By Dr. Asnat Raziel, bariatric surgeon specializing in obesity treatment, metabolic health and healthy longevity; Director of the Multidisciplinary Center for Obesity Treatment, Assia Medical, Assuta Ramat HaChayal, Tel Aviv
Genetics and longevity: how much is still in our hands?
The link between genetics and longevity is stronger than many earlier studies suggested. For years, we repeated the same line: genes account for only about a quarter of lifespan, and the rest is up to us. However, a new study from the Weizmann Institute of Science challenges that assumption.
According to the researchers, genetics explains about 55% of the differences in lifespan between people once you filter out the effects of accidents, infections and environmental hazards. The finding advances the science of aging. Even so, genes alone do not decide how long we will live, because lifestyle matters too.
The secret of centenarians: genes or habits?
When we meet someone who is 100 years old, we want to know their secret. What do they eat? How much do they move? How do they sleep? Who do they spend time with? Maria Branyas, who lived to more than 117, became a symbol of these questions. But behind them lies another question: how much of a centenarian’s advantage simply comes from the genes they inherited from their parents?
Earlier estimates of genetics and longevity
Until now, the accepted answer was modest. A large Danish twin study from 1996 examined 2,872 twin pairs born between 1870 and 1900. It estimated the heritability of lifespan at 26% in men and 23% in women.
A study published in 2018 in the journal Genetics went further. The researchers found similarities in lifespan even between in-laws, who share no blood relationship. Their conclusion: partners tend to choose each other based on similar traits, and this inflates the genetic estimate. By their account, true heritability is below 10%.
The accidents that hide the genes
The Weizmann study points to a bias in the opposite direction. In earlier generations, many people died of causes unrelated to aging: accidents, infectious diseases and environmental hazards. The researchers call these deaths “extrinsic mortality.” Such deaths add noise to the data and blur the effect of genes.
Imagine two identical twins with almost identical genes. One dies in an accident at a young age, and the other lives into old age. Someone looking only at age at death might conclude that genes had almost no influence. Yet the gap between them did not come from a different pace of aging. Instead, it came from external circumstances. Once you filter out cases like these, the genetic picture becomes much sharper.
Twins raised apart: a natural experiment in genetics and longevity
Ben Shenhar of Prof. Uri Alon’s group at the Weizmann Institute led the study, which appeared in the journal Science on January 29, 2026. The team combined mathematical models with data from three twin registries in Sweden and Denmark.
One of them, the Swedish SATSA registry, includes twins separated in childhood and raised in different homes. Twins like these are a kind of natural experiment: they share their genes, but the environment they grew up in is different. According to the institute’s announcement, this is the first time researchers have analyzed such a registry in the context of lifespan heritability.
The researchers used two mathematical models of mortality. With them, they calculated what heritability would be with no extrinsic mortality at all, starting from age 15. It’s important to understand that this is a theoretical calculation of “intrinsic lifespan.” In other words, it reflects lifespan determined mainly by the body’s own aging processes. In reality, no population lives free of external risks.
Genetics and longevity: the numbers behind the headline
55% – the combined estimate of the heritability of intrinsic lifespan, across all registries and models together.
33% – the estimate in the SATSA registry before correcting for extrinsic mortality. The gap between the two numbers shows how much noise extrinsic mortality adds.
13,794 twin pairs – the total across the three registries. The Danish registry contributed 2,872 pairs (the same twins as in the 1996 study). The historical Swedish registry added 9,880 pairs, and SATSA 1,042. In addition, the researchers validated the results in data on siblings of centenarians in the United States.
By type of disease – the researchers looked at people who survived to age 61. Among them, they estimated the heritability of the tendency to die of dementia by age 80 at about 70%. For cancer it was about 30%. For cardiovascular disease, it was about 50% at the earliest ages examined, declining at later ages.
Note: these are not odds of getting sick. For example, a heritability of 70% for dementia does not mean anyone has a 70% chance of developing dementia.
55% genetics. So does lifestyle no longer matter?
Heritability is a statistical concept. It describes what share of the differences between people in a particular population relates to genetic differences, under the environmental conditions at the time of measurement. However, it does not divide one person’s life into “genetic years” and “lifestyle years.”
