From Ending Aging by Aubrey de Grey and Michael Rae. Copyright © 2007 by the author and reprinted by permission of St. Martin’s Press, LLC. Aubrey de Grey is the chief science officer of the SENS Foundation.
nullImage: U.S. Department of Energy Human
Genome Program
In my view, we can probably eliminate aging as a cause of death this century—and possibly within just a few decades, soon enough to benefit most people currently alive.
What could that achieve, in humanitarian terms? I’ll start with some numbers. Around 150,000 people die each day worldwide—that’s nearly two per second—and of those, about two-thirds die of aging. That’s right: 100,000 people. That’s about 30 World Trade Centers, 60 Katrinas, every single day. In the industrialized world, the proportion of deaths that are attributable to aging is around 90 percent—yes, that means that for every person who dies of any cause other than aging, be it homicide, road accidents, AIDS, whatever, somewhere around 10 people die of aging.

Many people, when thinking about the idea of adding years to life, commit the “Tithonus error”—the presumption that, when we talk about combating aging, we’re only talking about stretching out the grim years of debilitation and disease with which most people’s lives currently end. In fact, the opposite is true. The defeat of aging will entail the elimination of that period, by postponing it to indefinitely greater ages so that people never reach it. There will, quite simply, cease to be a portion of the population that is frail and infirm as a result of age. It’s not just extending lives that I’m advocating; it’s the elimination of the almost incalculable amount of suffering—experienced not only by the elderly themselves, of course, but by their loved ones and caregivers—that aging currently visits upon us. Oh, and there’s the minor detail of the financial savings that the elimination of aging would deliver to society: It’s well established that the average person in the industrialized world consumes more health care resources in his or her last year of life than in an entire life up to that point, irrespective of age at death, so we’re talking about trillions of dollars per year.
I consider that if funding is sufficient we have a 50/50 chance of developing technology within about 25 to 30 years from now that will, under reasonable assumptions about the rate of subsequent improvements in that technology, allow us to stop people from dying of aging at any age—equivalent to the effect of today’s antiretrovirals against HIV. There are a few big caveats to that statement, though. The first is that it’s only a 50 percent chance. Any technological prediction as far in the future as 25 to 30 years is necessarily very speculative, and if you asked me how soon I thought we would have a 90 percent chance of defeating aging, I wouldn’t even be willing to bet on 100 years. But I think a 50 percent chance is well worth shooting for—don’t you? The second caveat is that aging won’t be totally defeated by the initial versions of this technology. We’ll have to carry on improving it at a reasonable rate in order to keep aging permanently at bay.
Cancer is a deal breaker for building an ageless organism. If we fail to make a breakthrough against this one disease, we can still expect to be dead in our mid-eighties. Diabetes and hypertension can be held at a safe, manageable level precisely because they are essentially stable diseases. By contrast, what makes cancer so fearsome a foe is that it’s a constantly evolving disease, a hive of genetic inventiveness that continuously finds new and better ways to outwit our attempts to control it. Within a single tumor exists such an astonishingly varied population of cells, each with its own combination of normal and abnormal genes, that at least some cells nearly always have a way to survive any particular attack. It ultimately just doesn’t matter if a given therapy kills 99 percent of the cells in a tumor.
We have a 50/50 chance of developing technology within about 25 to 30 years that will allow us to stop people from dying of aging.
To defeat cancer, we need a therapy that does not depend on anything that a cancer could escape through a mutation-driven change in gene expression. So any solution would have to have three key characteristics to be viable. First, it would necessarily involve denying cancerous cells access to some tool that is absolutely indispensable to their survival, so that they couldn’t just make up for its loss by tweaking some other gene expression pathway through mutating its other genes. Second, we would have to take away that tool in such a way that no mutation could restore it, either. And third, this tool would have to be one that our normal, noncancer tissues could do without.
As I considered this problem, I quickly saw the tool that I wanted to lock up: telo­merase. Our DNA comes equipped with a stretch of nonsense or “noise” DNA called the telomere. Telomeres are to our genes as the brief, silent stretch of leader tape at the beginning of a music cassette is to the songs on the tape: They give the “cassette player” (the DNA-replicating machinery) something to hold on to and advance over, so that it won’t skip over the essential information at the beginning of the very first “song” (gene) on the tape.
One key difference between telomeres and cassette leaders is that leaders stay intact as long as the tape does, whereas telomeres become ever-so-slightly shorter every time the cell replicates itself or is hit by damaging agents like free radicals. If it weren’t for telomerase, this gradual shortening would eventually lead to the complete loss of the telomeres in cells that replicate frequently during a life span, and thus the gradual erosion of the genes themselves. Telomerase periodically relengthens the telomere before it becomes critically short.
As with all of our other genes, the DNA that encodes the telo­merase enzyme is present in all of our cells—but because it’s needed only after quite a few cell divisions have occurred, it’s not needed in most cells for most or all of the time, so it’s turned off. This widespread lack of the need for telomerase is used by evolution as a key component of our defense against cancer, because having a limit to the size and renewal of telomeres prevents our cells from replicating themselves indefinitely—the crucial hallmark of cancer.