MY NAN WAS an active, outgoing, engaged senior citizen. She gardened, kneeling on a foam pad to protect the skin of her knees and her fragile bones, honeycombed with osteoporosis. She read books, the newspaper, did the crosswords. She looked after her neighbours’ children for an afternoon here and there, keeping those exuberant little minds occupied while their mothers and fathers worked or shopped or did the frantic tasks that parents squeeze into their tiny slices of child-free time.
She lent an ear – and sometimes a shoulder – to her granddaughter, listening patiently to my love woes, and offering such wise insights that I was sometimes taken aback by her modernity.
She sat among her raucous grandchildren at regular family get-togethers, a faint smile on her face that conveyed her joy at being in the midst of the happy banter, even when she didn’t always understand what we were talking about. She cared for her husband through more than a decade of dementia and managed his worsening and sometimes dangerous confusion.
She was doughty, bright eyed, determined. We all hoped she’d have a decade of quality ageing after Pa died; still active, still sharp, still Nan.
Then a stroke felled her while she ate dinner at a neighbour’s house. She was active, outgoing, engaged – until she wasn’t. i
Nan left her beloved neighbourhood in an ambulance. She never returned. Her last year of life was spent in slow, sad, uncomfortable decline in a care facility, trapped in a wheelchair or bed, struggling with nausea caused by the damaged part of her brain. We all visited her as much as we could, but leaving her there each time we departed was like cutting off a small piece of our hearts. This was not how it was supposed to go.
THERE IS THE promise of ageing, and then there is the reality.
The promise is tanned, linen-clad bodies – softer around the edges, but still a silhouette to be proud of – white teeth, confident smiles, full heads of silver hair gently stirred by coastal breezes, a late-afternoon sun shining on a beach walk or exercise in the residential-village pool. It’s medications to lower cholesterol, blood glucose and blood pressure, raise bone density and stabilise heart rhythms, soothe arthritic joints and quell the increasingly strident litany of petty aches and pains. It’s surgical procedures to replace joints and valves, even entire organs, and unblock clogged blood vessels.
But the gap between that promise and the experience of ageing for so many Australians – including my nan – is so profound that no amount of marketing or airbrushing can hide the cracks.
The reality is that around half of all Australians aged sixty-five years or older experience some form of disability. Among people aged eighty-five or above that figure rises to around 80 per cent. Men and women are differently impacted by severe age-related difficulties: 15 per cent of men and 22 per cent of women aged sixty-five and above need help with self-care, mobility or communication, rising to nearly two fifths of men and more than half of all women aged eighty-five and upwards.
The proportion of people who judge their health as fair or poor increases with greater age: from one quarter of people aged sixty-five to seventy-four to just under a third in the seventy-five to eighty-four age bracket, and just over a third of those aged eighty-five or over. ii The greatest burden of disease impacts sixty-five to sixty-nine-year-olds. This era is often anticipated as the prime time of post-retirement, but instead many grapple with heart disease, cancer, neurological conditions such as dementia and Parkinson’s disease, musculoskeletal conditions such as arthritis, and lung disease.
The unit used to measure the burden of disease is ‘disability-adjusted life years’ or DALY: this is what the World Health Organization describes as ‘one lost year of “healthy” life’. iii It’s a composite of time lost to premature death and time lost to disability, and it represents the gap between an ideal health situation ‘where the entire population lives to an advanced age, free of disease and disability’, and the actual, current health and wellbeing of a population.
In 2011, Australians aged sixty-five or over were denied more than 1.8 million of these DALY years. For every 1,000 people aged sixty-five and above, 600 years of ‘healthy’ life were lost. Nearly two thirds of this loss was terminal – the result of people dying prematurely from disease. The other third represented years where people might have expected to be living it up, free of work and with savings to spend – only to find themselves hampered by disease or disability.
Longevity is good if those additional years of life are healthy, happy and satisfying, says researcher Professor Nicolas Cherbuin, head of the Centre for Research on Ageing, Health and Wellbeing at the Australian National University in Canberra. But ‘it’s not terribly useful if it’s to prolong pain and disability’, he says. ‘And what we find is that the substantial portion of the added life years are actually additional years with disability, and in this sense they’re not as satisfying and as productive as if they were years of healthy life.’
