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Experts at AAAS Briefing Mull the Outer Limits of the Human Lifespan
ST. LOUIS — Imagine living to age 1,000 in a middle-aged body. Fantasy? Yes, for now. But recent genetic and molecular biological discoveries have dramatically extended the lifespan of several experimental animals, including mice and worms, and could have potential applications for increasing longevity in humans.
New research promises dramatic possibilities, such as — in the words of scientist Aubrey de Grey — postponing aging “indefinitely.” De Grey, a scientist from the University of Cambridge, contends that within 25 years there is a 50 percent chance of creating therapies which would give middle-aged people an extra 25 years of life.
De Grey is increasingly visible in the news media, and controversial among his colleagues. Many scientists believe that there are good reasons to doubt the imminent development of such therapies, and point out that there are potential drawbacks and side-effects to consider.
A panel of experts discussed the future of the human life span Friday 17 February at the 2006 AAAS Annual Meeting, and also examined the potential demographic and economic effects which such life-extension measures could have.
De Grey, a biomedical gerontologist who studies the biological and medical aspects of old age and the process of aging, believes aging may be postponed by repairing the “damage,” or the cellular and molecular “side-effects” that accompany metabolism.
“My view is that it would be much easier to repair and reverse, or at least to make harmless, those molecular and cellular things that are happening with aging rather than to prevent them in the first place,” he said. To that end he has developed a comprehensive plan, entitled “Strategies for Engineered Negligible Senescence” (SENS), which categorizes seven basic types of “damage” and groups each with a proposed repair method. Each type of damage becomes a target for a proposed therapy. For example, one category includes cell loss and cell atrophy, which de Grey proposes to repair or obviate by implementing stem cells, growth factors and exercise.
The proposed repair methods are technologies and therapeutics he believes may be sufficiently improved in the near future to effectively postpone getting old. Some therapies include new research on telomere modification which could have an impact on one of de Grey’s SENS targets, “accumulation of chromosomal damage which leads to cancer.” Another target, extracellular aggregates, could be alleviated by immune-mediated phagocytosis, explored recently in mouse models. Of course most of these therapies have only been achieved with experimental animals and remain — for the moment — theoretical for humans.
Nevertheless, de Grey envisions a day when therapeutic techniques improve more quickly than a person approaches death — thus reaching what he terms “longevity escape velocity.” If society ever reaches this point, he predicts, individuals may “never die from old age.”
But others believe the science of aging to be more complicated, including 28 scientists who dismissed much of de Grey’s work as “ill-defined speculation” in a 2005 report to the European Molecular Biology Organization. “In our opinion,” writes University of Minnesota biologist Huber Warner et al, “the items of the SENS programme… are not yet sufficiently well formulated or justified to serve as a useful framework for scientific debate, let alone research.”
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One of these 28 scientists, Steven Austad, an expert in mammalian aging and a gerontologist from the University of Texas Health Science Center in San Antonio, acknowledges the significant discoveries in the realm of experimental anti-aging techniques. But at the AAAS briefing Friday, he pointed out the enormous amount of lacking information that would be necessary for any human application—not to mention the side-effects these sort of applications could have.
Though we have succeeded in extending life expectancy, Austad said, there is much to be learned about the actual process of retarding aging. Some of the experimental animals whose lives have been extended suffer from significant side effects, such as susceptibility to infectious disease, reduced fitness and fertility problems, he said.
Assuming anti-aging therapies could increase life expectancy in the near future, Stanford biologist Dr. Shripad Tuljapurkar created a model examining the demographic and economic effects. Given a 20-year increase in life expectancy between 2010 and 2030 due to anti-aging therapy — which the panel scientists consider a “moderate” estimate — the model predicts that there will be twice as many American retirees relative to working people. Thus, the dependency ratio would double, as would the cost of Social Security and Medicare. In order to compensate, Tuljapurkar estimates, the retirement age would have to climb to 85.
Other notable predictions include an estimated 500 million extra people due to anti-aging technologies in India and China. Tuljapurkar noted that anti-aging technologies will be expensive and could therefore produce more inequality in terms of life expectancy, both between and amongst countries. In America, for example, where there already exists the highest level of inequity of age at death, if therapies are paid for with private resources, inequality could greatly increase, Tuljapurkar said.
While future models seem bleak to some, Dr. Eileen M. Crimmins, chair of gerontology at the University of Southern California, pointed out that there is much to be learned from the past. It may be more difficult to adjust to abrupt fertility changes than to anticipated increases in life expectancy due to mortality change, she said. Thus, since the developed world has already dealt with rising and subsequent falling fertility rates, she believes the future may not be as problematic as some believe.
“Now the question is: What will the adverse consequences of living a long life be?” she asked. “I think they will not be anything we cannot deal with… The issue will be adjusting to those changes with sensible policies which include changing the length of working life [by increasing the retirement age].”
Some of the debate surrounding anti-aging science derives from how one defines aging and thus how one goes about treating it. De Grey, for example, likens the effects of aging to “damage,” and anti-aging therapies to the maintenance of a house.
“The only real difference between houses and humans is that we didn’t design our own anatomy,” said de Grey. “We have to figure out how we work to sufficiently understand what to do in order to repair or obviate the effects of aging.”
Dr. Austad, however, defines aging more simply — and therefore envisions anti-aging therapy as more complicated.
“Aging is the progressive decline in function that virtually every living organism undergoes,” he said. Austad displayed a graph showing the decline in running speed of the fastest humans over the course of a lifetime, followed by a graph showing decline in various organ systems. Austad, like many others, sees SENS’ seven targets as overly simplistic. And even if they aren’t, problems remain.
Austad brought up the SEN target which includes tumor cells to illustrate his point. “Curing cancer hasn’t proved to be too easy,” he said.
Douglas M. Main
18 February 2006