The Prophet of Immortality

But funding experimental science that treads too far off the beaten path is, Archer says, “bloody hard.” And so de Grey’s bacterial project is moving along at a deliberate pace, not helped by Archer’s inability to find enough time away from the responsibilities of his primary, funded research and his young family to do the preliminary work necessary to jump-start a proper grant application. De Grey, who has no children and a monomaniacal amount of energy to pour into his projects, is not entirely sympathetic. “My emphasis is to get more people like John involved, preferably ones who aren’t so lazy,” he says, indifferent to the fact that Archer is sitting across from him, hearing every word. “It bounces off me,” the very British Archer tells me later. “Aubrey is a cross between Svengali and a Methodist firebrand preacher, and yes, he can drive you up the wall. But in science, people like him are far too rare.”


The minence grise of U.S. aging research, Leonard Hayflick of the University of California at San Francisco, says people are like cars, which reliably age “even though there’s nothing in the blueprints that shows a process for doing it.” In other words, there is no “death gene,” no mechanism that offs us after a certain time limit; aging is just a by-product of evolutionary neglect. Humans are mortal delivery systems for immortal genes. After we’ve made the delivery of those precious genes to the next generation through reproduction, evolution doesn’t care if we drive off a cliff. Which we all do, at various rates of speed. The mechanism here is natural selection. Because people who live a long time don’t generally have more progeny than people who have a middling life span, those long-lived genes don’t get selected for. Consequently, we have little protection against the bad things that happen to us later in life—the accumulation of metabolic waste products in our cells and harmful mutations in our genes that over time overwhelm the repair systems that, in most of us, work so splendidly when we are young.


The difference between a 20-year-old and a fit 30-year-old may seem relatively minor, de Grey points out, but something is going on in the cells of the latter, some ineluctable early-stage rot that explains why, statistically speaking, that 30-year-old is 10 years closer to his or her eventual demise. As gerontologists are fond of pointing out, you could solve all the major age-related diseases, and you’d still add only about 15 or 20 years to our current average life span of nearly 80. Even if we cured cancer and heart disease, we’d wind up dying of pneumonia or passing away in our sleep as frail geezers in our 90s. The problem with our bodies is that, absent a radical intervention of the sort that de Grey proposes, we simply wear out over time.


As de Grey explains, there are currently two ways of dealing with aging. The first, geriatric medicine, is a finger-in-the-dike approach that buys older people more time by battling, often at the symptomatic level, the diseases that typically characterize the last chapter of our lives: coronary-bypass surgery to improve circulation, pharmaceuticals to combat osteoporosis, radiation and chemo to blast away malignant tumors, and so on. This is a losing battle—yet from a certain point of view, so is life. Inarguably, there has been an enormous rise in the average American life span over the past century, thanks to vaccines, antibiotics, improved diet and a host of new treatments and surgeries, but we seem to have reached a point of diminishing returns, where further improvements are likely to bring only marginal life-span gains.


The second standard approach is the gerontologist’s, which consists of investigating the mechanisms of aging itself. Compared with the billions spent on disease research, this is penny-ante stuff. Still, in the past decade or so, a handful of prominent scientists—Cynthia Kenyon of the University of California at San Francisco, Leonard Guarente of the Massachusetts Institute of Technology, George Roth of the National Institute on Aging—have whetted the media’s and the public’s appetite for a genetic fountain of youth. Some researchers have put their lab animals on severe diets, a method known as caloric restriction, which results in longevity gains of about 30 percent. Others are closing in on genes that may be responsible for long-livedness in yeast, worms and rodents.


De Grey has carved a middle way between geriatric medicine and gerontology; he aims to reach what he calls “engineered negligible senescence.” His is a pragmatic approach, he tells me emphatically over another pint, because by the time the gerontologists have cracked the mysteries of cellular metabolism, we’ll all be worm’s food. We’re at an unprecedented time in the history of science, he says, having learned enough about the genetic and biochemical processes that lead to metabolic damage that we can begin to sketch out a plan to repair it. After all, it’s easier to play engineer and fix a problem than to play God and truly understand it. Unlike those researchers who theorize about some prime mover in the aging process—the usual suspect these days being “free radicals,” the unstable and thus troublemaking molecular by-products of metabolism—de Grey looks at aging as a group of interdependent processes that resist tidy prioritization. “We shouldn’t spend a lot of time navel-gazing, trying to figure out which things are more important than others,” he asserts. “We should just fix them all. And if we fix a couple things we didn’t need to, then no harm done, is what I say.”



Which brings us to de Grey’s Seven Deadly Sins of Aging, his formulation of the cellular and molecular culprits that he believes account for human decline. They are: the atrophying of tissues as a result of cell loss; the havoc caused by old cells that linger rather than self-destruct; waste buildup inside lysosomes, the garbage compactors of our cells; the waste products that build up between cells; the improper bonding of sugar and protein molecules that reduces the elasticity of our tissues; genetic mutations in the mitochondria; and genetic mutations in the cell nucleus that lead to cancer. Biologists are not convinced that these processes all contribute to aging, but de Grey is, and he has proposed solutions to each [see “Seven Deadly Sins,” below]. How practical or realistic those solutions are is another matter. “Aubrey will say something that’s the biological equivalent of 'Let’s build a 1,000-story building on the head of a pin, and then we can—,' and I’m like, 'Wait, wait, let’s go back to that first part again,'” says Judith Campisi, a top cell biologist at Lawrence Berkeley National Laboratory. (On the other hand, though Campisi has yet to feel compelled to do an experiment because of a conversation with de Grey, she
doesn’t rule it out. “I wouldn’t waste my time talking to him if I thought it would never happen,” she says.)