So far as we know, the last hundred years have been the most radical period of life extension in all of human history. At the turn of the twentieth century, life expectancy for Americans was just over 49 years; by 2010, that number had risen to 78.5 years, mostly on account of improved sanitation and basic medicine. But life extension doesn’t always increase our well-being, especially when all that’s being extended is decrepitude. There’s a reason that Ponce de Leon went searching for the fountain of youth—if it were the fountain of prolonged dementia and arthritis he may not have bothered.
Over the past twenty years, biologists have begun to set their sights on the aging process itself, in part by paying close attention to species like the American Lobster, which, despite living as long as fifty years, doesn’t seem to age much at all. Though some of this research has shown promise, it’s not as though we’re on the brink of developing a magical youth potion. Because aging is so biologically complex, encompassing hundreds of different processes, it’s unlikely that any one technique will add decades of youth to our lives. Rather, the best we can hope for is a slow, incremental lengthening of our "youth-span," the alert and active period of our lives.
Not everyone is thrilled by the prospect of radical life extension. As funding for anti-aging research has exploded, bioethicists have expressed alarm, reasoning that extreme longevity could have disastrous social effects. Some argue that longer life spans will mean stiffer competition for resources, or a wider gap between rich and poor. Others insist that the aging process is important because it gives death a kind of time release effect, which eases us into accepting it. These concerns are well founded. Life spans of several hundred years are bound to be socially disruptive in one way or another; if we’re headed in that direction, it’s best to start teasing out the difficulties now.
But there is another, deeper argument against life extension—the argument from evolution. Its proponents suggest that we ought to avoid tinkering with any human trait borne of natural selection. Doing so, they argue, could have unforeseen consequences, especially given that natural selection has such a sterling engineering track record. If our bodies grow old and die, the thinking goes, then there must be a good reason, even if we don’t understand it yet. Nonsense, says Bennett Foddy, a philosopher (and flash game developer!) from Oxford, who has written extensively about the ethics of life extension. "We think about aging as being a natural human trait, and it is natural, but it’s not something that was selected for because it was beneficial to us." Foddy told me. "There is this misconception that everything evolution provides is beneficial to individuals and that’s not correct."
Foddy has thought long and hard about the various objections to life extension and, for the most part, has found them wanting. This is our conversation about those objections, and about the exciting new biology of aging.
People usually regard life extension as a futuristic technology, but you begin your paper by discussing the ways that we’ve already extended the human lifespan. What’s driven that?
Foddy: The reason I present it that way, is that there’s always this background moral objection in enhancement debates, where a technology is perceived to be new, and by virtue of being new, is depicted as threatening or even strange. That goes for everything from genetic engineering to steroids to cloning and on and on. I think it’s always worth contextualizing these things in terms of the normal. So with human cloning it’s worth remembering that it’s exactly the same as twinning. With steroids, it’s worth remembering that in many ways it’s not that different from training and exercise, and also that people have been taking testosterone since ancient times. I think this way you can kind of resist the idea that something is wrong just because it’s strange.
When you’re talking about medicines that help us live longer, it’s important to realize how much we’ve already accomplished. In the last 150 years or so, we’ve doubled our life span from 40 to 80 years, and that’s primarily through the use of things you can characterize as being medical science. In some cases it’s clear that we’re talking about medical enhancement—vaccines, for instance, or surgical hygiene and sterilization. And then more broadly there are other, non-medical things like the sanitation of the water supply and the pasteurization of milk and cheese. All of these things have saved an enormous amount of life.
It used to be that people would die of an infectious disease; they’d be struck down when they were very young or when they were older and their immune system was weak. Now almost nobody in the first world dies of infectious disease; we’ve basically managed to completely eradicate infectious disease through medical science. If, at the outset of this process, you asked people if we should develop technologies that would make us live until we’re 80 on average instead of until we’re 40, people might have expressed these same kind of misgivings that you hear today. They might have said, "Oh no that would be way too long, that would be unnatural, let’s not do that."
So, in a way, we shouldn’t view it as being extremely strange to develop these medicines, but in another sense we’re at a new stage now, because now we’re at the forefront of having medicines that actually address the aging process. And that’s what I’m interested in talking about—the kinds of medicines that actually slow down the aging process, or at least some of the mechanisms of aging.
Can you explain how senescence, the biological process of aging, is unevenly distributed across species?
Foddy: There are different animals that are affected differently by various processes of aging. In my paper I go into the case of the American Lobster, which lives about as long as a human being. When you dissect one of these lobsters at the end of its life, its body doesn’t show much in the way of weakening or wasting like you see in a human body of advanced age. That suggests that aging can evolve differently in different species. Lobsters seem to have evolved an adaptation against the cellular lifespan. There’s this phenomenon where the DNA in our cells basically unravel after they’ve divided a certain amount of times, but lobsters have this enzyme that helps them replenish their telomeres—the caps that hold DNA together.
That’s one of the reasons why lobsters don’t seem to undergo aging in the same way that we do. Other species give off an antioxidant chemical in their bodies that prevent these oxidizing free radicals in our bodies from breaking us down. That’s why doctor’s recommend that you have a certain amount of antioxidants—some species are really good at producing those naturally.
There is this idea that when you’re evolving you make certain trade-offs. Lobsters and clams don’t really move around a lot; their bodies move and grow very slowly and one of the upsides of that is that they’ve been able to invest their evolutionary chips, so to speak, in resisting the aging process. Human beings, on the other hand, have to move around quite a lot. We have giant brains and we have to be able to run away from saber tooth tigers. As a result we have bodies that burn a lot of calories, and so that’s where our chips are invested. It’s just a difference in our evolutionary environment and that’s why we’ve evolved to live and die the way we do. But it could have easily not turned out that way—that’s the point I really want to make.