The Entropy Theory
Surprisingly, at what we believe to be the dawn of immortality, mankind currently
finds itself
without a unified theory of aging. And although the telomere theory is rapidly
rising in the spotlight, the ‘entropy’ theory of aging, in one of its various forms,
is still probably more popular among scientists and the general population alike.
The entropy theory of aging is basically that
we age from wear-and-tear. Or more precisely, that the corrosive effect
of our own metabolism, coupled with a host of other outside assaults, often in the
form of free radical damage, causes our bodies to wear down on multiple levels from
the cellular to the macroscopic, with glycation, Mitochondrial and Nuclear DNA damage
being at the forefront in various versions of this theory. Our bodies try to repair
this damage, but to the degree to which the repair mechanisms are imperfect or unable
to keep up with the damage, we age. In short, like an old house or car, we unravel.
Entropy's Conundrum - Immortal Cell Lines
This seems reasonable enough, but when we stop to consider the fact that cell lines
that maintain telomere lengths do not suffer from any of the 'wear-and-tear' damage
listed above, the theory begins to fray at the edges. This includes embyonic
stem cells, germ cells, and all immortal single-celled organisms, which are almost
all single-celled organisms. With respect to DNA damage in particular, this is because of the simple fact that allowing that
kind of damage in those cells types was simply not a luxury evolution could allow
life to entertain. If germ cells accumulated this sort of DNA damage across divisions,
every species would quickly be driven into the ground as that damage
accumlated in the germlines that spawned successive generations. The same is true
for immortal single-celled organisms. Life requires that the core cells that represent
its line maintain near perfect fidelity, otherwise life simply cannot work, and
the repair and renewal mechanisms of the cell have, billions of years ago, risen
to this challenge because they had to. And DNA damage is really the only cellular damage that matters because any other damage is not carried on across cell divisions. The proteins that make up
the new cell are coded, from 'scratch', from the newly copied strand of DNA. As a consequence these cells are indistinguishable
from those that came before them. Together the 'immortal' cells actually represent
the majority of cells on Earth, and the backdrop against which mortal multicellular
life evolved. The somatic cells in the bodies of various complex organisms, on the other hand, whose telemores do
erode, are unique in the world in that they accumulate damage across cell divisions.
Nature has a precise plan at the cellular level. Where it needs immortality, it maintains perfect telomere length and the result is pristine immortal cells impervious to wear-and-tear. Where it needs high
proliferative capacity, but not quite immortality, as in adult stem cells, it expresses telomerase, but not enough to halt telomere erosion over a lifetime. And where it needs neither, it lets telomere shortening run its course.
The question is: What is nature's plan for us? What does it need from us and what rights and powers of life have we been granted as a result?
Other Problems with the Entropy Theory
Also, consider these problems with the entropy theory:
- Every cell in your body is actually part of an immortal cell line going back to
the dawn of life, and they have suffered no damage from that 4 billion year trip.
This is possible because until now that trip was taken entirely in the immortal
cell compartment as germ and embryonic stem cells, as the journey in that line from
single egg to an egg in a fetal girl's (ie your mother's, grandmother's, etc) ovaries
was repeated. Why now, in the final 70 years of this journey, will wear-and-tear
get the best of most of your body's cells?
- It fails to explain Progeric syndromes - diseases of accelerated aging.
- It fails to explain the wide range of lifespans in the Earth's species and how the
ravages of wear-and-tear have already progressed throughout the body of a 2 year
old mouse, but have almost left a 28 year-old human relatively untouched.
- It fails to explain how some animals - the Lobster, Rainbow Trout, certain species
of Turtle, Sharks, Rays, Alligators, and the Bristlecone Pine age either not at
all or undetectably.
- It underestimates the body's capacity for renewal and repair. It views aging in
animals as similar to aging in a house, where entropy gradually gets the best of
it. But an animal is actually like a house whose every molecule is actively involved
in the house's maintainance and where entire structures are constantly broken down
and rebuilt on many levels. All of the systems mentioned above are in fact maintained
perfectly well for three decades as a human, but begin to breakdown inexplicably after
that. Aging is in our opinion, not the entropy inflicted on the house, but the gradual
failure - or more specifically the intentional abandonment - of the
repair mechanisms that maintain these systems.
- It fails to explain why the world's mortal and immortal species appear to be divided
precisely along the lines of those whose telomeres erode and those that do not.
- Above all, it looks for the 'efficient' cause of aging and not the 'teleological'
cause. That is, it does not think to ask the question: Does aging have a purpose?
Nature has precise control over all biologoical functions in the natural world and
they all exist for a reason. But aging, as universal as it is, is assumed to be
a lone exception to this, and this assumption is further assumed to be so self-evident
that it need not be defended, argued or really even pointed out.
