The Anglo-Irish poet Jonathan Swift said “Every man desires to live long; but no man would be old.”

In 1727, when Swift published those words in his “Thoughts on Various Subjects,” living long probably meant making it to 50. And in those days, when the most sophisticated treatment medicine could offer was blood letting, the longer you lived, the more parasite-ridden, painful and miserable your life would likely be.

How science has changed that. The average life span in Japan is 83 for women and 78 for men. The life span of British males went from 48 in 1901 to 75 in 2000; that of females from 49 to 80. The increase in life expectancy will probably continue. If it does, what will it mean for health care? Or for pension providers, governments, families, and society?

The social implications of medically slowing and even stopping aging are “potentially revolutionary,” according to Eric Juengst of the department of bioethics at Case Western Reserve University in Cleveland. In a paper in Science last week, Juengst and colleagues admit that the idea of interfering with the aging process in adults might seem far-fetched, but point out how biomedical advances “such as the cloning of mammals” can burst into public awareness without warning.

Juengst and the other authors identify three approaches adopted by researchers working on aging. The outcome of the most conservative approach, known as “compressed morbidity,” would be that humans stay healthy for a longer portion of their lives, but human life span in general would not increase. In the more moderate vision of “decelerated aging,” both average life span and life expectancy would increase. Finally, the goal of the most radical approach is to reverse the aging process altogether.

“Is aging as we have known it a human experience to be encouraged or discouraged, from the point of view of the public good?” Juengst and colleagues write. “If longer healthy life is an unalloyed social benefit, how should it be distributed? Serious ethical issues would arise if antiaging interventions were not universally available, but were distributed in response to status (economic, social or political), merit, nationality, or other criteria.”

There are two points here. First, an experience that is part of life in one generation need not necessarily be accepted in future generations thanks to advances in medical science. Dying after breaking a leg was once not uncommon, but when we learned how to protect people from infection and help bones mend, deaths from broken bones dropped dramatically. Granted, stopping aging is a bit more dramatic than healing bones, but you can be sure that if antiaging medicine becomes available, it will be used.

Second, “antiaging medicine” is already being used, in the sense that improved medical care and nutrition has increased the life span of many people in developed countries. Juengst and colleagues suggest there would be ethical difficulties if antiaging interventions were not universally available, but inequalities already exist. Medicine and food are not universally available, and where there are shortages, people die younger.

According to a U.N. report on world population expectations that was revised in 2000, the average life expectancy is 75 for developed countries and 63 for developing countries. AIDS in Sierra Leone has reduced life expectancy for babies born in 1999 to 25.9 years. Most people would agree that this constitutes an ethical issue, but you don’t see much being done about it. It seems unlikely that people are going to start worrying about something that isn’t even available yet, but Juengst urges that “public discussion of antiaging research is as deliberate and far-sighted as the research itself.”

Even with good medicine and nutrition, how can we increase life span even more? One way, ironically, might be to give people less.

Decreasing the amount of calories fed to rodents makes them more stress-resistant, and they live longer, say Valter Longo and Caleb Finch from the department of biogerontology, University of Southern California. (Biogerontology is the study of the biological mechanisms of aging; no surprise that there’s a research group in Los Angeles.)

It is not yet clear whether the lab rats live longer because they are more stress-resistant, but in other lab animals, such as worms, mutations which mimic calorie restriction make the animal more stress-resistant. Calorie restriction seems to work by protecting cells from oxidative damage caused by highly reactive “free radicals.”

This suggests new possibilities for antiaging drugs.

“By combining our knowledge of the conserved molecular pathways that regulate longevity and the starvation response mechanisms that slow down aging without collateral damage, we can begin to select candidate targets for antiaging drugs. Such an ‘evolutionary medicine’ approach could become a new strategy to prevent diseases such as cancer, Alzheimer’s and vascular diseases,” Longo and Finch wrote in Science.

And then there’s the genetic approach to antiaging. Research by Siegfried Hekimi and Leonard Guarente, respectively of McGill University, Quebec, and the Massachusetts Institute of Technology, in Boston, suggests that a relatively small number of genes may be responsible for aging.

Medicine and evolutionary theory indicate that aging is the result of many processes in the body breaking down, but the surprise is that in yeast, worms and mice, single genes (apparently those involved in preventing oxidative damage) seem to be responsible for aging.

“The aging process may be more specific than previously anticipated on evolutionary grounds,” the authors conclude in the same issue of Science.

There is then a real possibility that in the not-too-distant future, aging will be prevented or delayed. For the time being though, death, the ultimate human experience, is what defines our existence. It doesn’t look like it will be going anywhere just yet.

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