A century ago, we had pretty low expectations of old age. Most of us would have been lucky to make it to sixty, iv having long since succumbed to infectious disease, injury, hardship, childbirth or cancer. We didn’t live long enough to worry about heart disease, dementia, falls, osteoporosis or strokes. Which is not to say everyone died relatively young. Cherbuin says there is evidence that even thousands of years ago, some lucky humans lived into their seventies or even eighties, but far, far fewer than do so now.
Today, modern hygiene and medicine – at least in high-income countries and societies – have largely beaten infectious disease with vaccines, antibiotics and antivirals. We have reduced maternal and child mortality with advances in obstetric medicine and avoided injury with safety practices – and while we haven’t beaten cancer, we certainly have it on the back foot. We’ve cheated evolutionary selection pressures with technology, or at least changed the odds to be much more in our favour.
But we all have to die of something. The lucky ones go quickly, like my other grandmother who lived a mostly healthy and active life until a ruptured blood vessel took her with shocking but merciful suddenness.
WHY DO WE age? The American humanist Leon Kass wrote that ‘mortality makes life matter’. v The countdown – whether measured out in Prufrock’s coffee spoons or felt in every new ache or wrinkle – reminds us that we only have a finite time in this world and we should therefore get on with it, whatever our own ‘it’ might be.
Ageing is the tick-tock of a cellular clock. Each time a cell divides to create identical twins, it is one tick closer to what is called the Hayflick limit, after its discoverer Leonard Hayflick. In 1960, Hayflick overturned the existing dogma that cells could divide ad infinitum, instead demonstrating that a typical cell had around fifty divisions in it, coded into its genetic blueprint. vi Once it reaches that limit, a cell enters a state called senescence: it can divide no more and ceases to fulfil its biological role. As we age, these senescent cells accumulate, contributing to an overall decline in function in ways that are still relatively poorly understood.
The machinery of life also becomes creaky and unreliable with age. One of the most important tasks of this cellular machinery is to produce the proteins that keep life going. Sometimes – increasingly as we age – this machinery makes mistakes, producing aberrant proteins that are discarded and cleaned up by cellular cleaners. But as Cherbuin explains, as we age, this machinery starts to make more and more mistakes.
‘At the beginning these things are fixed as they go and very little damage is left behind,’ he says. ‘But it’s this little damage that just impairs slightly the cleaning mechanisms, the fixing mechanisms.’ As that damage piles up, it makes our bodies age.
At the same time, the genetic material that runs the show is subject to a host of environmental factors – some beyond our control, some partly under our control and some self-inflicted – that can increase the rate of these mistakes.
Our awareness of how big an impact such factors have on the ageing process has changed considerably. ‘We thought we could not do anything about ageing, that our body works in the way it works…and this has been really a prevalent thought for much of the last century,’ Cherbuin says. ‘It’s really only in relatively recent times that we’ve realised that in fact there is a great deal we can do about ageing, and that ageing is modulated by exposures to different risk factors.’
Unfortunately, many of those risk factors are lifestyle related, which make them both very easy and very difficult to alter. We could exercise more and spend less time sitting, but we don’t. We could eat more vegetables and wholegrains, but we don’t. We could drink less alcohol, smoke less tobacco, protect ourselves from the sun more, eat less red meat, but we don’t. We know what’s good for us, but bad habits are tough to break.
SO HAVE CENTENARIANS got the secret? Are those fortunate few – around 12,000 Australians in 2020 vii – who make it to one hundred years of age in possession of the secret to a long and healthy life?
A century ago, there weren’t enough centenarians to begin exploring, let alone answering, this question. But with increasing lifespans and longevity, there is now a big enough cohort that researchers can investigate the still relatively unique phenomenon of extreme long life. It’s what underpins the Sydney Centenarian Study at the University of New South Wales’s Centre for Healthy Brain Ageing, which has 410 Sydneysiders currently enrolled from all walks of life, predominantly female, and all at least ninety-five years old. viii Every six to twelve months, these volunteers answer detailed questions about their medical history and status, mental and cognitive state, diet, physical activity, social participation and social functioning.
Theirs is an altruistic contribution to humanity, says study co-ordinator Dr Catherine Browning. ‘The research that’s coming through, and the knowledge of the things that might help us…are informing the younger generations more than they’re informing the centenarians that I talk to,’ says Browning. But the participants in the study understand its importance.
