David Sinclair is a professor in the department of genetics and co-director of the Paul F. Glenn Center for Biology of Aging at Harvard Medical School. He is the author of Lifespan: Why We Age – and Why We Don’t Have To.
Matthew D. LaPlante is an associate professor in the department of journalism and communication at Utah State University, the author of Superlative: The Biology of Extremes and the co-writer of several books on the intersection of science and society.
A pill that costs pennies per dose could extend human lifespans by years. Artificial intelligence might help us predict and prevent diseases years before they would have taken hold. And the rapid development of gene therapies and the new science of cellular reprogramming may give us the power to actually reverse the aging of our tissues.
All in your lifetime.
When we tell people this, they sometimes respond with incredulity.
On a plane from Boston to Tokyo, a businessman curled his lip at the idea of extending healthy human lives past the years we already enjoy. “It sounds unnatural,” he said.
At a conference in Salt Lake City, a researcher wondered whether it was possible that science might finally be going too far. “Doesn’t death give life meaning?” he asked.
On social media, people warn again and again against “playing God.”
Why, they keep asking, can’t we just accept our own mortality?
That’s an understandable question. Our new book is optimistically, but also confidently, subtitled Why We Age – And Why We Don’t Have To. If you conclude from those words that we’re trying to cheat death, we get it.
Except for one thing: We’re not.
Against the breadth of our known universe, a human life is but a firing of a synapse, if that. If it were to be lengthened, what would that do? Give us the firing of two synapses? Or 20? Or even 200? Would that make us immortal? Alas, no.
We will all die. If not from aging, then from an accident, an act of violence, an ecological disaster, a cosmic event or a quickly evolving pathogen hell-bent on its own survival.
Death does not scare us. The prospect of going gently into its good night does.
It has always been this way. The quest to understand and potentially slow, stop or reverse aging is no different than the fights against smallpox and polio in the past and those against malaria, dementia and cancer today. We once considered infectious diseases and malignant tumours to be an inevitable part of life – if you lived long enough, one or the other would kill you. Today, we don’t accept these conditions as “natural” or unavoidable, even if we have not yet relegated them to the pages of medical history books. Nor have we concluded that we need these diseases to give life meaning; someone who did not die of polio cannot be said to have “missed out” on that experience.
Our decision to fight those diseases was perfectly in line with our nature – and the nature of all living things. Since the dawn of biological history, every species has raged against death, as individuals in many instances and collectively in many others. Pushed by death in one direction, life goes another, exploring new niches and evolutionary opportunities – fighting an endless war to survive and live robustly, if only a bit longer.
Our species is no exception. We formed families, villages and nations. We learned to harness fire and water. We domesticated plants and animals. We transformed our world with engines, electricity and flying machines. We trained doctors, built hospitals and created medicines. Those who were ahead of the curve in these and other developments were often accused of entering the realm of God – of not being able to accept things as they are.
But this is who we are. And so we have raged.
In doing so, we’ve increased the average human lifespan from around 30 years in paleolithic times to 70 to 80 years today. But we haven’t done nearly enough to keep up when it comes to health spans – the portions of our lives spent free of disease. Without significant improvement to the latter, increasing the former is pointless, even inhuman.
But because biological aging is the biggest driver of the conditions that all too often make the last decades of life so miserable, the distinction between longer and healthier life is moot; if we live healthier, we naturally live longer. We can have both.
And yes, this may happen quite soon.
New science about why we age is revealing what we can already do in our daily lives to have the greatest chance of living longer, including lifestyle changes and medicines. Human clinical trials are under way that will help us understand if other pills, some that have been on the market for decades but never used to treat aging – since aging was never before considered something that could be treated – might extend lifespans and health spans. More than two dozen companies have been started in the past five years, mostly in Britain and the United States, to develop revolutionary drugs that don’t just treat one disease but slow or reverse many, each aimed at the eight or nine known molecular processes that promote aging.
Precision medicine, meanwhile, is offering hope that when we couple our emerging understanding of genetic variability with the power of artificial intelligence to find order in chaos, we can head off both chronic and communicable diseases long before they become deadly.
And, in what could be the most revolutionary step in this effort, we might be able to “wipe away” aging from our cells. Over the past few years, many scientists have come to the realization that epigenetic, rather than genetic, changes are what truly paint the landscapes of our lives. How our cells turn genes on and off as we get older – “epigenetic noise,” so to speak – is far more important than the underlying genes themselves. Lifespan is only 20-per-cent genetically determined; the rest is epigenetic.
These numbers have made it fashionable to say that our genes are not our destiny, but there’s an even more important implication. Our newly emerging understanding of aging allows us to say something that many people will have an even harder time fathoming: Aging, as we know it, is not inevitable.
In 2016, the lab of Juan Carlos Belmonte at the Salk Institute, in San Diego, turned on genes normally turned on in embryos to induce cellular reprogramming in a mouse. Remarkably, it extended the lifespan of a short-lived mouse by 40 per cent. Now, new work from the Sinclair Lab at Harvard Medical School is showing that gene therapy can induce cellular reprogramming in the eyes of old mice. The process rewinds the biological clock and restores vision to that of young mice.
There is a great distance between reversing a disease of aging in an old mouse’s eyes and reversing all the symptoms of aging in human beings. But those who contend it’s impossible – a word that does not belong in any scientist’s vocabulary – are ignorant of what is happening in a rapidly increasing number of research laboratories around the world dedicated to understanding and solving aging.
The oldest among our species can reach 115 and, in exceptionally rare cases, only a few more years past that. But is a human lifespan stuck at that limit? We do not think so.
You can decry this future – or you can prepare for it.
Will extending human lifespans and health spans make things better or worse for our fate on this planet? That is an open question, for the laws and policies that guide our lives in a world in which most people are gone well before the age of 100 are not suitable for a world in which a person’s calendar age is no longer an indicator of their ability to contribute to our society, let alone a signal that they are near death.
We must begin to plan for this world. Because even though aging is not inevitable, our species’ collective fight against it is.
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