Are you, or is someone you know, ageing? Of course you are: though a handful of wellness influencers claim otherwise, the processes of biological ageing are ticking along within us all. But there’s good news – scientists now understand enough about those processes that we may one day be able to slow them down, or even reverse them. And that day might arrive sooner than you think.
While you should take the claims of social media biohackers with a very large pinch of salt, longevity science is beginning to uncover the mechanisms that make us grow old.
It goes far beyond vanity – such scientists aren’t just trying to create new anti-ageing skin creams to smooth fine lines and wrinkles, but real anti-ageing medicines that will slow the advance of those biological processes happening inside all of us.
The biology of ageing essentially causes diseases like cancer, cardiovascular disease and dementia. For example, while having high blood pressure roughly doubles your chance of a heart attack, being aged 80 rather than 40 multiplies that risk by 10.
That means understanding the biology behind these enormous risk increases could lead to the greatest revolution in medicine since the discovery of antibiotics. It could transform not just the treatment, but the prevention of disease in the first place.
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The prize, if we can identify and treat these underlying causes of ageing, is enormous. If we could make people in middle age a bit biologically younger with drugs that address the ageing process, we could improve everything from heart health to wrinkles, and delay the onset of cancer, dementia and frailty, all at the same time.
Scientists have identified several so-called ‘hallmarks’ of the ageing process – underlying biological and biochemical processes that are common to multiple, different diseases and dysfunctions associated with old age. By tackling these hallmarks, we could potentially prevent many of these problems simultaneously.
Although influencers’ claims fall short when it comes to good scientific evidence, that shouldn’t lead us to assume that these treatments are a fantasy, or something only future generations might benefit from.
We’ve got dozens of ideas that work in the lab already, keeping animals from worms to monkeys healthier for longer, and some treatments have even entered human clinical trials.
This isn’t about immortality, or spending millions a year on medical tests and every waking hour following health-optimising protocols – these treatments will transform healthcare.
For all the fuss about weight-loss drugs in the last couple of years (much of which is largely justified), imagine if medicine could reduce our biological age as well as our waistlines. Such medicines really might keep us slim and biologically younger for longer.
So, what are these biological hallmarks, and what might treatments to slow or stop their currently relentless march look like? Here are the five most promising.
A miracle drug from Easter Island
Easter Island, which you probably know for its giant stone heads, is also the origin of one of our most promising drugs to improve longevity: rapamycin.
Discovered in a soil sample returned by a Canadian expedition in the 1960s, it was named after the Polynesian name for Easter Island, Rapa Nui.
The molecule, produced by a species of bacterium, is a pharmaceutical Swiss army knife, with applications ranging from treating cancer, to suppressing transplant patients’ immune systems to help prevent organ rejection. And we could soon add ‘slowing down the ageing process’ to that list.
It all comes down to one of the hallmarks of ageing: the accumulation of dysfunctional proteins as we get older.
Proteins are the nanoscopic machines that keep our bodies running and, if they go awry, can do anything from gum up our biology, to being outright toxic.
Thankfully, there’s a process called ‘autophagy’ – literally, ‘self-eating’ – that allows our cells to recycle these malformed molecules and turn them into fresh, functional proteins. Rapamycin can increase our cells’ ability to engage in this anti-ageing spring-cleaning.
The end result is one of the most robust anti-ageing interventions we know of, it’s extended the average lifespan in mice by 20 per cent in some of the most rigorous, carefully validated mouse-longevity experiments yet conducted.
Even more excitingly, you don’t necessarily have to start taking the drug early in life – in fact, rapamycin was shown to be effective in mice aged 20 months, which equates to about 60 years in human terms.
We also know that rapamycin offers benefits in many different areas of mouse biology, from heart health to gum disease. It extends the lifespan in yeast, worms and flies, and we recently found out that it also works in marmosets, a tiny species of primate (meaning they’re much more closely related to us than mice). Human trials also suggest similar drugs could improve immunity in older adults.
Frustratingly, despite all this positive evidence, no one has stumped up the cash to do a proper randomised trial in older people to see if it really can keep us stay healthier for longer. While it might not give us the longevity of those massive stone heads, rapamycin is one of our most exciting near-term prospects as an anti-ageing drug.
A drug in your medicine cabinet
There are several contenders for drugs that you might already be taking that could improve how long and healthily you live. In fact, one recent paper attempted to rank existing approved drugs by evidence that they might make people or animals live healthier for longer.
Topping the table were diabetes drugs known as SGLT-2 inhibitors – meaning that, if you’re taking canagliflozin, dapagliflozin or empagliflozin, you might be getting a health and even lifespan benefit, beyond helping with your blood sugar. These drugs have been shown to improve wider health in patients that take them, and canagliflozin extended lifespan by 14 per cent in male mice.
Other top contenders include two more diabetes drugs (metformin and acarbose), ‘bisphosphonate’ drugs (usually used to reduce bone loss), plus – a late new entrant – weight-loss treatments like semaglutide, more commonly known under brand names like Wegovy or Ozempic.
Given that restricting the amount animals eat is one of the most effective ways to make them live longer, it wouldn’t be too surprising if drugs that make that easier in humans had similarly wide-ranging effects.
And here’s the really exciting bit: because these treatments are already in use, we know a lot about their dosing and safety, so we could start a trial right now to see if they really do slow down ageing in healthy people.
A cellular spring clean
In 1961, a young scientist called Leonard Hayflick was experimenting with cells in the lab. For decades, scientists had thought that cells could reproduce indefinitely outside the body. Cells reproduce by copying themselves and splitting into two, a process known as cell division.
But Hayflick found that, after about 50 divisions, the fibroblast cells he was experimenting with couldn’t divide any more. They also looked very strange under the microscope – and he christened these fried-egg-resembling cells ‘senescent’, after the scientific word for growing older.