Nature Abandonment Theory
There are some popular variants of the Entropy Theory that begin to introduce the
concept of the individual's interests taking a back seat to those of the species,
which is the right direction. But they don't go far enough.
The Nature Abandonment Theory, for example, states that nature doesn't care about
us after our fertile years, because at that point we've already handed down our
genes and will not be handing down any more. If a gene exists which disposes us
to a heart attack at age 50, as opposed to 12, that gene will most likely get handed
down, and in such a way the genes that abandon us in old age are passed along, and
that this is essentially what aging is. We're getting warmer with this theory, but it still has problems:
- In response to the question 'Why are our lifespans limited the way they are?', to
answer by first assuming a fertile life with a finite window of a particular length
begs the question.
- It is predicated on some mechanism by which the genes change effect, or expression,
over time, for a gene to be able to suddenly cause damage late in life. But this in a nutshell presupposes
a fundamental aging mechanism in order to explain it. In fact there is such a mechanism
- it is called the telomere position effect, which is sufficient in itself to explain
aging.
In sum, Nature Abandonment assumes a finite life and relies on a fundamental aging mechanism in order to explain those very things and still offers no explanation of a downward pressure on age.
Extrinsic Causes of Death
Certain animals live longer than others. But why don't they all live for hundreds,
or thousands of years? What is the downward selection pressure on age putting a cap
on this? It has been understood for a while that the likelihood of death by extrinsic
causes (i.e., predation) is controlling the ages of various species. Species that are
likely to get picked off within a few years anyway, such as mice, have lifespans
that don't go much beyond that. On the other end of the spectrum we have animals
like certain seabirds and Humans which have few predators and are relatively long-lived.
Interestingly, the immortal species (Lobsters, Rainbow Trout, certain species of
Sharks, Rays, Turtles) score pretty low on the extrinsic likelihood of death scale
as well. The explanation for the mouse's shorter life is, under a corollary of the Nature Abandonment Theory, that a mouse
isn't going to get much procreation payback for living for 10 years, since it is
likely to get eaten before then anyway, so evolution does not select for for a longer-lived
trait.
The lifespans of various species do seem to be pretty neatly organized along this
axis. First and foremost, this should tell us something though - that nature is
in the driver's seat of longevity. Nature is not a helpless victim of entropy, but
can, on the contrary, easily increase the lifespan of a species by 150 times (Shrew versus Giant Tortoise) if evolutionary
conditions give it motivation for doing so. This should really alone put any wear-and-tear
theories of aging to rest, and should also tell us that any theories of aging without
a 'teleological' cause component should be questioned. In other words, there will
always be wear-and-tear. The question of aging is: When, why and how does nature
abandon its repair and renewal mechanisms that combat it?
As a theory to explain the underlying reason for the variance in different species'
lifespans, the Extrinsic Causes of Death theory succeeds. But it has been used for
more than that and taken too far. It has, in a way very closely related to the Nature Abandonment Theory, been used to explain aging
per se, by positing that aging is simply the result of thousands of time-bomb genes
in our DNA that have been allowed to slip in undetected because our ancestors essentially
died of other causes first, and that therefore evolution did not have the opportunity
or motivation to weed them out.
But we have a question for those who follow this theory of aging:
If you really were to put an immortal mouse into the wild, what are the true chances
that it would die of extrinsic causes before that species' natural lifespan, say
two years? Is it really over 99.9%? Because if it's not, the extrinsic causes/ nature abandonment death theory
is no good. The slightest edge in the game of procreation and survival is borne
out in the game of evolution. Has anyone ever observed mice, or any other species in the wild, to determine
conculsively that they die overwhelmingly of extrinsic causes before their natural
lifespan is up? There is not really any evidence out there demonstrating that this
is the case. And if there were, it should be rejected as defense of the nature abandonment theory, because it would be logically
bound to the conclusion that no animals in the wild die of old age.
In a nutshell, the extrinsic causes theory of aging fails to offer a source of downward selection
pressure on age needed to explain aging and death per se. Without it, only
a positive procreation payback, however small, could come from a long-lived mouse
and there would be nothing stopping a continual age increase of all animals as evolution
progressed.
The downward selection pressure, we believe, comes from supraindividual evolutionary
forces - i.e., species vs. species competition, as we will explain later. This can be seen as balancing
against the forces of individual evolution which push only upwards, where the compromise between the two
forces is the life span of the species. But a better perspective, really, is to see the life span of the individual
as a trait of the species, in precisely the same way that the lifespan of a red blood cell is a trait and function of the body and not
of the cell. Quick or slow turnover is a survival strategy for the species, meant to match environments where those species are at the bottom or top
of the food chain, respectively. Quick turnover allows the species not to be hunted to extinction, for species where there is a danger of that.
Slower turnover, where that luxury exists, allows the species to develop larger and more complex animals that can occupy and maintain
more complex and demanding niches.
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