‘We’re working on this to predict what might help us to age better, rather than to just age and live with what our lot is in life.’
The secrets to longevity are not as exciting as one might imagine, having glimpsed the occasional centenarian on television over the years insisting that the elixir of long life is a tot of whisky before bed every night. That’s not (unfortunately) one of the options on the list of factors that study participants are given to choose from when asked what they think is the most important factor in their longevity.
It turns out physical activity is what one third of these centenarians credit with keeping the grim reaper at bay. ‘They can reflect on their lives as being physically active, either incidentally through their work or deliberate exercise like swimming in the ocean every day, or taking a walk,’ Browning says.
Physical activity is as close to a magic bullet for the diseases of ageing as we’re going to get, at least for the time being. There’s a growing body of evidence that physical activity in midlife is associated with better brain health in older age. ix It’s also associated with a lower risk of heart disease x – or, rather, physical inactivity is associated with a higher risk of heart disease – and lower risk of the symptoms of anxiety and depression.xi But the evidence isn’t always consistent: xii the Whitehall II study, a large UK study of over 10,000 civil servants who were followed for an average of twenty-seven years, did not find a protective effect of exercise against dementia. However, they did find that people who went on to develop dementia exercised less in the nine years leading up to their diagnosis, and suggest that maybe as people feel the early effects of dementia, they go out and exercise less. At the same time, other studies have found an association between fitness in older adults and improved brain function. xiii ixv The possibility is that exercise improves cardiovascular fitness, and that in turn reduces the risk of dementia, but it’s a tricky and complex association to tease apart, especially when you take into account other risk factors such as smoking and diet.
The second most favoured ingredient for a long and healthy life is the company you keep, and how often you keep it: 16 per cent of the Sydney Centenarian cohort believe that their relationships are the thing that keeps them going. Scientific research supports this, at least for men: married men are healthier and live longer than unmarried men, and they’re less likely to die from heart disease. xv Women haven’t always enjoyed the same health and longevity benefits from marriage, but curiously that appears to be changing: in the past few decades, married women have edged in front of single women in lifespan, although no one is quite sure why the switch has happened. xvi One suggestion is that in the past, married women were largely confined to home responsibilities, but the recent advances in female workforce participation have seen the health benefits of marriage shared more equally between men and women. xvii
And in a close third place is diet and nutrition. ‘We’ve got a few participants in our study who immigrated to Australia after the Second World War and some of them are from Europe, so we often hear of the Mediterranean diet or Mediterranean-type diet,’ Browning says. ‘They’re very proud to tell me that that’s how they’ve lived all their life and they have that knowledge…that nutrition is important.’ Science backs this up: there is now a wealth of evidence that a diet of vegetables, fruits, wholegrains, beans, nut and seeds, and olive oil each day, plus fish, poultry and eggs on a weekly basis supplemented by moderate amounts of dairy and limited red meat, is best for the heart. xviii And what’s good for the heart is also good for the mind.
But the study also gives its centenarians the opportunity to tell researchers, in their own words, what they think their secret to longevity is. And ‘a lot of them say it’s luck,’ says Browning. ‘Some of them are just bewildered and stumped, and they say that they were lucky.’
Perhaps most important of all is picking your parents wisely. Browning says their research suggests around 30 per cent of longevity comes down to your genes.
HEARTS AND MINDS. These are the things that so often betray us in old age, if we manage to dodge the cancer bullet. Cancer might be the second leading cause of disease burden in the over sixty-fives, but its prevalence actually decreases after a peak around retirement age. Data from the US shows that around one quarter of new cancers are diagnosed in people aged sixty-five to seventy-four, but only 7.8 per cent are diagnosed in those over the age of eighty-four. ixx
But one in ten Australians aged over sixty-five has dementia. It’s the single biggest cause of disability in the over sixty-fives, the second leading cause of death in Australia overall, and the numbers are increasing. xx This phenomena may well be a function of people living longer – dementia is most commonly a disease of older age – but it could also reflect increasing rates of cardiovascular disease and diabetes in the population, which are thought to play a role in causing dementia.
Dementia is the most feared diagnosis of older age, says Dr Katya Numbers, study co-ordinator for the Sydney Memory and Ageing Study at the Centre for Healthy Brain Ageing at UNSW. In 2000, this study enrolled around 1,000 individuals aged between seventy to ninety years, without dementia, and has been following them ever since.
