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 asssuming 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 resistent, 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.
See Further:
