Hey… about that bunker, starting to look good. 
1 Like
A lot of people who write these stories don’t understand the broadness of people’s situations in countries such as the UK. There are many people whose health is so bad in say their 40s or even 30s that they move towards a form of inactive participation in everything.
Lots of these problems are like accelerated age related diseases such as diabetes, COPD, heart disease. If we overcome these problems it will improve the lives of many people in their 30s and 40s.
2 Likes
AI will become something like this.
1 Like
Where could you even hide from an AGI in this universe?
Alpha Centauri? (…)
Takes a robot a few decades at most to reach and start mining/hunting.
Hence a good place to hide from AGI.
Then we might need human biostasis, or how do we get there?
Big money in anti-aging researching areas we already are reading about on rapamycin.news… "Yamanaka factors” – rapamycin and metformin.
Ageing: The longevity secrets billionaires are betting their fortunes on
Link: Ageing: The longevity secrets billionaires are betting their fortunes on
The 2 existing drugs that could become anti-ageing pills
The world’s wealthiest are betting billions on an almost unbelievable idea: that getting older can be slowed or reversed. Here is the science behind it.
Scientists in fields such as epigenetic reprogramming are working on a series of potentially world-changing breakthroughs in extending the human lifespan. Bethany Rae
Euan Black Health and wellness reporter
Aug 22, 2025 – 5.59am
Katia Dowling’s idea of living a long and healthy life probably differs from yours. The former engineer and founder of Lumen Longevity has set her sights on reaching her 200th or 300th birthday.
“I hope that within my lifetime something will be created that will allow me to live to that age, and if not, I can use cryopreservation,” the 40-year-old says, referring to the process of preserving human bodies after death.
Although it may sound like the work of science fiction, Dowling is not naive. She doesn’t think she will live that long simply by jumping into ice baths, taking bucketloads of supplements or getting high-dose infusions of vitamin C every week. She accepts her ambition for an exceptionally long life will only be realised if there is a “very serious” scientific breakthrough.
But depending on who you ask, that breakthrough is perhaps not as far away as you might think. For while no serious researcher will claim to know exactly what causes ageing and how they can slow or reverse it, the field is brimming with ideas and studies that could soon yield answers – perhaps not enough for centuries of life, but maybe 120 or 150 years of healthy living.
For now, most agree that the best things we can do today to improve our chances of staying healthy for longer relate to diet, exercise, sleep, social engagement and stress management. But scientists are also pulling the thread on a series of potentially world-changing breakthroughs.
Researchers in the field of epigenetic reprogramming have rejuvenated individual human cells in laboratory settings, essentially turning back the clock on ageing. Several human trials are under way to assess whether medicines indicated for diabetes management and immunosuppression could slow ageing, following promising animal trials.
And scientists are also working hard to overcome a major hurdle within the field – the difficulty of conducting the types of trials needed to test whether a given intervention can actually extend human lifespan – by discovering molecules, genes and biological characteristics within humans that we can track over time to determine how quickly an individual is ageing.
The two words that perhaps carry the most excitement in the field of human ageing today are “Yamanaka factors” – particularly if you place any stock in the flow of investment dollars as a signal of potential value.
Amazon founder Jeff Bezos is reportedly the major backer of ageing-research biotech Altos Labs, which raised $US3 billion ($4.6 billion) in funding in 2022 and is pursuing the biological reprogramming technology made possible by the discovery of “Yamanaka factors”, while the King of Saudi Arabia and OpenAI chief executive Sam Altman are throwing significant funds at researchers exploring similar technologies.
The excitement stems from a 2006 paper by Japanese researcher and Shinya Yamanaka. The former surgeon discovered four transcription factors (proteins that regulate gene expression) that could rewind the clock on an adult mouse cell, turning it back into an embryonic-like state known as an “induced pluripotent stem cell”, or iPS cell.
Scientists had known that a specialised adult cell could be reprogrammed since the 1960s. That’s when the British developmental biologist John Gurdon transferred the nucleus from a frog’s intestinal cell into a frog egg and watched it grow into a healthy tadpole – not into an unhealthy frog as you might have expected given its old-nucleus beginnings.
It wasn’t until Yamanaka’s discovery in 2006, however, that scientists had a recipe for replicating the process. Yamanaka discovered you could turn back the clock on a cell’s age by adding to it just four transcription factors – Oct3/4, Sox2, c-Myc and Klf4 – which came to be known as “Yamanaka factors”. A year later, he proved the same method worked on human cells taken from a 36-year-old woman and a 69-year-old man.