‘There’s a real feeling of inevitability associated with dementia in our cohort,’ Numbers says. ‘There’s a lot of worry about feeling like they’ve noticed signs of decline, a lot of talk about parents and family members who have had dementia.’ Part of the challenge in understanding, preventing and treating dementia is that ‘dementia’ is actually an umbrella term for a complex range of patterns of neurological degeneration and symptoms.
There’s Alzheimer’s disease, vascular dementia, frontotemporal dementia, Parkinson’s disease with vascular dementia and Lewy body disease, to name just a few. xxi Some present in middle age, some in older age. Some are associated with memory loss and confusion, others with personality changes and hallucinations. All have different presentations, different features, different pathologies and different origins, although the causes of dementia in whatever form is a wide-open question.
‘What we’re finding more and more, especially as people are living longer and longer, is there’s almost no such thing as a pure dementia,’ Numbers says.
One factor that does stand out as being common to many forms of the disease is heart health. Studies suggest that the risk factors for heart disease – high blood pressure, smoking and diabetes – are also risk factors for dementia.
Heart disease was responsible for 27 per cent of all deaths in Australia in 2017, and one in six Australians is affected by it. xxii It’s the leading cause of death in people aged sixty-five and older, accounting for 13 per cent of all deaths in older Australians. xxiii And it becomes more prevalent with age: just over one third of Australians aged fifty-five to sixty-four have heart disease, but two thirds of those aged seventy-five and older. ixv
Here’s the rub: modern medicine is actually very good at preventing and treating heart disease. Research tells us clearly what needs to be eaten, done or avoided to reduce the risk in midlife. There are medications to reduce all the risk factors for heart disease – cholesterol, blood pressure, blood sugar – and there are interventions to open up plaque-blocked arteries around the heart to allow the oxygen-carrying blood to nourish those essential heart muscle cells without interruption. We know this stuff. Doctors know this stuff, and they’ve done so for a long time. As far back as the seventeenth century a physician observed that heart disease was linked to reduced blood flow through the arteries of the heart. xxv The concept of atherosclerosis – the build-up of plaque in the arteries of the heart – was introduced in 1949, and in the 1950s the connection was made between low-fat diets and low rates of heart disease.
So why are so many older Australians still suffering with and dying from heart disease?
Cardiologist Dr Sonali Gnanenthiran has long been perplexed by this apparent contradiction. Her research suggests that a big part of the problem is that while the elderly are the main victims of heart disease, the disease is studied and its treatments tested in younger people – those of middle age.
‘Most cardiovascular disease events actually happen in the elderly but when you look at studies, recruitment of the elderly is usually very small; if you’re lucky it’s a third, but usually far less,’ says Gnanenthiran, a visiting medical officer at Canterbury Hospital, who also works at the Sydney Adventist and Concord hospitals. This is problematic because the risk factors for heart disease in the elderly, and the way it behaves, seem to be quite different to those risk factors and behaviours observed in younger – middle-aged – people.
‘Going through the factors that contribute to cardiovascular disease, the things that we understand as being predictive, such as blood pressure and cholesterol, are actually less predictive in older people,’ she says. Take blood pressure. While there’s understandable focus on reducing high blood pressure as a risk factor for heart disease, there’s now emerging evidence that lowering it too aggressively in older people is associated with a higher risk of death. xxvi
The same pattern is emerging for cholesterol. A recent study by Gnanenthiran and colleagues found that low total cholesterol – a composite of the so-called ‘good’ HDL cholesterol and ‘bad’ LDL cholesterol and triglyceride levels – is actually associated with an increased risk of major heart disease events in men aged seventy years and older. xxvii They suggest that low cholesterol in these older men could actually be the result of frailty or underlying disease, such as cancer or infection, which might explain the association with increased risk of heart disease because these conditions are all mediated in various ways by inflammation.
The gold standard method for working out an individual’s risk of experiencing a heart disease event, such as a heart attack, has long been an algorithm called the Framingham Risk Score. This takes into account blood pressure, cholesterol levels, smoking and gender to predict the risk of a heart attack within ten years, and therefore guide decisions on preventive treatments such as blood pressure-lowering or cholesterol-lowering medications. The data used to develop this algorithm came from a landmark, ongoing, multi-generational study of a group of (mostly white) residents of the town of Framingham in Massachusetts. But, as Gnanenthiran points out, that study only includes people aged thirty to sixty-two at study entry.
