The Question That Refuses to Die

In 2021, a team of researchers at Singapore’s Gero and the Roswell Park Comprehensive Cancer Center published a paper suggesting that the human body’s ability to recover from stress declines predictably with age, and that this resilience would disappear entirely somewhere between 120 and 150 years. The finding was widely reported as a “hard limit” on human lifespan. It was not. It was a model, built on blood-test data and mathematical extrapolation, and it came with caveats that rarely made the headlines.

Five years later, in 2026, a different team at the Skolkovo Institute of Science and Technology ran a simulation asking a narrower question: if every other mechanism of aging could somehow be paused, how long would random DNA mutations alone allow a human body to function? Their answer, published in npj Aging, was roughly 146 to 194 years depending on the model—with a median around 156. Again, headlines declared that “150” was the new ceiling.

These studies are serious science, and they tell us something real about the biological constraints on lifespan. But they are also a useful entry point into a larger question: what does it actually mean to say humans cannot live to 150? Is it a hard biological wall, a soft limit that medicine might push against, or simply a number generated by models that are still being refined?

The honest answer is that nobody knows. What the research does show is that aging is not a single process. It is a collection of biological failures that accumulate over time, and the question of whether 150 years is possible depends on which failures turn out to be fixable—and which ones do not.

Why Do Humans Age?

For most of medical history, aging was treated as an inevitable background condition. You aged, you developed diseases, you died. The diseases were the problem; aging was just the context.

That view has changed. Geroscience—the study of aging as a biological process in its own right—now treats aging as the shared risk factor behind most chronic diseases. Cancer, heart disease, dementia and frailty all rise exponentially with age, not because they are separate failures but because they share underlying cellular mechanisms.

In 2023, a major review in Cell consolidated these mechanisms into twelve “hallmarks of aging”. They include:

• Genomic instability — DNA damage accumulates over time.
• Telomere attrition — the protective caps on chromosomes shorten with each cell division.
• Epigenetic alterations — the chemical marks that control gene expression drift.
• Loss of proteostasis — the cell’s protein-folding and recycling systems decline.
• Deregulated nutrient sensing — metabolic signalling pathways become less responsive.
• Mitochondrial dysfunction — the cell’s energy factories become less efficient.
• Cellular senescence — damaged cells stop dividing but do not die, secreting inflammatory signals.
• Stem cell exhaustion — the body’s repair cells lose their capacity to regenerate tissue.
• Altered intercellular communication — inflammation and other signals become chronically dysregulated.

Not all hallmarks are equally important, and not all are equally well understood. One 2026 review went further, arguing that among the twelve, only telomere shortening has a clear causal role, and that other hallmarks may be consequences rather than drivers. That is a minority view, but it illustrates an important point: the map of aging is still being drawn.

What Determines the Maximum Human Lifespan?

There is a difference between average lifespan and maximum lifespan. Average life expectancy has risen dramatically over the past century, from roughly 30 years in many pre-industrial societies to over 70 globally today, driven by sanitation, vaccines, antibiotics and reductions in infant mortality. Maximum lifespan—the age reached by the oldest individuals—has barely moved.

The oldest verified person in history, Jeanne Calment, lived to 122 years and 164 days. No one has credibly exceeded that record. The number of people reaching 110—supercentenarians—has increased, but the maximum age at death has remained remarkably stable.

The 2026 Skolkovo simulation offers one explanation. The researchers modelled what would happen if somatic mutations—random DNA changes that accumulate in cells throughout life—were the only aging mechanism left. They found that non-dividing cells, such as neurons and heart muscle cells, are particularly vulnerable because they cannot be replaced. When mutations accumulate in these “fixed” cells, organ function eventually collapses. Under that model, even perfect repair of every other system would cap the median at around 156 years, with the upper range approaching 194.

A separate line of evidence comes from demographic studies of supercentenarians. Analyses of international longevity databases have suggested a plateau in mortality rates at extreme ages, implying a biological limit somewhere between 120 and 125 years. The 150-year figure is not a measured limit. It is a theoretical ceiling generated by models that make specific assumptions about what aging is and what can be fixed.

Secrets of the World’s Longest-Living People and Blue Zones

If you want to know what a long life looks like, the Blue Zones are the obvious place to start. These are five regions—Okinawa (Japan), Sardinia (Italy), Nicoya (Costa Rica), Ikaria (Greece) and Loma Linda (California)—identified by demographic research as having unusually high concentrations of centenarians.

The Blue Zones narrative is appealing: eat plants, move naturally, have purpose, stay connected, drink wine (in moderation). It has spawned best-selling books, documentaries and a small industry of longevity advice.