The breakthrough led to Nobel prizes for both Yamanaka and Gurdon in 2012, and gave birth to the modern field of “epigenetic reprogramming”. Scientists had a way of reversing an individual cell’s age without altering its underlying DNA sequence. The next question was: could they do the same across an entire body?
Early attempts to do this in mice had disastrous consequences, leading to what are known as “teratomas”. This is because while adult cells perform a specific set of functions based on their identity (skin cell, hair cell, liver cell etc), stem cells are immature cells that have not yet undergone the process of cell specialisation, meaning they have no specific function and can develop into any type of cell in the body, and not just the cell types they used to be.
Associate Professor Lindsay Wu is the head of the Laboratory for Ageing Research at the UNSW. The centre researches fundamental mechanisms and interventions that could maintain healthy ageing. Dominic Lorrimer
“Now, you hope that they turn back into the cell types you want, but there’s a good chance that they won’t,” says Lindsay Wu, head of the Laboratory for Ageing Research at the University of New South Wales.
“So, you can end up with these structures called teratomas. They’re not quite tumours. They are lumps of tissue that have differentiated into the wrong tissue type.”
Google “teratomas”, and you will find an array of distressing images that illustrate the risk involved with this approach. Yet, undeterred, scientists shifted their focus to “partial reprogramming” instead. The question was: could they ever so slightly turn back the clock – enough to rejuvenate the cell, but without taking it all the way back to a stem cell and erasing its original identity? “That’s where the field’s at today,” Wu says.
So far, animal trials have delivered promising results . One reversed age-related vision loss in old mice. Another achieved the same result in non-human primates, a result described as an “unprecedented step forward” in a review published in the journal Ageing Research Reviews last year. And scientists have also rejuvenated multiple tissues and extended the healthy lifespan of mice by 15 per cent when they applied the partial reprogramming early in life.
Life BioSciences, a US-based company that Wu helped set up, is now trying to use the same technology to restore sight to people who experienced damage to their optic nerve, which can lead to glaucoma.
“Some cell types in the adult body just don’t regenerate, especially nerves. So the idea is that, by using this partial reprogramming approach, you could restore them,” Wu explains. The human trials for this have not yet begun, but the work leading up to them is well under way.
Given it could solve the problems of teratomas and inadvertent erasures of a cell’s identity, the partial reprogramming approach has attracted plenty of media attention and significant financial investment. But it’s not without risks – perhaps the biggest of which is cancer.
The same factors used to rejuvenate cells can cause tumours if the process is uncontrolled or goes too far. Wu says recent approaches have attempted to minimise this risk by leaving out one of those factors, c-Myc, which was the greatest cause for concern in early reprogramming work, and by “building in controls that fine-tune the degree of reprogramming”.
There are also safety concerns related to the way these factors are transported to old cells: through an inactivated virus. And then there are the many ethical and philosophical dilemmas associated with the technology: Is ageing a disease that needs to be cured? Could epigenetic reprogramming lead to overpopulation? Will such expensive interventions only be accessible to the rich and famous, worsening inequality? And, far lower down the list of priorities, what would it mean for romantic relationships – would 200 years of healthy marriage be a realistic ambition?
Former environmental engineer Katia Dowling has faith in scientists’ ability to crack the ageing condundrum, citing discoveries such as the “Yamanaka factors”. Louise Kennerley
The list of unanswered questions is scary and long. But the excitement is palpable. The term “Yamanaka factors” comes up repeatedly when AFR Weekend interviews researchers for this piece. So it’s perhaps unsurprising that Dowling mentions it when I ask her what scientific discoveries to date give her confidence that living to 200 or 300 is a realistic ambition.
“Discoveries like that prove to us that [it could be] possible,” she says. “[It could be achieved by] reprogramming cells, or getting rid of zombie cells [called] senescent cells, so clearing the body of the cells that cause inflammation and ageing.”
Dowling, whose company Lumen Longevity organises public conferences on human ageing to raise awareness of longevity science and encourage investors to support local scientists, also mentions “nutrient sensing” and “metabolic health”.
She never utters the words “hallmarks of ageing” – the 12 interconnected biological processes which scientists believe are the main drivers of the lifelong, ageing process – but that’s what she’s getting at.