‘They incorporate traditional cardiovascular risk factors but fail to account for changing distribution of cardiovascular risk factors in the elderly,’ she says. Just being old is considered a risk factor for heart disease, but the algorithms designed to predict that risk aren’t taking those same elderly into account. Gnanenthiran and her colleagues are working on their own cardiovascular risk model specifically designed for elderly populations that takes into account other factors such as frailty, and looks at death from all causes rather than just cardiovascular causes. The aim is to take a more holistic view of health in the elderly, she says: ‘There’s no use putting someone through a complex coronary intervention if they’re going to die next month from bleeding.’
ANTI-AGEING IS big business. Whether it’s creams, supplements, extreme fad diets, therapies such as cryotherapy or vitamin infusions, or even more extreme experimental treatments such as injecting oneself with essence of monkey testicles xxviii (don’t try this one at home), there is an endless supply of largely unproven or even untested therapies purporting to keep the body fresh and youthful.
Medicine is also on this quest, hunting for that miracle molecule that will wind back the cellular clock. ixxx Professor Elizabeth Blackburn won the 2009 Nobel Prize in Physiology or Medicine for her discovery that the tips of our chromosomes – called telomeres – wear down with age, but there is an enzyme, telomerase, that can slow or even reverse that process. xxx Blackburn has argued that stress, poor diet, poor sleep and lack of exercise all contribute to the demise of those telomeres. But, inevitably perhaps given our desire for a quicker easier fix, there are companies selling telomerase as an anti-ageing treatment – despite the lack of evidence that such an approach works or is even safe.
Some existing medications, such as metformin – a common treatment for diabetes – are showing signs in animal studies that they may have life-prolonging benefits beyond their anti-diabetic effects. xxxi Another compound that caused some excitement – possibly because red wine is a rich source – is the antioxidant resveratrol. xxxii But again, the studies are often preclinical – meaning they’re done in cell cultures or animals, not humans – so the leap to real-world outcomes in humans is a big one.
One area of research into anti-ageing compounds has Nicholas Cherbuin intrigued. Senolytics – drugs that target the senescent cells accumulating in the ageing body – are generating excitement in research and investment circles, leading to predictions that these drugs might be available in five to ten years. xxxiii The principle is that these drugs help to clear out those senescent cells – or ‘zombie’ cells, as is their new and catchy descriptor – therefore reducing their toxic effects.
One of the few human studies that used a combination of the two senolytic compounds, dasatinib and quercetin, in people with a lung-scarring disease called idiopathic pulmonary fibrosis, suggested improvements in walking distance. But it was a small study without a control group for comparison, so the results are not a resounding endorsement. They are, along with studies in mice, certainly intriguing. But there is a long research path to be walked, and the usual pitfalls that claim so many promising new therapies before they make it to commercialisation still need to be overcome.
I’M IN MY forties. I’m starting to feel a few unexplained aches and pains; I might expect more in later life. My eyes have lost a bit of their clarity in the past year or so. My hair is edging towards what might charitably be called ‘salt and pepper’. I’m a bit more careful of flinging my body around in space than I might have been twenty years ago. I’m also acutely aware that the lifestyle train I set in motion now will probably decide the course of my later life, so I have started running; I drink less alcohol; I try – but usually fail – to resist the lure of butter.
I feel like I’m doing the right things to increase my odds of a healthy and productive older age, but I also know that’s mainly wishful thinking. There are still so many ‘known unknowns’ and especially ‘unknown unknowns’ in my biological future that I may have only tipped the scales slightly in my favour.
For all the promise of research and medicine, and many drops of anti-ageing snake oil, there is still a long way to go before every limitation or indignity of ageing can be banished, if that is even possible to achieve. And for all our fears about ageing, the alternative is far less attractive.
I’ve heard it said that the best thing to do if you want to live a long and healthy life is pick your parents carefully. And so, in that respect, I am lucky.
‘I don’t feel seventy-two,’ says my mother, sitting across from me at the kitchen table, both of us nursing cups of tea. ‘When I think of what my image of a seventy-two-year-old would be, it’s someone old.’ She laughs at the incongruity of that statement. ‘I think of my grandparents being seventy-two, and being old and dithery.’
From her perspective, my mother is pretty happy with the hand that ageing has dealt her. She’s mobile – so much so that most of the time I have no idea where she or my father might be in Australia, let alone on the planet. She eats well, she enjoys the many delights that Australia’s cultural scene has to offer, she spends plenty of time with her grandchildren, and she’s still as sharp and feisty as she was when I was a child.
Like many of her generation, she dreads dementia, especially after seeing it rob her father of his mind over more than a decade. She also carries a heavy burden of grief over Nan’s – her mother’s – last year in the nursing home, and the injustice of her suffering just to prolong life by a few more months.
But Mum is not afraid of dying.
‘We do have to accept that everyone dies,’ she says. She has a fierce objection to the idea of prolonging life at all costs. There is a finite amount of money in the health budget, ‘and I don’t think it should be spent on someone who’s lived a good life for eighty years, just to live another four or five years,’ she says.
‘If I’ve reached eighty and I’ve been like this? Brilliant. What a great life and I’m happy for it to finish.’
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ii Australian Institute of Health and Welfare (2018). Older Australia at a glance. 10 September. https://www.aihw.gov.au/reports/older-people/older-australia-at-a-glance
iii World Health Organisation (2019). Health Statistics and Information Systems. https://www.who.int/healthinfo/global_burden_disease/metrics_daly/en/
iv Queensland Government (2018). Vital Statistics: Life Expectancy. Life expectancy at birth by sex, Queensland and Australia, 1881-1890 to 2016-2018. 31 October. https://www.qgso.qld.gov.au/statistics/theme/population/vital-statistics/life-expectancy
v Kass, L.R., (1983). ‘The case for mortality’. The American Scholar. pp.173-191.
vii UNSW (2019). Centre for Healthy Brain Ageing (CHeBA). Sydney Centenerian Study. https://cheba.unsw.edu.au/research-projects/sydney-centenarian-study
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ix Alzheimer’s Society (2020). Physical exercise and dementia. https://www.alzheimers.org.uk/about-dementia/risk-factors-and-prevention/physical-exercise
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xi de Oliveira, L.D.S.S., Branco, C., Souza, E.C., Rodrigues, R.A.S., Fett, C.A. and Piva, A.B., (2019). The effects of physical activity on anxiety, depression, and quality of life in elderly people living in the community. Trends in psychiatry and psychotherapy. 4 Feb 2019. doi: 10.1590/2237-6089-2017-0129.
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xxvii Gnanenthiran, S.R., Ng, A.C., Cumming, R., Brieger, D.B., Le Couteur, D., Waite, L., Handelsman, D., Naganathan, V., Kritharides, L. and Blyth, F., (2019). Low total cholesterol is associated with increased major adverse cardiovascular events in men aged≥ 70 years not taking statins. Heart, pp.heart jnl-2019.
xxviii Grundhauser, E. (2015). ‘The True Story of Dr.Voronoff’s Plan to Use Monkey Testicles to Make Us Immortal’. Atlas Obscura. 13 October. https://www.atlasobscura.com/articles/the-true-story-of-dr-voronoffs-plan-to-use-monkey-testicles-to-make-us-immortal
ixxx Klimova, B., Novotny, M. and Kuca, K. (2018). Anti-Aging Drugs-Prospect of Longer Life?. Current medicinal chemistry, 25(17), pp.1946-1953.
xxx Corbyn, Z. (2017). ‘Elizabeth Blackburn on the telomere effect: ‘It’s about keeping healthier for longer’. The Guardian. 29 Jan. https://www.theguardian.com/science/2017/jan/29/telomere-effect-elizabeth-blackburn-nobel-prize-medicine-chromosomes
xxxi Reynolds, G. (2019). ‘An anti-aging pill? Think Twice’. The New York Times. 19 June. https://www.nytimes.com/2019/06/19/well/move/an-anti-aging-pill-think-twice.html
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xxxiii Fleming,A. (2019). ‘The science of senolytics: how a new pill could spell the end of ageing’. The Guardian. 2 Sep. https://www.theguardian.com/science/2019/sep/02/the-science-of-senolytics-how-a-new-pill-could-spell-the-end-of-ageing