Welcome to our
lecture on How Nature, Nurture
and Chance Shape How We Age.
My name is George Martin.
I am a Professor Emeritus at
the University of Washington
in Seattle, Washington, USA.
This slide provides a brief
outline of the lecture.
We will be dealing with
three fundamental questions,
why organisms age?
Why various species
age so differently?
And, of special interest
to our own species,
why one observes such
in patterns of aging among different
members of the same species?
As a pathologist, I have done many
autopsies on geriatric subjects.
I have never seen
two individuals who
have aged in exactly the same
way, either qualitatively
All biology students fully
appreciate that phenotypes result
from both genes and environment, as
well as their various interactions.
But there is usually less interest
in the issue of chance events, one
reason why I will give
that component a good deal
of attention in this lecture.
Let's start with the question
of why organisms age.
I shall be presenting
what is often referred
to as the classical evolutionary
biological theory of why we age.
It is important to first understand,
however, that that theory is based
upon what could be called
age structured population
of iteroparous organisms.
By age structured,
I mean that we are
dealing with populations
that consist of individuals
of a wide range of ages.
By iteroparous, I
mean that these are
populations that have multiple
routes of reproduction
during their adult lives.
That scenario contrasts with groups
of organisms that undergo what
might be called
semelparous, or big bang
reproduction, namely single
terminal episodes of reproduction,
followed by death.
This slide gives two such examples.
On the left is a dying Spawning
Salmon and on the right
an Australian Marsupial Mouse.
These mice only manage to reproduce
in connection within a very short
period of rainfall, an event that is
essential for the growth of plants
and thus sufficient
food for progeny.
When the season is right,
males undergo a massive release
of stress hormones while they fight
for females, copulate and then die.
One could use the term programmed
aging for these two species
and also for many flowering plants.
Many of my colleagues, however, will
argue that even iteroparous species
like us undergo programmed aging.
Many of them believe that aging is
simply an extension of development.
We should, of course, always
welcome such alternative views,
but one can make strong arguments
against that proposition, which
that aging is adaptive.
That it is good for the
species to have organisms
die, as it preserves
for the younger population.
A famous late 19th
August Weismann published such
views early in his career,
but later changed his mind.
Suffice it to say that the majority
of geroscientists believed that
aging is non-adaptive and that it
cannot be explained by the type
of determinative sequential adaptive
alterations in gene expression
that characterize development.
This is not to say,
however, that development
is not an important determinant
of health span and lifespan.
I like to think of us as
protein synthesizing factories.
How well you build those factories
and how well you design the quality
controls will obviously
make a big difference
in how well these factories
function, and how long they last.