We often think of ageing as nature’s one unbreakable law. Everyone gets older. Cells slow down, tissues wear out, and eventually, the body gives in. But over the past thirty years, science has begun to challenge that assumption. Ageing isn’t just a background process ticking away in our bodies, it’s something with mechanisms, pathways, and weak spots. And in animals, at least, researchers have learned how to push back against it.
The question is beginning to change from “is ageing modifiable?” to “how much can we safely shift it in humans?”
The Biology of Ageing
A landmark review in Cell in 2013, often called the “Hallmarks of Ageing” paper, laid out the biological foundations of ageing in nine categories (López-Otín et al., 2013). Instead of one switch, ageing is a cascade of failures. DNA repair falters, telomeres shorten, mitochondria sputter out, proteins lose their shape and clog up cells. Senescent “zombie cells” accumulate, spreading inflammatory signals to their neighbours. Even stem cells, the body’s natural repair toolkit, lose their ability to regenerate tissues.
It sounds bleak, but each of these problems is, in theory, fixable.
What Worms and Mice have Taught Us
The first hints came from simple organisms. In 1993, Cynthia Kenyon’s lab discovered that altering a single gene in the insulin signalling pathway of roundworms doubled their lifespan (Kenyon et al., 1993). Instead of 20 days, the worms lived for 40.
Mice brought even more dramatic results. Rapamycin, a drug that inhibits the growth-related mTOR pathway, extended lifespan even when given late in life (review). In another experiment, scientists engineered mice so that their senescent cells could be selectively destroyed. Clearing away these “zombie cells” improved heart and kidney function, restored muscle strength, and even extended overall lifespan (Baker et al., Nature, 2016).
What about humans?
Animal data is exciting, but humans are harder. We live much longer, our biology is more complex, and safety risks are larger. Still, some interventions are making their way into clinical trials.
Metformin, a drug prescribed for type 2 diabetes for decades, is at the centre of the TAME trial (Targeting Ageing with Metformin). Epidemiological studies suggested that patients on metformin had lower rates of cancer and cardiovascular disease than those on other treatments. The trial is now testing whether it can broadly delay the onset of age-related conditions, not just diabetes.
Rapamycin has also crossed into human studies. In a small trial, older adults given a rapamycin derivative before flu vaccination mounted a stronger immune response (Mannick et al., 2014). That’s not proof of longer lifespan, but it’s a sign that modulating ageing pathways can improve human biology.
Senolytics are at an even earlier stage. A pilot study in patients with idiopathic pulmonary fibrosis used dasatinib plus quercetin, drugs that target senescent cells, and found reduced markers of senescence with some signs of improved function (Justice et al., 2019). It’s far from a miracle cure, but it shows the mouse findings aren’t limited to the lab.
The most headline-grabbing trials have been those inspired by parabiosis experiments; connecting the circulatory systems of old and young mice. In animals, young blood seemed to rejuvenate tissues in the old partner. In humans, plasma transfusion studies have been attempted in Alzheimer’s patients, but results so far are modest, and the approach remains controversial.
Why it’s so hard
If the science is this exciting, why aren’t we already taking “anti-ageing pills”? The answer is complexity. Ageing isn’t one disease; it’s a network of processes. Fixing one pathway might break another. A drug that extends lifespan in mice could raise cancer risk in humans. Even measuring success is tricky. You can’t run a 70-year clinical trial just to see if people live longer. Instead, researchers rely on “biological clocks” based on DNA methylation and other biomarkers, but these are still being validated.
And then come the ethical questions. If we did find a way to add decades of healthy life, would it be accessible to everyone, or only to those who could afford it? Would societies strain under the weight of longer lives? And should we even be trying to “cure” ageing at all, or should medicine focus on making the years we already have as healthy as possible?
Healthspan vs Lifespan
Most scientists in the field now emphasise healthspan. Immortality isn’t the goal. What matters is whether people can spend their later years free of frailty, disease, and decline. Living to 90 with the health of a 60-year-old is a far more realistic target than living to 150.
And that’s where the next 20–30 years may take us. Drugs like rapamycin, senolytics, and metformin probably won’t grant eternal youth. But they may compress the years of illness into a much smaller fraction of life. That’s not science fiction anymore, it’s the direction of current clinical research.
So…?
We can’t cure ageing yet. But we’re no longer asking whether it can be slowed. We’re asking how much, and at what cost. The idea that biology can resist time itself? That’s no longer a dream. It’s a research programme, and it’s happening now.
So the question becomes personal: if staying healthy was guaranteed, how long would you want to live?
Thanks for reading! If you want to learn more, check out the YouTube video at the top 🙂
