The Old Assumption About Lifespan
For decades, scientists and the public have shared a reassuring belief: how long you live is largely up to you. Lifestyle choices — diet, exercise, sleep, stress management — were thought to carry most of the weight. Genetics, by contrast, contributed only a modest 20 to 25 percent to your lifespan. That number came from landmark studies of Scandinavian twins conducted in the late 19th century and became the dominant view in aging research.
Uri Alon, a physicist-turned-systems biologist at the Weizmann Institute of Science in Israel, was never quite satisfied with that figure. “That makes you think: what’s the rest of the 80 percent? Is it the lifestyle? Why should we study genes for lifespan if they’re not that important? It kind of bothered me,” he said.
His unease, it turns out, was scientifically justified.
What the New Study Found
A Landmark Revision in Aging Science
A major new study, published in the journal Science in January 2026, dramatically revises our understanding of longevity. Researchers at the Weizmann Institute, led by biophysicist Ben Shenhar and Uri Alon, used mathematical modelling to re-examine the role of genetics in determining human lifespan. Their conclusion is striking: once you remove deaths caused by external factors, genetics account for roughly 50 to 55 percent of the variation in how long people live.
That figure more than doubles the previously accepted estimate. Furthermore, it puts lifespan heritability in line with other complex biological traits — such as height, body fat distribution, and muscle composition — which are all considered at least 50 percent heritable. In other words, longevity was always an outlier in the data. Now, the new study suggests it no longer needs to be.
Why Earlier Estimates Were Off
The Problem With Historical Twin Data
The original heritability estimates came from studies of twins born between 1870 and 1900. That era was defined by high rates of “extrinsic mortality” — deaths caused not by biological aging, but by external forces: infectious diseases like tuberculosis and pneumonia, accidents, violence, and poor sanitation. These factors killed indiscriminately, regardless of a person’s genetic makeup.
“At that time, people died of pneumonia and tuberculosis and not a lot of people made it to their 40s,” Alon explained. “In that situation, who cares how long your parents lived? Genes don’t have a chance.”
How the Research Team Fixed the Flaw
Shenhar and his team drew a clear distinction between two types of death: intrinsic mortality, driven by internal biological decline and genetic factors, and extrinsic mortality, driven by environmental hazards, infections, and accidents. By building a model that stripped out extrinsic deaths, they were able to see how much of the remaining variation in lifespan came from genes alone.
The results were consistent across multiple datasets. When the team applied their model to databases of Swedish and Danish twins — born between 1900 and 1935, a period of steadily improving medicine — they found that heritability rose from one generation to the next as extrinsic deaths fell. They also applied the model to data on siblings of centenarians who lived to at least 100. In both cases, heritability climbed to around 50 percent.
“They have lower and lower extrinsic mortality, and we see that their heritability goes up and up,” Alon said.
The Genetic Set Point Explained
How Your Family History Shapes Your Future
Alon describes genetics as a “genetic set point” — a kind of built-in biological ceiling that influences, but does not entirely determine, lifespan. How old your parents and grandparents were when they died carries some predictive weight. Families with exceptional longevity — including centenarians and those who live beyond 105 — tend to share protective genetic variants that shield them from age-related diseases.
Thomas Perls, a longevity researcher at Boston University and founder of the New England Centenarian Study, agrees that genetics play a significant role, particularly at the extreme ends of old age. At the very oldest ages — 105, 110, and beyond — genes are a decisive factor. However, Perls also points to research suggesting that even without a favourable genetic hand, the average person can likely reach 88 years (for men) and 93 years (for women) through healthy living.
Key Genes Linked to Longevity
So far, only a handful of genetic variants have been clearly linked to long life. The most notable include:
- FOXO3 — associated with resistance to age-related disease
- APOE2 — protective against Alzheimer’s and cardiovascular disease
- SIRT6 — involved in DNA repair and cellular aging
However, as Eric Verdin of the Buck Institute for Research on Aging notes, these genes are not found in all centenarians. Longevity is almost certainly polygenic — shaped by hundreds of interacting variants, not a single lucky gene.
Does Healthy Living Still Matter?
The Upside Is Real, But Has a Ceiling
The new findings do not mean healthy habits are pointless. They do, however, reframe the picture. Alon thinks of lifestyle as capable of adding years — but with an asymmetry that matters: bad habits can shave decades off a lifespan, while good habits add a more limited number of years.
Longevity scientists differ slightly on the exact figure, but most agree that a healthy lifestyle can add 5 to 20 years to a person’s life. Importantly, there is real “play in the system.” Alon himself continues to eat well and swim regularly. A 2018 study in the journal Circulation estimated that even average people, without exceptional genes, can reach their late 80s to early 90s through consistent healthy behaviours.
Additionally, researchers at Tufts University note that the new framework — removing extrinsic deaths from analysis — could improve future genetic studies. By focusing on intrinsic lifespan, scientists may more easily identify the specific gene variants that influence how long people live from within.
What This Means for Future Medicine
New Urgency for Longevity Drug Research
The most immediate consequence of this research is scientific. If genetics play a larger role than previously believed, then studying longevity genes becomes far more worthwhile. Sofiya Milman of Albert Einstein College of Medicine — who studies centenarian biology — captures the ambition well: the goal is to understand how some people’s unique biology protects them from age-related disease, then translate that into therapies. “We’re hoping to create therapies that will mimic those intrinsic factors, and make them accessible to people who didn’t win the genetic lottery,” she said.
Daniela Bakula and Morten Scheibye-Knudsen of the University of Copenhagen, writing in a commentary in Science, called the new findings consequential for the field. A substantial genetic contribution, they argued, strengthens the case for large-scale efforts to identify longevity-associated variants, refine polygenic risk scores, and link genetic differences to specific biological pathways that regulate aging.
Meanwhile, Shenhar’s next focus is the environmental side of the equation — trying to understand how much of lifespan variation comes from inherent randomness versus deliberate lifestyle choices.
Key Takeaways
- Genetics account for roughly 50–55% of lifespan variation, not the 20–25% previously believed.
- Earlier studies were skewed by high rates of extrinsic death in historical populations.
- Healthy living still matters and can add years to your life — but the ceiling is lower than once assumed.
- Longevity-related genes like FOXO3, APOE, and SIRT6 offer promising targets for future therapies.
- The new study resets the debate, giving scientists stronger reason to pursue genetic research into aging.
