From: Robert J. Bradbury (bradbury@aeiveos.com)
Date: Wed Jun 16 1999 - 13:18:28 MDT
I thought I would comment on the threads regarding life expectancy,
longevity quotient and telomeres & cloning.
a) Long telomeres DO NOT EQUATE with long lives.
Mice have longer telomeres than humans but much shorter lives.
b) Short telomeres do equate with reduced cancer rates.
Humans have shorter telomeres and that probably plays a
role in the 10-100x lower cancer rate humans have (compared
with smaller organisms with many fewer cells).
c) Short telomeres equate with reduced replicative capacity of cells.
So, short telomeres (whether in normal humans or "clones") will
reduce the replication potential of normal cells and tend to have
a limiting effect on health (or longevity) in those situations where
increased cellular replacement capacity is necessary.
The studies have demonstrated that in non-cancerous cells
(i.e. those that have not accumulated deleterious mutations),
long telomeres provide increased replicative capacity (to
several hundred divisions). So *IF* you could reduce the
mutations that lead to the development of cancer (that come
from *both* environmental hazards and the natural mutation
level that occurs when replicating DNA), then engineering
long telomeres would provide increased longevity (until
something else goes wrong).
One's "longevity quotient" is only ~50% related to the longevity
of one's parents. The rest is unrelated to parental longevity
(it could be related to parent's intelligence, personality traits
related to risk taking behaviors, or environmental factors).
Leonid & Natalia Gavrilov and T. Kirkwood, I believe,
have published recent papers showing that the relative portions
of your l.q. contributed by mothers & fathers (of different ages)
to sons & daughters (different sexes) varies. Any generalizations
will likely be innacurate.
Leonid & Natalia's recent work point out that continued increases
in "longevity" predicted by other demographers, may not be
certain, because the "longest-lived" may possess unique genomes.
I.e. there is a fundamental difference between extending longevity
to the maximum allowed by the "average" genome, and the maximum
allowed by the "optimal" genome.
The only way around this problem is to switch from engineering the
external environment (sterile techniques, sanitation, pollution, etc.)
that have provided most of the longevity increases historically,
to engineering the internal environment (optimal genomes,
nanoenhancment, etc.).
Robert Bradbury
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