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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 at sixty look noticeably younger. Others begin to feel the effects of aging much earlier. A person's date of birth alone therefore tells us surprisingly little about how well their body has actually aged. This is precisely where modern research steps in: it distinguishes between chronological age as recorded in a passport and biological age, which aims to describe the condition of cells, tissues, and organs.
Researchers are working to make these differences measurable using what are known as epigenetic clocks. 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 placed environment and living conditions front and center, while a study published in 2026 attributes a surprisingly large role to genes.
The concept of healthy aging reflects a shift in focus. The question is no longer solely 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 core distinction:
• Chronological age: the number of years since birth. Unchangeable, and advancing at the same rate for everyone.
• Biological age: the functional state of cells, tissues, and organ systems.
The fact that this difference can be quantified at all is a relatively recent achievement. Biostatistician Steve Horvath, then at UCLA, introduced a method in 2013 that sounds technical at first but is, in effect, quite remarkable: it reads the methylation status at 353 defined DNA sites and uses this to calculate an age that matches a person's chronological age to within about 3.6 years.
From this first generation, new models with different objectives have since emerged. While Horvath's original clock was primarily designed to reconstruct chronological age from DNA methylation, models such as GrimAge focus more on health risks and mortality.
DunedinPACE, in turn, is not primarily intended to express biological age in years, but rather to capture the pace at which a person is aging. A large comparative study from 2025 confirms that these newer clocks can outperform first-generation models in predicting age-related diseases.
Anyone who wants to understand what is actually happening inside these cells will sooner or later encounter a paper that has shaped aging biology over the past decade more than almost any other.The team led by Carlos López-Otín described in 2013 in Cell nine so-called hallmarks of aging — common biological denominators underlying the decline that accumulates over the years. Three more were added in 2023. The twelve hallmarks include, among others:
• Genomic instability and shortened telomeres
• Epigenetic alterations (see above)
• Stem cell exhaustion and disrupted cell communication
• Chronic, low-grade inflammation ("inflammaging") and dysbiosis of the gut microbiome
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 first appear: how much of this is actually within our control, and how much is simply given — written into our genes long before anyone makes their first choice for or against a healthy lifestyle?
Anyone who has attended a longevity talk over the past thirty years is probably familiar with this figure: it comes from a twin study by Anna Maria Herskind and colleagues, which 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 family tree analyses temporarily pushed the figure below 10 percent. The message that stuck for years was both convenient and reassuring: how we live matters far more than what we inherit.
This interpretation gained additional weight in 2025 — through a study of a scale rarely seen before.M. Austin Argentieri and her team analyzed data from 492,567 UK Biobank participants. They examined how strongly numerous 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 regular physical activity and 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 with classical heritability estimates.
Then, barely a year later, Ben Shenhar and a team led by Prof. Uri Alon at the Weizmann Institute in Israel revisited three large Scandinavian twin cohorts — including, for the first time, twins raised apart — and systematically removed all deaths unrelated to aging itself: accidents, infections, violence.
Their argument: this confounding factor had systematically led earlier studies to underestimate the genetic contribution. Once it is removed, the heritability of "intrinsic" lifespan rises to 50 to 55 percent — more than double the old rule of thumb. For specific diseases such as dementia, the team calculates a heritability of around 70 percent up to the age of 80.
This did not go unchallenged. In a Perspective article in the same issue of Science, Daniela Bakula and Morten Scheibye-Knudsen raise several methodological concerns about the model, including the argument that the direction of the higher estimate is already built into the structure of the statistical approach.
Independent voices also urge caution against over-interpreting the figure: biologist Chiara Herzog from King's College London noted to the Science Media Centre that heritability estimates are statistical measures for whole populations, not predictions for individuals. And bioinformatician Steve Hoffmann from the Leibniz Institute on Aging in Jena put it 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 statistically be attributed to genetic differences. The percentage figures from each study therefore cannot be directly compared.
How much of lifespan ultimately comes down to genes is a question that will likely keep researchers busy for some time — perhaps also because science is reluctant to settle on a single number when three studies yield three different ones. For everyday life, however, these debates change surprisingly little about the practical takeaway.
Even the study attributing the greatest role to genetics does not dispute that modifiable factors matter: not smoking, physical activity, diet, sleep, stress management, and social connection. Genes apparently shape the framework within which aging unfolds — but they do not entirely determine the individual trajectory. It is precisely within that margin that healthy aging comes into play.
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