The “hallmarks” were coined by Spanish biochemist Carlos Lopez-Otin and his colleagues in a 2013 paper published in the journal Cell. The paper identified nine biological processes at the cellular and molecular level, but these were refined and expanded to include 12 hallmarks in an update to the framework published in 2023.
That consensus exists on the importance of these hallmarks is encouraging. Because, as the 2023 paper makes clear, one of the three criteria that a biological process must meet to be considered a hallmark is that it provides an opportunity to “decelerate, stop, or reverse ageing” via therapeutic interventions that target it. And so, if scientists could just find a way of slowing down these hallmarks – which include things like genomic instability, telomere attrition, mitochondrial dysfunction and chronic inflammation – the theory is they could help humans age slower and live for longer.
This idea is linked to another promising theory known as the geroscience hypothesis, which posits that physiological ageing is the root cause of many chronic diseases and conditions, such as cancer, diabetes, cardiovascular disorders and neurodegenerative diseases. Targeting the hallmarks of ageing directly – rather than each individual disease – could therefore help us delay or prevent the onset of multiple age-related diseases all at once.
Many of the hallmarks relate to metabolism and metabolic health, which is another area of focus for Wu and his laboratory at UNSW. While many scientists have focused on the effect of whole-body metabolism, leading to the discovery that mild-to-moderate caloric restriction could be the most potent intervention for extending human lifespan, Wu and his colleagues have instead focused on energy metabolism within our cells.
“There’s this vitamin co-factor called nicotinamide adenine dinucleotide, or NAD+, and it is required for about 45 per cent of all biochemical reactions that occur in the cell. It’s really important for almost every step of metabolism,” Wu says. NAD+ levels decline with age, which can lead to “blocks in energy metabolism”. But these problems can be overcome by restoring NAD+ levels, leading to improved health and longevity.
“For example, a few years ago, we showed that we can make old mice run further on a treadmill by restoring NAD+ levels, [which] improved their microvasculature,” Wu says. “And really excitingly, when we give NAD precursors to old animals, we reverse their infertility. Egg cell quality improves, and they become fertile again.”
Other promising areas of research involve so-called senolytic drugs – molecules that help to clear cells that have stopped dividing but continue to secrete harmful molecules that drive the ageing process (“senescent cells”) – and the compounds rapamycin and metformin. Neither of these drugs were designed to be anti-ageing drugs, but preliminary research suggests they could be used for that purpose.
“In every species that it’s been tested, [rapamycin] extends lifespan quite potently,” Wu says. “Even when it’s delivered late in life to older animals, or if it’s delivered briefly in the middle of life, it extends lifespan by a good margin. We’re talking 20 to 30 per cent overall, which is super exciting.”
For some individuals, the preliminary evidence is encouraging enough for them to experiment with taking the drug off-label in the hope of slowing down ageing – even though its primary use in the healthcare system is as an immunosuppressant.
Stanford-trained physician and popular podcaster Peter Attia has spoken about his experience taking the drug and how it led to a common side effect of painful mouth ulcers. “I woke up this morning in an unbelievable amount of pain,” he told his 1.3 million Instagram followers in a post from 2023. Another public figure who takes the drug for its potential anti-ageing effects is the renowned American biologist Brian Kennedy.
Kennedy, who is now the director of the Centre for Healthy Longevity at the National University of Singapore, told Attia’s podcast last month that his team was undertaking a six-month trial in people aged 40 to 60 to see if a weekly dose of rapamycin led to improved health metrics in healthy adults. He noted, however, that it was difficult to know which metrics to track given the scientific community had not yet worked out the best surrogate measures for ageing.
“I try all kinds of different things on myself,” Kennedy said. “One of the things I notice is when I take rapamycin, if I do a hard run … I don’t have good runs within 24 hours of taking rapamycin.”
Rapamycin extends an animal’s lifespan by preventing their cells from producing more protein and forcing them to break down the junk that accumulates in their cells in a process known as autophagy. The same process is also triggered when animals fast.
Metformin is believed to induce autophagy, too. The drug is cheap and one of the most prescribed medications globally for treating type 2 diabetes, but, as with rapamycin, some people also take it off-label in the hope it may extend their lives. A 2013 study in Nature Communications found that giving a low dose of the drug to one species of male mice increased their average lifespan by almost 6 per cent. Studies in humans, meanwhile, have found that metformin is associated with an improvement in cardiovascular risk factors. It is not yet known why metformin appears to reduce a patient’s risk of multiple diseases, but scientists are hopeful it is because the drug targets the underlying hallmarks of ageing.
