When 103 ageing researchers were asked in 2024 whether average lifespan in developed countries would rise by more than ten years in the next two decades, most said yes. It is one of the most optimistic numbers the field has ever produced. It is also one of the least likely, if you look at demography and at what drugs have actually achieved so far.

This article draws on an essay by biologist Adiv Johnson in the September issue of Lifespan Magazine and on his paper in the journal Biogerontology. It asks a simple question: where are we today, what would have to be true for life to get a decade longer, and what does that mean for someone who wants to live longer now?

Where we are: around 80, and the pace is slowing

Average life expectancy in developed countries now sits around 80 years. In the UK it is roughly 79 for men and 83 for women. Over the last century that is an enormous leap, but most of the gain has one cause: the defeat of infectious disease. Strip the eight most common infections out of the data since 1900 and the overall improvement shrinks considerably.

Demographer Jay Olshansky and colleagues showed in Nature Aging in 2024 that in the longest-lived populations the growth in life expectancy has been slowing since 1990. By their estimate it is unlikely that most people will live to 100 in this century. In other words, the easy wins have been taken. What remains is ageing itself, a much harder opponent than bacteria.

Where life expectancy has moved, and where it would have to go for the optimists to be right
US, year 1900 about 47 years Developed countries now about 80 Survey target in 20 years 90 plus

1900: life expectancy at birth in the US from national mortality statistics. Today: approximate figure for developed countries (Johnson 2025). Target: the statement from the survey by Gladyshev et al. 2024 that most respondents agreed with.

What would have to be true: a 12.5 percent jump

Johnson does the arithmetic plainly. At a typical lifespan of 80 years, a drug or intervention would have to extend life by more than 12.5 percent to push the average past 90. That sounds modest until you look at what such a jump means in experiments.

The US National Institute on Aging runs the Interventions Testing Program, in which dozens of compounds are tested in mice at three independent labs. Out of the whole list, only four things cleared the 12.5 percent bar in both males and females: rapamycin, acarbose, rapamycin combined with acarbose, and rapamycin combined with metformin. Everything else, including many substances sold as anti-ageing supplements, either did nothing or added a few percent.

And that is still mice. A mouse lives two to three years. Carrying the size of an effect over to humans is unreliable, according to a systematic review in the BMJ: treatments that worked in animals often diverged from expectations in clinical trials. The road from discovery to treatment also takes 10 to 15 years. For the survey’s optimistic scenario to come true, enormous and expensive human trials would have to be running already. They are not.

Why even scientists are prone to hope

Johnson uses an instructive example from the field’s history. In 1956 Denham Harman published the theory that ageing is caused by free radicals. The paper has more than ten thousand citations and gave birth to a decades-long antioxidant industry. But the theory turned out to be far too simple: free radicals are essential to normal cell function, and boosting antioxidant defences did not extend life in animals. Oxidative stress plays a part in ageing, just not the part that was expected.

The lesson is not that science failed. It is that the longevity field tends to run enthusiastically after one explanation before the data arrives. The 2024 survey also showed that researchers do not even agree on the basic principles of what ageing is. Where there is no consensus on the cause, a quick cure is hard to expect.

What is being studiedWhat the studies showedWhere we are in humans
RapamycinRepeatedly extends mouse lifespan by more than 12.5% (ITP)Small safety and marker trials, no lifespan study
AcarboseOver 12.5% in mice, mainly in males (ITP)Established diabetes drug, effect on ageing in humans unproven
MetforminNot enough alone, works combined with rapamycin (ITP)A large human trial (TAME) has been in preparation for years, no lifespan results
AntioxidantsTheory from 1956, no lifespan gain in animalsSupplements with no proven effect on lifespan
Biomarkers of ageingEpigenetic clocks and blood panels are developing fastPromising as a yardstick in shorter studies, not as a diagnosis

What could change the sceptics’ minds

Johnson himself writes that he would be glad to be proven wrong. Two things could change the picture. The first is artificial intelligence in drug development: if it really shortens the path from idea to molecule to trial, the pace of discovery could accelerate. The second is measuring biological age. If there were a reliable biomarker of how fast a person is ageing, trials would not have to wait decades to see who dies. It would be enough to watch whether the clock has slowed.

