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Hello, my name is Robert Arking,
I'm a professor
of Biological Sciences
at Wayne State University.
I've long been interested
in understanding
the genetic aspects
of the biology
of longevity and aging.
I've been asked to discuss
with you today
the topic of human
senescent phenotypes,
what are they,
how do they begin,
do they use the same
or different mechanisms,
can they be averted,
and most interestingly,
can they be reversed.
Let us begin.
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We experience our life
as being a long
and continuous
sequence of events.
Our conscious experience is not,
however, a reliable guide,
for the lifespan
is actually composed
of several different phases.
Each distinguished by different
patterns of gene expression,
functional levels,
and mortality rates.
These phases
are the developmental span,
the health span,
the transition phase,
and then the senescent span.
The developmental span
begins at our conception,
or for certain epigenetic
based events,
it might well begin
when your mother was a fetus
in your grandmother's womb.
Much of this phase is concerned
with proper physical
and mental development
and ends by about
20 years of age
when we reach
our maximum physical fitness.
The minimum human age specific
mortality rate has reached
just prior to sexual maturation.
Humans differ from most
other mammals in the fact
that we are sexually mature
long before
we are developmentally mature.
The health span occurs roughly
from ages 20 to 55 or 60 or so.
Gene-dependent longevity
assurance mechanisms
are operative.
There are high levels of repair
and maintenance,
high levels of homeostasis,
and sufficient reserve capacity
to deal with various stressors.
If you are healthy,
the age specific mortality rate
usually increases
at a very slow rate
and is at a low level
to begin with.
The transition phase
is when the age
specific mortality
begins
to significantly increase,
beginning
at about 55 to 60 years.
When the age related
senescent human phenotypes
begin to make themselves felt
and experienced.
The senescent phase extends
form age 55
until the end of life.
And many senescent phenotypes
that steal away
our functional ability
are highly individualized.
In all cases, what occurs
is that the cells burden
of damage increases
and we undergo
a loss of homeostasis.
Eventually,
a critical threshold is passed
and cell function ceases.
Note that aging can be reversed
in certain highly controlled,
entirely different situations
in laboratory animals.
Thus, the idea that aging
is non-reversible
is not strictly true.
But there are for now
no obvious ways
of translating
these exceptional reversals
into a more ordinary event.
Although the research
is very encouraging, I must say.
Perhaps, one of you might be
involved in that work some day.
Thus the senescent human
phenotypes occur mostly
during the last 20 years
of the ordinary human life
but as you will see,
they mostly have
their beginnings
much earlier
in the health span.
