When I tell people that anti-aging drugs are no longer a distant prospect, they often assume I'm talking about the quest for immortality. That's not surprising, given the buzz generated in recent years by visionaries who speculate about re-engineering the human body to last thousands of years. But actually I don't find that far-out prospect very interesting -- it bears the same relationship to serious aging science that warp-drive spaceships do to aeronautical engineering. What really grabs me are experimental advances that may impinge on the lives of people I know, maybe even mine.
Last year, for instance, research convincingly showed for the first time that a drug could extend life span in mammals. That has momentous implications, but I bet you can't name the drug. Give up? It's rapamycin, a medicine prescribed to prevent rejection of transplanted organs. Despite its reputation as an immune inhibitor, earlier studies with worms and flies suggested that it might mimic the anti-aging effects of calorie restriction, a curtailing of food intake that has long been known to brake aging in rodents and many other species. And when researchers at three different U.S. labs gave it to late-middle-aged mice, the results were stunning: the life expectancy of the aged males was boosted by 28 percent, and that of females by 38 percent.
It will take a lot more work to translate this discovery into safe, effective anti-aging medicines, but knee-jerk skeptics who routinely dismiss anti-aging research as the Deepwater Horizon of snake oil are now on very shaky ground. In fact, even before the rapamycin breakthrough, a group of prominent authorities on aging including the late Robert Butler, founding director of the National Institute on Aging, had publicly stated that it now seems "realistically achievable" to develop anti-aging drugs that can delay the onset of all age-related diseases by about seven years. If widely used, such drugs might boost life expectancy by a similar amount.
That's gotten much less attention than dreams of bioengineered immortality. But consider this: if we were able to totally eliminate cancer, U.S. life expectancy would rise by only about three years. (The reason the gain would be so small is that the risk of many fatal diseases soars after age 65, so even if we were suddenly immune to cancer, those other killers would prevent average life span from rising much.) Thus, the seemingly minor gain in healthy life span that Butler believes we could achieve with anti-aging drugs would actually shrink death's dominion far more than winning the war on cancer would. Writ large, this point represents one of my new book's main messages: the only practical, near-term way to substantially increase healthy life span today is to simultaneously lower the risk of all diseases of aging. The way we now mainly buy time -- administering therapies for one progressive, old-age disease at a time when it's too late to do much good -- can't do that. Anti-aging drugs could, and at the same time they would go a long way toward ending the ruinously costly game of diminishing returns we're playing in geriatric medicine, as we eke out incremental gains with ever pricier palliatives. In effect, they would be preventive medicines of unprecedented scope and efficacy, drastically lowering the risk of everything from Alzheimer's to osteoporosis to wrinkles in the way that hypertension drugs now cut heart-attack risk.
The downsides?
The two possibilities brought up most are overpopulation and the chance that the drugs might prolong late-life disease and disability -- naysayers picture 70 million boomers on anti-aging drugs re-enacting their hell-no-we-won't-go days in nursing homes. Both concerns seem overblown to me. For one thing, birthrates have long been dropping across the globe, so it's not clear that a modest increase in life expectancy would significantly increase world population at this point. Besides, lifestyle trumps raw population numbers -- if everyone on earth burned as much fossil fuel as the typical American, the planet would soon be toast, and that fact alone utterly overshadows the risk to sustainability posed by a potential modest increase in world population. As to prolonging misery, consider the pertinent data: all the anti-aging interventions shown so far to work in animals -- including gene mutations that extend life span, calorie restriction, and drugs that mimic effects of calorie restriction -- appear, at worst, to postpone the onset of diseases of aging without lengthening their typical courses. And there's some evidence that such interventions can abbreviate late-life decline. When pathologists examine tissues of calorie-restricted rodents after death, for instance, they've found no visible signs of severe age-related diseases in a fourth to a third of the animals, a post-mortem finding that's made in only about 6 percent of control animals. It's as if the rodents had lived to extraordinarily ripe old ages and then suddenly passed away without any terminal decline at all.
Like all profoundly life-altering technologies, anti-aging drugs would confront us with some taxing changes -- we'd need to stockpile bigger nest eggs, for example. But no other investment of medical research dollars promises bigger returns than developing such drugs. And while immortality isn't in the offing, I think we'll be eternally sorry if we don't do what it takes to make them real and widely available as soon as possible.
David Stipp is the author of The Youth Pill: Scientists at the Brink of an Anti-Aging Revolution. A freelance science writer, formerly with the Wall Street Journal and Fortune, he has extensively covered the topic of gerontology since the late 1990s. He recently started a blog on aging science. For more info, please visit www.davidstipp.com.