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August 28, 2026
Birgitta Dunckel
Why do some people age faster than others? For a long time, lifestyle was considered the decisive factor. But a new study attributes a surprisingly large role to genes — and in doing so, challenges a long-standing rule of thumb in aging research.
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Some people look noticeably younger than their age at sixty. Others feel the effects of aging much earlier. A date of birth alone therefore says surprisingly little about how well a body has actually aged. This is precisely where modern research comes in: it distinguishes between chronological age as recorded on paper and biological age, which is meant to describe the condition of cells, tissues, and organs.
But why do some people age faster than others? How much is genetically predetermined, and how much can we influence through our lifestyle? A major 2025 study highlighted the role of environment and living conditions, while a 2026 study attributed a surprisingly large role to genes.
Behind the concept of healthy aging lies a shift in focus. It is no longer just about how long a person lives, but about how long they remain mobile and mentally and physically fit. Longevity research provides the scientific foundation for this. Both concepts revolve around the same distinction:
• Chronological age:the number of years since birth. Unchangeable, and progressing at the same rate for everyone.
• Biological age:the functional state of cells, tissues, and organ systems.
To make differences in biological aging measurable, researchers have developed various biomarkers and models. These include so-called epigenetic clocks, which analyze specific changes in DNA methylation. The foundation was laid in 2013 by biostatistician Steve Horvath, who developed a method capable of predicting the age of tissue samples with remarkable accuracy using 353 DNA methylation sites.
More advanced models, such as GrimAge and DunedinPACE, have since been developed. These aim not only to reflect age, but also to capture health risks and the pace of biological aging processes. How these epigenetic clocks work, why different tests can yield different results, and how lifestyle influences epigenetic changes are all explained in detail in our article on epigenetics.
Anyone who wants to understand what is actually happening in thesecellswill sooner or later encounter a paper that has shaped the biology of aging over the past decade more than almost any other.described inin 2013 nine so-called "Hallmarks of Aging" — common biological denominators to which the deterioration seen over the years can be traced. Three more were added in 2023. The twelve hallmarks include, among others:
• Genomic instability and shortened telomeres
• Epigenetic alterations
• Stem cell exhaustion and disrupted cell communication
• Chronic low-grade inflammation ("inflammaging") and gut microbiome dysbiosis
Which of these mechanisms can be influenced is one of the most active areas of healthy aging research. Above all, though, there is a question more fundamental than it might initially appear: how much of this is actually within our own control, and how much is simply given — written into our genes long before anyone makes their first decision for or against a healthy lifestyle?
Anyone who has attended a longevity talk in the past thirty years is probably familiar with this figure: it comes from a twin study by Anna Maria Herskind and colleagues, who in 1996 calculated a genetic contribution to life expectancy of around 22 percent based on 2,872 Danish twin pairs born between 1870 and 1900.
Later, even larger genealogical analyses temporarily pushed the figure below 10 percent. The message that lingered for years was both convenient and reassuring: how we live matters far more than what we have inherited.
This interpretation gained additional weight in 2025, through a study of a scale that had rarely been seen before.M. Austin Argentieri and her teamanalyzed data from 492,567 participants in the UK Biobank. They examined how strongly a range of environmental and lifestyle factors — the so-called "exposome" — and polygenic risk scores for 22 major diseases were associated with mortality.
The results were clear: the genetic risk scores examined explained less than 2 percentage points of additional mortality variance, while the exposome accounted for around 17 percentage points. Smoking emerged as the single strongest adverse factor, while regularexerciseand higher socioeconomic status were among the factors identified as protective.
It is important to note, however, that this does not mean genes in general account for less than two percent of lifespan. The study did not capture the full genetic influence on longevity, but rather specific genetic risk variants. Its percentage figures are therefore not directly comparable to classical heritability estimates.
Then, barely a year later,Ben Shenhar and a team led by Prof. Uri Alonat the Weizmann Institute in Israel revisited three large Scandinavian twin cohorts — including, for the first time, twins raised apart — and systematically excluded all deaths unrelated to aging itself: accidents, infections, and violence.
Their argument: it was precisely this confounding factor that had led earlier studies to systematically underestimate the genetic contribution. Once it is removed, the heritability of "intrinsic" lifespan rises to 50 to 55 percent — more than twice the old rule of thumb. For specific conditions such asdementia, the team even estimates heritability at around 70 percent up to the age of 80.
This did not go unchallenged. In aPerspective articlein the same issue ofScience, Daniela Bakula and Morten Scheibye-Knudsen raised several methodological concerns about the model, including the argument that the higher estimate was effectively built into the structure of the statistical approach itself.
Independent voices have also urged caution in interpreting the figure: biologist Chiara Herzog from King's College London pointed out to the Science Media Center that heritability estimates are statistical measures for entire populations, not predictions for individuals. And bioinformatician Steve Hoffmann from the Leibniz Institute on Aging in Jena summed things up in a way that reads almost like a punchline: even a higher heritability estimate would not lead him to start smoking again.
Only at first glance. The studies ask different questions and use different methods. The 2025 UK Biobank study compared measured environmental factors with specific genetic risk scores and examined their association with mortality.
The 2026 study, by contrast, used twin data to estimate what proportion of the variation in intrinsic lifespan within a population can be statistically attributed to genetic differences. The percentage figures therefore cannot be directly compared or set against each other.
How much of lifespan ultimately comes down to genes will likely keep researchers busy for some time — perhaps because science is reluctant to settle on a single number when three studies produce three different ones. For everyday life, however, these debates change surprisingly little about the practical conclusion.
Even the study attributing the largest role to genetics does not dispute that modifiable factors play an important role: avoiding smoking, exercise, diet, sleep, stress management, and social connection. Genes appear to influence the framework within which aging unfolds — but they do not fully determine the individual trajectory. It is precisely in this margin that healthy aging comes into play.
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