age is much smaller than in the original human environment, would continue to exist for a million year or so, natural selection would promote genes that would make us live longer. (when we are speaking about an evolution towards cybernetic immortality, however, we mean a quite different phenomenon, on a much shorter time scale. This evolution would take place on the level of memes rather than genes. ) In fact, a similar evolution has been artificially produced in fruit flies: by only allowing the fruit flies to reproduce at an advanced age, there was a selection for longevity instead of a selection for quick reproduction. Thus, in a few years, time researchers were able to double the (very short) life span of the flies. This is an experimental confirmation of the disposable soma theory.
In conclusions, such genetic theories of aging seem to imply that death is not necessary for evolution: it is only a side-effect of the fact that a gene can spread more quickly by early reproduction than by long-term survival of its carrier, depending on the average life-expectancy (and reproduction expectancy) in the given environment. From the point of view of the selfish gene, there is no reason whatsoever why it should destroy older copies of itself in order “to make room for the newer ones” (a quote from our Cybernetic Manifesto). This is merely an anthropomorphization of “Nature” as an intelligent agent, looking ahead and concluding that the new generation should be promoted at the expense of the older generation. All genes are selfishly striving for survival, and the only thing that would make one of them give up the fight is because it is less fit than its rivals, not because it is “older”.
From that point of view, I would even reject the more careful formulation that mortality “may be useful for genetic evolution”. The only reason for mortality would be that not having it (i.e. maintaining the necessary apparatus for unlimited self-repair of cells and organisms) would take away many resources from reproduction, for a very small return in terms of reproductive fitness. But I would hardly call that “being useful”.
Different causes of aging
As to the process of aging, there seems to be a multitude of effects involved, so that we should not expect any single genetic mutation to solve the problem. One of those is the production of “free radicals” (a type of oxidyzing agents, damaging proteins necessary for the functioning of the cell) during energy production. Much of the damage done by free-radicals is repaired by the cell, but in the long term damage tends to accumulate. One of the suggested therapies to increase life-span (life-extension) is to combat free radicals by antioxydant chemicals such as selenium, Vitamin C and Vitamin E, or to minimize their production by calorie restriction diets.
Another one is an apparently inbuilt limit on the number of times a cell can divide (mitosis). This so-called Hayflick limit (of the order of 50 divisions) is well beyond the one that is reached during normal life, and should thus not be interpreted as a preprogrammed death. The hypothesis is that it functions to limit the risks for the development of cancer or tumors (characterized by unrestricted reproduction of cancerous cells). The mechanism seems to be that during each splitting of a cell, the chromosomes are copied incompletely, with a small stretch of DNA on the outer extremum being cut off during the split. The outer stretches of DNA (telomeres) for a young cell are not functional, so that losing them does not impair function. But after a sufficient number of divisions, the process would start to cut off functional DNA, thus making it impossible for the cell to survive. The cutting off does not happen during cell divisions (meiosis) producing sex cells (sperm or egg cells). Otherwise each subsequent generation would have less DNA than the previous one. This reminds us of the fact that the loss of DNA is not an unavoidable effect of increase of entropy or a similar physical principle leading to aging.
Very recently, researchers have managed to synthetically produce the enzyme telomerase, which is capable of produce new telomeres. This open up new avenues to combat those forms of again linked to the Hayflick limit.
- Theories of Aging FAQ
- Theories and Causes of Aging from the Aeiveos Science Group
- KIRKLAND, J. L. 1989. Evolution and ageing. Genome, 31: 398 – 405, a paper
- Medline references for Aging Reviews
- The Aging Research Centre
- Aging: a quick review of theories
- Life Extension by Brian Delaney
- a series of articles on aging in the Chicago Tribune