A study in the United States should hopefully provide more clarity. The Targeting Aging with Metformin (TAME) Trial is a series of nationwide, six-year clinical trials led by 14 leading US research institutions. Involving more than 3000 individuals aged 65 to 79, it aims to provide strong evidence to shore up a controversial theory: that ageing can be treated, just like we treat diseases.
“If ageing is made an indication, the TAME Trial will mark a paradigm shift: from treating each age-related medical condition separately, to treating these conditions together, by targeting ageing per se,” reads the trial’s official website, managed by the American Federation for Aging Research.
The scientists involved have settled on the study’s design, but the trial’s website says it still needs “visionary donors” to help launch the project.
That the trials are not yet under way points to a significant challenge within the field of human ageing and longevity. By definition, the experiments needed to prove whether a given intervention extends human lifespan would take a lifetime (and be difficult to control) – and that’s obviously too long to wait for anyone alive today.
There are potential workarounds to this problem, which we’ll get to later. But it’s perhaps the biggest hurdle for longevity science, and a good reason why you should be sceptical of social media influencers who claim to know how to slow down or reverse ageing, says Steven Zuryn, a molecular geneticist at the University of Queensland.
“Delaying or preventing ageing is a physical challenge, and anything that is a physical challenge can, theoretically, be solved,” Zuryn says. However, he warns that some of the claims made today in relation to longevity are often based solely on findings from animal trials, which, while important, do not always translate to humans. This is why people should be cautious about buying supplements that claim to have anti-ageing effects, or experimenting with drugs off-label before clinical trials have been conducted.
“For example, Alzheimer’s disease can be treated in mice in many different ways,” Zuryn says. “But we are yet to find an effective treatment that works in humans, because mice and humans, although similar, still have differences in biology.”
The conundrum of how to scientifically test whether a given intervention is slowing or reversing the ageing process in humans, without conducting an extremely long clinical trial, is a keen area of interest for researchers. Some are using the onset of age-related diseases as a proxy measure for ageing, the idea being that if an intervention could delay or prevent the onset of multiple age-related diseases rather than just one, then this could be a sign that it is targeting the hallmarks of ageing directly.
Others, like Alexey Terskikh, head of the Perkins Chromatin and Ageing Laboratory at the University of Western Australia, are trying to develop biomarkers for ageing – biological metrics that can be measured to track the ageing process within individuals.
In 2024, Terskikh and his colleague Kenta Ninomiya revealed in the journal Nature Aging that they had developed the world’s first “imaging-based biomarker capable of quantifying ageing and rejuvenation at a single-cell level”. In other words, they had developed a new way of measuring the ageing process, within individual cells.
“By offering a detailed snapshot of cellular ageing, we can better understand the effects of interventions such as caloric restriction and partial reprogramming, potentially paving the way for new strategies to extend healthy lifespan,” Ninomiya said in a press release accompanying the research in 2024.
“For instance, the biomarker showed increased ageing following chemotherapy treatment and decreased ageing after caloric restriction or partial cellular reprogramming.”
In an interview with AFR Weekend, Terskikh says the novel approach developed by his laboratory gives his team a better chance of understanding the mechanisms of a particular intervention and its capacity to influence healthspan (the number of years that we remain healthy, free from disease and functionally active) and lifespan (the total number of years we live).
“If you know mechanistically what is happening and in which cell type it is happening, then there’s a greater level of assurance that what you’re doing makes sense, as opposed to the snake oil people telling you, ‘take this and it’s going to work’. Well, how do you know?” Terskikh says.
“We need to do a lot of experiments in C elegans [roundworms], mice, and other model organisms. The key question is how the mechanisms we learn in animal models are translated into humans.”
Given the extent to which drugs like rapamcyin and metformin have extended the lives of animals, and given how Yamanaka and other scientists have rejuvenated human cells in controlled experiments, it’s no surprise that there is plenty of excitement about the possibility of one day being able to take a pill or undergo a procedure to slow or reverse ageing. But some scientists would rather we focused more on the things we can do today to help us stay healthy as we age.
Sarah Hilmer, a geriatrician and clinical pharmacologist at Royal North Shore Hospital, says significant improvements to quality of life can often be achieved through seemingly simple interventions.
Sarah Hilmer, a geriatrician and clinical pharmacologist at Royal North Shore Hospital, says it’s important for people to understand that “there are a lot of things that we actually can do right now to help us with healthy ageing”. These include doing exercise that builds muscle, eating healthily, avoiding obesity and maintaining as much social engagement as possible.
“The final one, which is where I work, is around optimising our medical care to prevent and manage disease, and to minimise the adverse effects of medications on our ability to function physically and cognitively and socially,” Hilmer says.
She is best known for developing a clinical risk assessment tool called the Drug Burden Index, which is a measure of all the drugs taken by a patient that have anticholinergic and sedative effects (the former refers to drugs that block the neurotransmitter acetylcholine).
Covering a wide of range of medicines such as sleeping tablets, antihistamines and drugs for urinary incontinence, the index calculates the extent to which a patient’s medications are slowing them down physically and mentally, so that doctors and pharmacists can make more informed decisions about future prescriptions and other components of their treatment plans.
“If someone’s just a little bit slow physically or mentally, you might just think they’re getting old, or you might think it’s because they’re sick,” Hilmer says. “So it’s really important to be able to recognise the medication-related effects because those are potentially reversible.”
It’s an example of how significant improvements to our quality of life can often be achieved through seemingly simple interventions. Or, as Hilmer puts it, by focusing on what we know works, and “delivering it to help people age well”.
Andy Philp, who heads the Centre for Healthy Ageing at the Centenary Institute and University of Technology Sydney, is another researcher with his feet firmly in the healthspan over life span camp. He also is keen to stress that interventions to promote healthy ageing should be started in midlife or earlier, as ageing is a lifelong process.
“If you extend healthspan, you will probably live longer as a consequence of that. But this idea that you want to live to 200 or 300 – to me, that’s not really a narrative that I’m that bothered about,” says Philp, who also convenes the national network of scientists focused on the biology of ageing known as the Australian Biology of Ageing Network.
“I’d rather live happily and healthily for as long as I possibly can, go to sleep one night and not wake up, right? I don’t want to be in hospital for a decade. I want to spend time with my kids, hopefully my grandkids, travel, enjoy retirement, and to me, that’s a successful healthspan.”
“There are beautiful studies showing that if you resistance-train 80-year-olds, they get stronger and they get better.”
— Andy Philp, Centre for Healthy Ageing
What’s concerning to Philp is that – despite all the advances of modern medicine – we actually appear to be heading in the wrong direction when it comes to healthy ageing.
Research by the Australian National University last year concluded that life expectancy was stagnating for Australians under the age of 50, while separate data from Cancer Australia shows the rates of several cancers among Australians aged 30 to 39 has more than doubled between 2000 and 2024. The prevalence of prostate, pancreatic and colorectal cancers, for example, has jumped by 500 per cent, 200 per cent and 173 per cent respectively.
“To me, the narrative should be about trying to avoid that [getting age-related diseases earlier in life],” Philp says.
The good news is he believes there is powerful evidence to suggest we can significantly influence what our last decade looks like. Getting old, Philp says, doesn’t have to mean suffering through years of illness and frailty. “That isn’t inevitable. It is modifiable, and it doesn’t need to be modified by million-dollar treatments”.
A particularly powerful intervention is resistance training, which helps offset the age-related decline in fast-twitch muscle fibres. This is important because losing these fibres makes us more susceptible to falling over and breaking a bone, which can be extremely difficult to recover from later in life.
The flipside is that inactivity actually accelerates ageing. Philp and his team have found that healthy 70-year-olds lose about two kilos of muscle mass if they are confined to a bed for five days, meaning that older people come out far weaker from a short hospital stay than when they went in.
“There are beautiful studies showing that if you resistance-train 80-year-olds, they get stronger and they get better. They have functional improvements from 12 weeks of resistance exercise,” Philp says. “You can remodel muscle when you’re older. You can get better. There’s a narrative that we don’t know that, but we definitely do know that. So you can absolutely modify healthspan, which I think is the exciting thing”.
The irony, perhaps, is that the people who most need to hear that probably aren’t the people reading this article. The audience for this piece probably already eat well, exercise fairly regularly and do their best to sleep seven or eight hours each night.
Dowling is among them. She also tries to stick to organic food, cooks as many of her meals at home as possible, and practises Vipassana meditation to manage her stress. She is doing all these things because “while we’re waiting for miraculous drugs and innovative things to be discovered, we do need to get there in good health”. But she does believe that those discoveries will be made.
“It’s very complicated to figure out the formula [that] will allow us to live longer,” she says. “But it is happening.”
1 Like