That is exactly why epigenetic clocks and blood panels of ageing are developing so quickly. For now they are research tools with wide scatter, not something you should change treatment on. But the direction is right: measure, do not believe.

What this means for you right now

If you are waiting for a pill to rescue you within twenty years, the data is against you. If you want to use the years that are within reach, the strategy is well known and a little dull:

  1. No smoking, and alcohol only rarely. The two biggest removable causes of early death, both with overwhelming data behind them.
  2. Movement, including strength. Aerobic fitness and muscle mass are among the strongest predictors of survival in middle and older age.
  3. Sleep and food without excess calories. No diet works miracles, but excess weight, high blood pressure and high LDL cholesterol can be measured and kept in check.
  4. Prevention guided by your own numbers. Blood pressure, LDL, glucose, weight and body composition show risk years before disease arrives. Those who know their values and watch the trend fix problems while they are still cheap.
  5. Experimental drugs and supplements only with a doctor. Rapamycin is not a vitamin. Anyone who wants to try it belongs in a trial or in a doctor’s office, not on a web shop.

The best news in this whole debate is, paradoxically, the sober one. A decade of extra life may not arrive. But extra healthy years, which is what people actually want, are largely in each person’s own hands, and can be tracked in their own data.

FAQ

What people ask

What is average life expectancy in developed countries today?

Around 80 years, with differences between countries and between men and women. In the UK it is roughly 79 for men and 83 for women, in the US a little lower. The rate of improvement has slowed since the 1990s.

What does it mean that a drug would have to extend life by 12.5 percent?

At a typical lifespan of 80 years, 12.5 percent is ten extra years. That is what it would take for the average to cross 90. In mice only a handful of compounds cleared that bar, and in humans none has.

Does rapamycin work in people?

In mice it extends lifespan repeatedly and reliably. In humans there are smaller trials, mostly on safety and partial markers. According to systematic reviews, effects seen in mice usually shrink or vanish in people. It is not an anti-ageing drug you should start on your own.

Why do most mouse results fail in humans?

A mouse lives two to three years, a human eighty, and ageing runs along different tracks in each. A systematic review in the BMJ found that results from animal experiments often disagree with human clinical trials. On top of that, the path from lab to treatment takes 10 to 15 years.

What is biological age and what is it for?

An estimate of age from blood markers or epigenetic marks that can differ from your birth date. It serves as a faster yardstick in short studies: instead of waiting decades to see who lives longer, you watch whether the clock has slowed. For now it is a research tool, not a diagnosis.

So what should I actually do if I want to live longer?

Stick to what has strong data: no smoking, minimal alcohol, movement including strength work, sleep, food without excess calories, and prevention guided by your own numbers (blood pressure, LDL cholesterol, glucose, weight). Supplements and experimental drugs only after talking to a doctor.

Sources

What this article is based on

Peer reviewed papers and primary sources the text draws on. Links go to the original.

  1. Gladyshev VN et al.: Disagreement on foundational principles of biological aging. PNAS Nexus, 2024Survey of 103 ageing researchers, including expectations of more than 10 years of added lifespan.
  2. Olshansky SJ et al.: Implausibility of radical life extension in humans in the twenty-first century. Nature Aging, 2024Slowing gains in life expectancy in the longest-lived populations since 1990.
  3. Johnson AA: Realistic expectations for changes to average human lifespan in the near future. Biogerontology, 2025The 12.5 percent threshold and the ITP compounds.
  4. Olshansky SJ, Carnes BA, Cassel C: In Search of Methuselah: Estimating the Upper Limits to Human Longevity. Science, 1990Eliminating cancer would add only about three years.
  5. Perel P et al.: Comparison of treatment effects between animal experiments and clinical trials: systematic review. BMJ, 2007Divergence between animal and human results.
  6. Harman D: Aging: A Theory Based on Free Radical and Radiation Chemistry. Journal of Gerontology, 1956Origin of the free radical theory, now considered too simple.
  7. Lifespan Magazine, September 2026: How Long Can We Actually Expect to Live in the Coming Years? (Adiv Johnson)The essay this article draws on; published by the Lifespan Research Institute.