Dr. Michael Fossel, M.D., Ph.D., gave a presentation on "Reversing
Human Aging" at the National Institutes of Health's Natcher Center on
April 16, 1996.  The presentation was sponsored by the Smithsonian
Institution's Smithsonian Associates.  LES members and subscribers
were notified of the talk, and a number of LES members attended.

For years, Dr. Fossel has studied progeria and related accelerated
aging syndromes.  He is convinced that the evidence from these
diseases, together with the fact that germ cells and cancer cells
do not age, indicates that aging is a regulated process, that is, a
function of gene expression, and not a function of "wear and tear."
His recent book, "Reversing Human Aging," reviews recent research into
"telomere" that identifies a mechanism for the regulation of aging.

This research shows that telomere, or "nonsense" DNA at the end of
each chromosome, is shortened with each cell division in dividing
cells.  Telomere functions like the tip of a shoelace.  Snip off
the tip bit by bit, and eventually the shoelace will unravel.  Once
telomere in a dividing cell becomes too short, the cell unravels,
that is, it ceases to divide, senesces, and dies.

This explains why we have limited life spans, why calorie restriction
and other methods that slow down metabolism and cell division may
extend life, and why progeria victims have short lives (they are born
with already-shortened telomere).  Why, then, don't we just stay young
and healthy, then drop like rocks at our appointed time?  The answer
is that on each chromosome the regulatory genes are located near
the tips, that is, near the telomere, and the expression of these
regulatory genes is influenced by telomere length.  With each division
beyond a certain point, the regulatory genes in dividing cells get a
little more out of whack.

Germ cells and cancer cells are the exception.  They are immortal
because they produce an enzyme, telomerase, that replaces the telomere
that otherwise would be lost in each division.  It doesn't restore
already lost telomere, but it prevents further losses.

Organisms with telomere-limited cells have a survival advantage
because damaged or mutated telomere-limited cells die off before they
can kill the organism.  Cancer, in which telomerase production is
turned on, is the exception.

Although gene expression leads to cell disfunction after numerous
divisions, changes in gene expression early in life are important to
individual development, maturation, and reproduction.  Telomere may be
involved in the master "clock" that regulates both maturational and
senescent changes in gene expression.  (Death, then, would be the
inadvertent byproduct of the continued ticking of the "clock" after
maturation and reproduction had been taken care of.)

Unfortunately, achieving immortality is not simply a matter of
introducing telomerase into normal cells.  First, some types of cells
do not divide (heart muscle or brain cells, for instance).  Second,
many potentially cancerous cells fail to become immortal and die off
because they do not also become telomerase-producing.  Introducing
telomerase wholesale would enable runaway mutant cells to divide

Perhaps some day we will be able to enable normal cells to produce
telomerase and to limit telomerase production in abnormal cells.
Right now, research into telomerase inhibition (cancer control) is
ahead of research into telomerase induction.

Dr. Fossel cautions that advances in telomerase induction may not
significantly extend lives right away.  There are still too many other
things -- viruses, bacteria, trauma, poison, genetic errors -- that
can happen to bodies.