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Recently in Salon Health & Body

Urge: Naked World
Cruisin' is confusin'
A British bereavement group called Cruse will change its name.
By Jack Boulware
[03/29/00]

Nobel dude
Kary Mullis revolutionized genetic research but thumbs his nose at the scientific establishment. It thumbs its nose right back.
By William Speed Weed
[03/29/00]

Urge
Stop raping my loved ones
Dating a victim of sexual assault means learning, awfully, how rape touches everyone.
By Andrew Strickman
[03/28/00]

Urge
The conversation
There comes a time in every relationship when I've got to talk about my rape.
By Jenn Shreve
[03/28/00]

Urge: Naked World
Battle of the bra barons
There's a cat fight brewing over who is the mother of the latest cleavage creator.
By Jack Boulware
[03/28/00]

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Some human tissues that divide indefinitely, such as reproductive cells producing sperm and eggs, contain telomerase. So do cells in embryos, but the telomerase gene is inactivated in most cells after birth.

Reactivating telomerase could replenish lost cells. Warner mentions the possibility of restoring epithelial cells in the retinas to restore lost eyesight. Telomerase genes have been successfully reactivated in retinal epithelial cells grown in tissue culture, in work done at the University of Texas Southwestern Medical Center and the Geron Corporation. Geron has filed for patents on hTRT, the telomerase reverse transcriptase protein. Warner notes, "The problem with turning telomerase back on is that's one of the things that happens in cancer." Cancer cells are all about telomerase and unrestricted cell division.

Steven Austad is a zoologist who studies aging. In his lucid, engaging book "Why We Age," he describes his study of opossums on a Georgia barrier island -- Methuselah opossums who had smaller families, often bred two years in a row instead of one, and aged more slowly, living a whopping three years instead of two.

Austad notes that when we discover and examine genes in the human genome that can increase longevity, they may prove to come with trade-offs. "Of all these genes in these small animals [that extend longevity], none of them are ever found in nature. And they all have downsides. People have not been eager to investigate the nature of their downsides."

Cancer obviously could be a downside, as could altered fertility.

Austad says he's been snorted at by other scientists when he argues that we should study the cells of long-lived animals like whales and elephants instead of short-lived ones like mice and fruit flies if we want to understand how we might live longer. "Elephants contain about 40 times the numbers of cells we do, and whales as many as 600 times as many cells. Yet elephants and whales live, to a reasonable approximation, just as long as we do. Therefore, their cells must be 40 to 600 times more resistant to turning cancerous than our own. Could we perhaps learn something about cancer resistance from studying these cells?" he has written.

So far, Austad himself isn't working with elephants. Instead he's looking at parakeets. "They live up to 20-plus years," he says admiringly. "That's seven times as long as a mouse, and they're the same size. They have unbelievable resistance to oxidative damage ... if we could somehow mimic that in humans ..."

So, downside or no, Austad also thinks findings from the Human Genome project will help us increase human longevity. "We already know that there are some genes that are associated with longer life in animals. I think we'll find the [corresponding] genes in humans that have a small but measurable effect on how long we live. And it won't be too many years before we have gene therapy for all kinds of things. It hasn't worked too well yet, but that's just a technical problem."

Is there any theoretical limit that would keep increased longevity from becoming immortality? Warner says "There's no theoretical limit. There's a balance between constant damage and repair. It's like a car. Theoretically you should be able to keep a car going forever -- not yours, maybe, and not mine -- but if you keep replacing the parts the car could last forever. Maybe the individual could live forever."

"The only limit is that there is no such thing such as immortality because accidents still happen," says Austad. "The theoretical limit is human behavior, not human physiology. If teenagers didn't drive cars like crazy people, that would probably have more effect on life expectancy than curing cancer."

Dr. Leonard Hayflick takes a darker view of longevity research than many scientists do. Hayflick's view of significantly increased longevity is, basically, that it won't happen, it can't happen, and if it did happen it would be a bad thing.

Hayflick, a professor of anatomy at the University of California at San Francisco's school of medicine, is the author of "How and Why We Age," and has been thinking about longevity for 30 years, ever since he discovered what's now called the Hayflick Limit. Until his research, it was thought that animal cells growing in tissue culture were immortal and could divide forever. In a series of meticulous experiments, Hayflick showed that normal cells in culture have life spans: They flourish and divide for a while, but after a certain number of generations, divide no longer and eventually die. The cell lines that do go on forever are cancer cells.

People fail to distinguish between curing disease and ending aging, Hayflick says. If all the diseases currently written on death certificates in developed countries were resolved, you could add perhaps at the most 15 years to human life expectancy. "And that's it. Period."

Aging itself will not be affected. "Aging is an inexorable process that begins at about the age of 30 in humans and continues indefinitely. If you resolve disease you then expose or reveal the underlying real cause of that vulnerability, and hence death."

Hayflick doesn't believe that we will be able to go beyond resolving disease to slowing or stopping the process of aging. You can replace parts all you want he says, but what will you do when you have to replace your brain?

It's true that people object to aging as well as to death. Long life, while much admired, isn't sought after so much as long healthy life, or perhaps long youth. We want to be 100 years old and dewy fresh.

Dr. Pier Paolo Pandolfo, one of the scientists who studied the mice that live 30 percent longer, told the New York Times that a drug to block the self-destruct protein p66shc (the one the mice were engineered not to have) could be applied in the form of a cream to reverse wrinkling and blemishes on aging skin.

Can we have both long life and long youth? "I would say that there's no question about that," says Austad. "Most people would say that if you can't have better function there's no sense in keeping people alive."

It's increasingly easy to imagine replacing our parts, renewing our tissues, and rewriting our DNA. We would also need to fix our memories. They can hold a great deal, but never needed to hold an infinite amount of experience. Yet there are various ways we might deal with that, such as adding memory chips to our brains. Or perhaps we'll even figure out how to get rid of unneeded, unpleasant old memories and provide room for delightful new memories. It'll be doable, eventually.

Next page | I see no reason why we won't eventually learn how to live forever and to live forever young