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 indefinitely. 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.