Evolutionary necessity of senescence?

Francis Heylighen fheyligh at vnet3.vub.ac.be
Mon Feb 15 05:10:20 EST 1993

It is sometimes said that mortality through senescence is "necessary" in
genetic evolution. For example, V. Turchin and C. Joslyn in their
"Cybernetic Manifesto" (published in Kybernetes, Vol. 19, Nos. 2-3, p.
63-65) state the following:

"16.  Evolution and immortality

[...] In natural selection, the source of change is the mutation of the
gene; nature creates by experimenting on genes and seeing what kind of a
body they produce.  Therefore, nature HAS TO destroy older creations in
order to make room for the newer ones.  The mortality of multicellular
organisms is an evolutionary NECESSITY.  [...]"
[EMPHASIS added]

The statement that individual mortality is necessary for evolution is
rather strong. Therefore, in a later text, I have reformulated this idea
in a somewhat more prudent way:

"Natural selection entails survival and development as the essential
values. Although the death of individual organisms MAY BE USEFUL for
genetic evolution (genes themselves being immortal), it is no longer
necessary for cultural evolution. Hence the maximisation of survival
leads to the striving toward immortality."  [emphasis added]

This view was influenced by my study of 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.

A paper in a recent "Scientific American" issue (I don't have the
reference at hand), summarizing the most recent theories of aging, leads
me to an even more skeptical view. Though some theories seem to 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, and 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). 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 30-40 years. 

Now, if you are likely to die around the age of 35 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 35, 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. 

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. 

Another one is an apparently inbuilt limit on the number of times a cell
can divide (mitosis). This 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 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.

In conclusions, those genetic models of aging seem to imply that death is
not necessary for evolution, as Turchin and Joslyn originally stated:  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". 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". 

More information about the Ageing mailing list

Send comments to us at biosci-help [At] net.bio.net