It has also attracted serious criticism. A 2024 Ig Nobel Prize–winning analysis by Australian researcher Saul Justin Newman argued that many supposed centenarians in these regions may not be the age they claim, because poor birth records, pension fraud and age misreporting were common in the relevant historical periods. A 2025 essay in a public health journal went further, arguing that the Blue Zones concept suffers from biased population selection and uncontrolled confounding, and that the longevity attributed to these regions may be partly an artefact of flawed data.

Defenders of the Blue Zones have pushed back. A 2025 paper in The Gerontologist described the extensive age-validation process used in each region, cross-checking multiple independent documentary sources to eliminate errors and fraud. The authors concluded that the age data from the classic Blue Zones are “valid and reliable” and that these populations “still have much to teach the world”.

The most defensible reading is that the Blue Zones are real but complicated. Extreme longevity in these regions is not a myth, but it is also not a simple lifestyle formula. Genetics, record-keeping quality, population history and environmental factors all interact. The Blue Zones are a useful starting point for studying healthy aging—not a guaranteed recipe for living past 100.

Can Genetics Influence How Long We Live?

The heritability of human lifespan has been one of the most contested numbers in aging research. Twin studies have traditionally estimated that genetics accounts for only about 20 to 25 per cent of lifespan variation, with the rest driven by environment and lifestyle. Some large pedigree studies put the figure even lower, around 6 per cent.

A 2026 analysis in Science challenged those numbers. The researchers argued that previous estimates were confounded by extrinsic mortality—deaths from accidents, infections and other external causes—which dilute the genetic signal. By mathematically removing extrinsic deaths, they estimated that the heritability of intrinsic lifespan is around 50 to 55 per cent.

That is a significant revision, but it does not mean that genetics is destiny. Even a 55 per cent heritability leaves substantial room for environmental influence. And the genetic architecture of longevity is not a single “longevity gene.” It is likely a large number of small-effect variants, interacting with each other and with the environment.

Some specific genetic factors have been identified. Variants in the FOXO3 gene, for example, have been associated with exceptional longevity in multiple populations. But these variants are neither necessary nor sufficient for a long life. They are part of a probabilistic picture, not a deterministic one.

How Diet, Exercise, Sleep and Stress Affect Aging

The lifestyle factors that influence aging are well known, even if the mechanisms are still being worked out. The most rigorous evidence comes from studies that measure biological age using epigenetic clocks—chemical marks on DNA that correlate with age and predict health outcomes.

The CALERIE trial, a two-year randomised controlled trial of 12 per cent caloric restriction in healthy adults, found that the intervention slowed the pace of biological aging as measured by the DunedinPACE algorithm. The effect was modest—roughly a 2 to 3 per cent reduction in aging rate—but it was measurable, and it persisted after controlling for weight loss.

Exercise has similarly been linked to slower biological aging. A 2026 review of lifestyle interventions concluded that caloric restriction, moderate exercise and quality sleep all decelerate the aging process from the standpoint of biological age. The mechanisms include improved mitochondrial function, reduced inflammation and enhanced autophagy—the cell’s recycling system.

Stress is harder to measure, but chronic psychological stress has been associated with accelerated telomere shortening and epigenetic age acceleration. Sleep is another modifiable factor: poor sleep quality and short sleep duration have been linked to faster biological aging, while adequate sleep supports the glymphatic system’s waste-clearance function.

The practical takeaway is not a specific diet or supplement. It is that the fundamentals—moderate eating, regular movement, adequate sleep, stress management and social connection—have measurable biological effects. They do not guarantee a longer life, but they shift the odds.

Anti-Aging Research, Gene Therapy and Cellular Rejuvenation

The most speculative area of longevity science is also the one that generates the most excitement. Researchers are exploring several approaches to slowing or reversing aging at the cellular level.

Senolytics are drugs that target senescent cells—the “zombie” cells that accumulate with age and secrete inflammatory signals. In mouse models, clearing senescent cells improves frailty and extends lifespan. In humans, early clinical trials have shown reductions in senescent-cell burden, but functional benefits have been modest and variable.

Epigenetic reprogramming uses transcription factors—most famously the Yamanaka factors—to partially reset the epigenetic marks that drive cellular aging. In aged mice, partial reprogramming has extended median remaining lifespan by as much as 109 per cent. In humans, the technology is still in early stages. A 2026 review noted that no clinical trials for aging have yet been conducted using reprogramming, and that delivery to target tissues, off-target effects and durability remain major challenges.

