This Mortal Coil
William Mair is the Assistant Professor of Genetics and Complex Diseases at the Harvard T. H. Chan School of Public Health. He explains how and why we all age…
Words William Mair
Illustration Christopher DeLorenzo
Humans are ageing — not individually, but as a collective. For the first time in our history, people over 65 will soon outnumber those under five years of age. This dramatic shift is the dual effect of lower birth rates coupled with a remarkable rise in longevity.
In 1900, the average life expectancy in the US was just over 47, but by 2000 it had rocketed to 77. Think about that for a moment — 30 years of extra life added in one century. And while overall life expectancy is higher in developed countries than the developing world, this Methuselah-like rise in longevity is not a luxury of the wealthy; life expectancy has grown in every continent, and the gaps between them are narrowing. In 1955, worldwide life expectancy was 46; in 2015 it was 65, and if we project forward to 2100, the average human on our planet can reasonably expect to make it to 83 before drawing their last breath. The outcome of this fantastical rise in humanity’s ability to not die is that by 2050 there will be one and a half billion people over the age of 65 — more than the current population of China.
That’s the good news. The bad news is that while we may be living longer, we are not ageing any slower than a century ago. There has been little change in the maximum lifespan achieved by healthy outliers, which would be expected if somehow we had reduced the rate of ageing itself. In fact, not only are we ageing at the same speed, but modern medicine has had little to do with our greying population.
By far the greatest contributor to this demographic shift is public health — education, sanitation, vaccination and communication — which have alleviated many of those things that previously killed us before retirement. Remarkable success at prevention, coupled with better cures, has squared the curve of human survival so that many more of us make it into advanced age. Although such human achievement is surely cause for celebration, this life extension has come at a cost: our bodies are not built for the task of old age that we’re setting them.
Sadly, each of us has a built-in obsolescence of sorts, revealed as an increase in frailty and disease risk as we age. To understand why this is and what we might do about it, we have to get to the very heart of why ageing exists in the first place.
Why does ageing exist? Ask most people (even many geneticists in the field of gerontology) and you often get similar responses: “We age because things break down, like a rusting car” or “We age because telomeres, the caps at the end of your chromosomes, get shorter”. Besides being wrong — some species don’t age, and not all cells divide and therefore suffer shortened telomeres — these are in fact answers to a different question, namely “How do we age?”, not why ageing as a thing exists.
“If ageing does not exist as a coalition of the willing and is actually built into our DNA, why did natural selection, which chooses survival of the fittest, lead to the evolution of bodies that age?
Pushed further to explain “Why ageing?”, we often hear, “To get old people out of the way so the younger generation can flourish”. Although a compelling concept, this answer lacks a true understanding of natural selection, which does not have a plan. One cannot explain the existence of something in biology by using that thing as part of the explanation — getting rid of failing old people to help the vigorous youth makes the assumption that old age failure is both inevitable and existed already, that ageing’s existence explains its evolution. The British evolutionary biologist Sir Peter Medawar called this a “vicious figure of eight”, and such thinking can only end up in a muddle. Species don’t work together as a group to maintain their existence by ageing — all it would take is one ‘cheating’ longer-living mutant to upset this delicate agreement, and simple maths would make that mutation spread even if the catastrophe of extinction was the result — ask the 99.9% of species no longer in existence.
If ageing does not exist as a coalition of the willing and is actually built into our DNA, why did natural selection lead to the evolution of bodies that age? The answer is that rather than ageing being selected for, it could not be selected against. Look around at the natural world and you won’t see many old animals. We see old pets in our houses and old animals in zoos, but not many in the wild. This is of course explained by how much harder life is in the wild. In the wild things die of predation, disease and falling off a cliff — the chance of making it through to old age is so small, we hardly see it.
Therefore, if a field mouse can only expect to live to a year or so before being killed, there is little reason for mice to evolve the capacity to live to 300. Sure enough, when you put mice in a zoo they only live for a couple of years, even when all the killers of the wild are kept at bay. But what if during their evolution mice could have taken away some of the things that killed them — say, removing predator risk by growing wings to escape, or finding an environment with no predators at all? Then longevity becomes a worthy thing to evolve.
“Ageing has evolved as a negative side effect of things that make us better when we are young.”
And sure enough, winged mice (which most people instead call “bats”) live to 30, as does the cancer-resistant naked mole rat, which lives in tunnels in the desert, far from any predators.
So now we know why a mouse does not live to 300, but why does it age so much faster than us? The clue here lies in the phrase “survival of the fittest” — not survival of the oldest. If a mouse can only reasonably live to six months in the wild, a random mutation in a gene that might make that mouse live three years instead of two doesn’t make that mouse fitter in the evolutionary sense: It’s likely been eaten by a cat before the benefit of that mutation kicks in. But what about a mutation that helps the mouse to escape that cat in early life? Maybe it makes it faster, better able to sense the cat, or hide. Evolution is blind and driven by probability alone; lots of mice make it to four weeks, so the advantage this early benefit gene offers affects many individuals. Now we have a fitter mouse, and that mutation will spread like a forest fire. It won’t just spread, it will spread even if a side effect of that early fitness benefit causes disaster in old age, even if it causes the ageing process itself.
Small advantages early in life greatly outweigh even huge disadvantages in old age, particularly in a wild world where old age is a pipe dream. Ageing has therefore evolved as a negative side effect of things that make us better when we are young. Species have only evolved the capacity to maintain themselves for the amount of time they can reasonably expect to escape death in the wild. Take away external hazards — by putting animals in a zoo, or in our case by developing a fantastic public health and medical infrastructure — and now suddenly we push bodies past the point to which they have evolved to survive.
Suddenly ageing and frailty are everywhere…
To explore the subject of ageing we teamed up with The Powerful Now, an IDEO + SYPartners initiative poised to creatively redefine ageing as a path of continual growth instead of decline. Together we wanted to explore the ways in which health, money, work and communities will exist in our future, and initiate discussions to find radical new solutions.
This article is taken from Weapons of Reason’s third issue: The New Old. Weapons of Reason is a publishing project to understand and articulate the global challenges shaping our world by Human After All design agency.
