With hindsight, the fact that aging is at least somewhat coherent should be obvious. The fact that we start to suffer simultaneously from a diverse family of ailments, each with their own complex underlying causes, should set off scientific alarm bells. The clogged arteries of heart disease, the dying brain cells in dementia and the out-of-control cells of cancer don't seem to have much in common—so why do they all happen at once? It might seem like just a cruel coincidence, if it weren't for our long-lived, hungry rats in which all of these are delayed together: what this suggests is that there is an underlying, ticking clock which, with surprising synchrony, unleashes a phalanx of terrible diseases on our bodies.
The fact that aging is malleable could save and improve billions of lives. The aim of anti-aging medicine is to replicate in people what we've seen at work in so many dietarily restricted species: to keep us fit and disease-free for longer. This is sometimes referred to as increasing "healthspan"—prolonging the period of life lived without disease or disability.
Dietary restriction is just the beginning. After all, when the first results were published in 1935, we didn't know the structure of DNA—in fact, back then we weren't even entirely sure that DNA was the medium of heredity. Nowadays, we can read an organism's entire DNA sequence in a few hours. Our understanding of how life works has expanded exponentially, thanks to an array of biological tools and techniques which would have sounded fantastical a century ago. Our modern understanding of aging biology, like all science, comes from researchers standing on the shoulders of their forebears—and research into aging runs the gamut from ecology to lab biology.
There's inspiration to be drawn from the diversity of life on Earth, involving an ensemble cast of incredible animals which, it turns out, age at remarkably different rates. We've already met negligibly senescent tortoises which have mastered biological immortality. How could they evolve when aging seems universal? Even if we stick to animals more closely related to us, mammals have lifespans ranging from just a few months for some unfortunate kinds of rodents to probably centuries in the case of whales. How has this diversity of lifespans evolved, and what tricks might these creatures be able to teach us about how to age well?
Then, there's what we know from the lab. We've uncovered huge results in tiny nematode worms: a change in a single gene, indeed a single letter of DNA, can extend a worm's lifespan tenfold. We've also had success in animals with physiologies far closer to our own: we can routinely improve the aging process in mice via dozens of different treatments. We've discovered drugs which can slow aging, or turn back the clock entirely, some of which are already being tried in patients.
This collection of observations and evidence is tantalizing and foreshadows a future where aging will be treated. And this future may not be so far away: in the last decade or two we have finally been able to say with confidence what aging 'is'. And once you know what something is, you can start to work in earnest to target it.
We now think that aging isn't a single process, but a collection of biological changes which make old organisms different from young ones. These phenomena impact every part of us—from genes and molecules to cells and whole systems inside our body—and go on to cause the aches and pains, worsening sight, wrinkles and diseases of the elderly. We are now at a stage where we can draw up a list of these changes and conceive treatments to slow or reverse each of them.
The ideas for treating aging processes aren't pie-in-the-sky theoretical biology—they are being tested in labs and hospitals around the world today. One such phenomenon is the accumulation of aged "senescent" cells in our bodies. Few in number in our youth and accumulating with time, senescent cells are associated with a number of age-related diseases. In 2011, the removal of these cells in mice was shown to defer multiple diseases and extend lifespan. By 2018, drugs which destroy these cells were undergoing clinical trials in people.
The dream of anti-aging medicine is treatments that would identify the root causes of dysfunction as we get older, then slow their progression or reverse them entirely. They would address many conditions at once, and would also be preventative rather than palliative—reducing your odds of getting diseases, and tackling the more everyday symptoms like wrinkles and hair loss at the same time. We wouldn't wait until patients were old and sick to start with treatment, as we do today; instead, we'd give them in advance, and stop people from becoming ill and infirm in the first place.
Treating aging itself rather than individual diseases would be transformative. Much of modern medicine targets symptoms, or at least takes aim at factors several steps removed from the root cause of many illnesses. For example, if someone has high blood pressure (as many people do, especially as they get older), they will often be prescribed medication to lower it. Many common blood pressure drugs work by relaxing the muscles around the arteries, causing them to widen, and allowing blood to flow more freely. This doesn't address the stiffening of the artery walls, or the clogging of their interiors which are actually causing the rise in blood pressure. It's not that these treatments are useless—blood pressure is reduced by these pills, and patients live longer as a result—but these drugs and others are workarounds and, ultimately, they can never be a cure.