The obvious question raised by this finding was whether senescent cells give rise to senescent animals and humans: as our cells divide throughout our lives, do they eventually hit this limit, stop working and cause wider signs of ageing in the body?
The answer seems to be yes – we all accumulate these cells in increasing numbers as we get older. The good news is that scientists now have a range of drugs and other treatments that can seek out and destroy these cells, while leaving the rest of the cells in our bodies intact.
The most wide-ranging results were published in 2018, when scientists using a combination of dasatinib (a chemotherapy drug) and quercetin (a ‘flavanol’ found in fruit and veg) managed to excise the senescent cells from aged mice and make them live longer in good health.
They weren’t just free from diseases like cancer and heart problems, either – they also did better when sent to the mouse equivalent of the gym. They walked further and faster on a tiny treadmill, hung from a wire for longer and were more generally active in their cages.
Dozens of subsequent papers have shown similar results for a range of age-related problems, and there are now over 20 companies trying to commercialise both drugs, and many other so-called ‘senolytic’ treatments. If any of them succeed, senolytics could be the first type of medicine on the market expressly designed to target the process of ageing.
Bottling up a baby’s biology
Newborn babies are one of the wonders of biology and you don’t need to be a cooing new parent to appreciate them. It might sound obvious, but babies are born young. This means, on some level, biology has already worked out how to reverse the ageing process.
Decades-old cells from a child’s parents can nonetheless give rise to a baby born with an age of zero. And this has happened with no noticeable degradation for millions of generations of different forms of life. The question is, can we work out how babies do it, so that we adults can get in on the action too?
A species known as the immortal jellyfish (Turritopsis dohrnii) seems to have this figured out. These tentacled sea creatures can, in times of stress, simply revert their biology to the junior ‘polyp’ stage and then grow up all over again, seemingly as many times as they like.
In other words, ageing backwards isn’t against the laws of biology. But is it possible in humans? And without turning us into polyps? Surprisingly, it might be.
The 2012 Nobel Prize for Medicine was awarded to Prof Shinya Yamanaka and Prof John Gurdon for their work showing how the clock could be turned back in adult cells.
Yamanaka’s contribution was particularly impressive, finding just four genes that could take an adult cell and turn it back into a ‘pluripotent’ cell, a type of stem cell that’s normally only present at the very start of embryonic development.
Unfortunately, turning these four genes on in adult mice proved to be disastrous. Pluripotent cells, all-powerful though they are in terms of their ability to grow up into any type of adult cell in the body, are singularly useless at performing those same adult cells’ functions.
However, later work found that mice with a modification that enabled these genes to be turned on for two days a week, rather than constantly, enjoyed significant benefits.
How exactly we’ll turn these exciting results in genetically modified mice into human treatments we’re not sure, but investors including Amazon founder Jeff Bezos are confident enough in the possibility to sink £2.3 billion ($3bn) into a company called Altos Labs to try and find out.
Preliminary results, announced in a recent interview, show that a mouse’s lifespan can be extended by 25 per cent by activating these ‘Yamanaka genes’ later in its life.
If this result holds up when the results are published in full, it’ll be exciting news. And, if Altos Labs succeeds in creating a human treatment from this work, Yamanaka could become the first person in history to deserve a second Nobel for the same discovery.
Mixing it all up
Reading about the promising effects of these drugs when taken independently might leave you wondering if combining them would have a bigger effect. Scientists have wondered this too and it seems like the answer could be yes.
The current record-holder for extending mouse lifespan is a combination of rapamycin and the anti-diabetes drug acarbose. They weren’t picked at random – it’s known that rapamycin can worsen control of blood sugar in mice and humans who take it.
So, the theory went that perhaps a diabetes drug could dampen this effect. The results were astounding: on average, male mice lived nearly 40 per cent longer with this combination, and female mice 30 per cent longer.
But could another blend of drugs be even more effective? That’s what the Robust Mouse Rejuvenation study hopes to find out. It’s following 1,000 mice, in 10 groups, that are receiving different combinations of up to four treatments (rapamycin, a senolytic, a therapy to strengthen the protective caps on their DNA and a bone marrow transplant).
The experiment isn’t yet complete, but early results show that the mice receiving all four are living the longest.
Given that ageing is caused by multiple processes – scientists have identified 12 hallmarks of ageing so far – it seems unlikely that there will ever be a single magic pill that makes us younger in every way. But understanding these hallmarks helps us develop treatments for each of them, which could affect the age-related diseases and dysfunctions that each hallmark is connected to.
We now have so many ways to slow the ageing process in mice that it would be wildly unlucky if none of them worked in people. Ageing biology, as a field, needs more funding to begin human trials for the promising interventions.
If it gets it, there’s no reason why some of these real anti-ageing medicines couldn’t be approved within a decade, allowing everyone who’s ageing (so that’s all of us except those longevity influencers, apparently) to stay healthy for longer.
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Experts in this article
Leonard Hayflick was a pioneering American biologist best known for discovering the Hayflick Limit, which demonstrated that normal, somatic cells have a finite number of divisions before they stop replicating. His work challenged the previously accepted belief that cells could divide indefinitely, significantly influencing the fields of ageing and cell biology.
Throughout his career, Hayflick made major contributions to understanding cellular ageing, human health, and the development of vaccines, particularly his work on the cultivation of viruses for vaccine production.
Prof Shinya Yamanaka is a Nobel Prize-winning stem cell researcher. After earning his PhD at Osaka City University in 1993, he spent several years at San Franciso's Gladstone Institute at the University of California.
Later, he joined the Nara Institute of Science and Technology and started his prize-winning research on the reversal of human ageing.