Stem cell therapies aim to restore the body’s regenerative capacity. Stem cell exhaustion is one of the hallmarks of aging, and researchers are engineering stem cells to resist senescence and maintain their function. These approaches are promising but early. Most are still in preclinical or early clinical testing.

The common thread across these fields is that biological age reversal has been demonstrated in animal models and, in some cases, measured in humans through epigenetic clocks. What has not been demonstrated is a durable, safe, clinically meaningful extension of maximum lifespan in humans.

Can AI and Modern Medicine Help Humans Live Longer?

Artificial intelligence is becoming a tool for aging research in several distinct ways.

AI-powered aging clocks can estimate biological age from blood tests, genetic data, imaging and even retinal photographs. Deep learning models can capture non-linear patterns that traditional clocks miss, improving the accuracy of biological age prediction. These clocks are not just diagnostic tools. They are essential for evaluating whether an anti-aging intervention actually works.

AI-driven drug discovery is being used to identify compounds that target aging pathways. In 2025, researchers used AI to discover a dual-action candidate for aging-related neurodegeneration, mapping a reproducible “AI-to-clinic” pathway. Autonomous AI agents are now being deployed to scan millions of molecular profiles for age-modifying interventions.

AI in clinical care is already improving outcomes for age-related diseases. AI-assisted imaging detects cancers and cardiovascular disease earlier. Predictive models identify patients at risk of frailty and falls. These advances extend healthspan—the number of years lived in good health—even if they do not extend maximum lifespan.

The honest assessment is that AI is accelerating the research pipeline, not delivering a longevity breakthrough on its own. It makes aging research faster, cheaper and more precise. It does not change the fundamental biology.

What Scientists Still Don’t Know About Aging

Despite decades of research, several fundamental questions remain unanswered.

Why do different organs age at different rates? The brain and heart, composed largely of non-dividing cells, appear to be the limiting factors for lifespan, while the liver and skin regenerate continuously. The mechanisms that govern this differential aging are poorly understood.

What is the relative contribution of damage accumulation versus programmed decline? The telomere hypothesis argues that aging is driven by progressive cellular damage. The programmed-aging hypothesis argues that aging follows a genetic timetable. The evidence supports elements of both, but the balance is unresolved.

Can biological age be reversed safely and permanently? Partial reprogramming has reversed epigenetic age in mice, but it has also caused tumours in some experiments. The safety profile in humans is unknown.

What is the role of inflammation? Chronic low-grade inflammation—“inflammaging”—is associated with almost every age-related disease, but whether it is a cause or a consequence of aging is still debated.

These are not niche questions. They are the core unresolved problems of geroscience, and they are unlikely to be settled within the next decade.

What the Future of Human Longevity Could Look Like

The most plausible near-term future is not a sudden leap to 150 years. It is a gradual extension of healthspan—more years lived in good health—driven by incremental improvements in prevention, diagnosis and treatment.

Within the next decade, AI-assisted diagnostics, personalised prevention and senolytic drugs may reduce the burden of age-related disease. Average life expectancy in high-income countries may continue to rise slowly, but maximum lifespan is unlikely to change dramatically.

Further out, epigenetic reprogramming and stem cell therapies could, in principle, extend the period of healthy life. But the challenges—delivery, safety, durability, cost—are substantial, and the timeline is uncertain.

The 150-year question is, in the end, a question about the plasticity of human biology. If aging is a collection of fixable damage, then the ceiling may be higher than we think. If some damage—particularly in non-dividing cells—is irreparable, then the ceiling may be closer than the optimists hope.

The most useful way to think about longevity is not as a number to be maximised, but as a distribution of probabilities to be shifted. Every year of healthy life is a gain, regardless of whether the absolute maximum ever moves.

Conclusion: A Longer Life Is Not the Same as a Better One

The science of aging has moved from fatalism to active investigation. We now know that aging is modifiable, at least at the margins. Caloric restriction, exercise, sleep and stress management have measurable biological effects. Senolytics and reprogramming are being tested in humans, even if the results are early. AI is accelerating the research pipeline.

What we do not know is whether the fundamental limits identified by the Skolkovo model—the accumulation of mutations in cells that cannot be replaced—can be overcome. If they cannot, then 150 years may remain a theoretical ceiling rather than a realistic target. If they can, then the ceiling may move.

The more important question may be not how long we can live, but how long we can live well. A 120-year life spent in frailty and dependency is not a triumph of medicine. A 90-year life spent in good health, with purpose and connection, is. The future of longevity research will be judged not by the maximum age reached by a handful of outliers, but by the number of people who reach old age with their minds and bodies intact.

That is a goal worth pursuing, whether the number is 90, 120 or 150.