So you cannot say that someone who lived to 100 got 55 years from their genes and 45 from their lifestyle. Nor can you conclude that healthy habits only affect “the part that’s left.”
Height is a familiar example. It is a highly heritable trait, yet average height has risen over recent generations thanks to better nutrition and living conditions. Similarly, when living conditions across a population become more alike, genes explain a larger share of the remaining differences. And still, improving the environment has lengthened many people’s lives. In short, a high genetic contribution and a major role for the environment can exist side by side.
What genes don’t tell us: the power of habits
Other studies remind us how large the impact of what we do can be. A study from the University of Oxford, published in 2025 in Nature Medicine, examined almost half a million participants in the UK Biobank database. Environmental and lifestyle factors explained 17% of the differences in risk of death. By contrast, genetic predisposition explained less than 2%.
Smoking, socioeconomic status, physical activity and living conditions topped the list. Interestingly, for dementia and breast cancer the genetic risk was more dominant, similar to the Weizmann finding on dementia.
Is this a contradiction? Not necessarily. The British study measured polygenic risk scores based on known variants, not the full hereditary effect. In other words, the two studies answer different questions.
A Harvard study followed 123,219 participants and looked at five habits. These were not smoking, 30 minutes a day of moderate-to-vigorous physical activity, a healthy weight, a high-quality diet and moderate alcohol intake. The researchers estimated the effect from age 50. Women who adopted all five habits would live an average of 14 years longer, and men 12.2 years longer, than those who adopted none of them.
Genetics and longevity: the debate isn’t over
In February 2026, researchers posted a critical preprint on medRxiv, a repository of scientific papers that have not yet undergone peer review. According to the preprint, susceptibility to severe infections is also largely heritable. Therefore, classifying death from infection as “extrinsic” may skew the estimate. The preprint also raises questions about survivor selection and about the interplay between genes and environment.
The critique does not refute the study published in Science. Still, it is a reminder that this is an estimate resting on the assumptions of a mathematical model, not final proof. The accurate wording is “the researchers estimate,” not “science has proven that half of our life is predetermined.”
The hunt for longevity genes
According to the Weizmann Institute, the finding strengthens the search for genetic variants linked to longevity. Such variants could reveal mechanisms of aging and open new avenues for treatment. There are already several candidates.
For example, a study of Japanese-American men in Hawaii linked the FOXO3 gene to reaching extreme old age. Follow-up studies in other populations have partly supported this. In addition, a study from Leiden identified a rare variant in the CGAS gene in families that age more slowly. This gene plays a role in regulating inflammation.
The Max Planck Institute for Biology of Ageing notes that in worms and fruit flies, switching off certain genes can even double lifespan. But the fact that such mutations have not spread in nature suggests they also carry a biological cost. After all, what works in a worm is not yet a treatment for humans. I discuss other mechanisms of aging in my article on zombie cells and autophagy.
What about NAD+, peptides and genetic tests?
The study did not examine NAD+ infusions, peptides, supplements or commercial tests that promise to predict how long you will live. It neither supports them nor disproves them. Recommending a specific treatment requires research that tests it directly. I have written at length about the gap between promise and evidence in the world of biohacking, NAD+ and peptides.
Genetics and longevity in practice: what can you do?
So what does the research on genetics and longevity mean for you? First, family history is an important tool. It’s worth knowing at what ages illnesses appeared in your family and what the causes of death were. It also helps to know whether relatives lived long lives in good health. Share this information with your doctor. However, the 55% figure on its own does not call for any particular test, drug or treatment plan.
Not just how many years, but how many good years
There is a big difference between lifespan and healthspan, the number of years we live in good health and good function. A person can reach a very old age and still live many years with disability. Moreover, the Weizmann study looked at lifespan only and says nothing directly about years of independence and function.
This is where intrinsic capacity comes in. The measure is gaining ground, and it looks at what we are still able to do, not just how old we are. Research on genetics and longevity may open new directions in the medicine of aging. I describe how this field is reaching the clinic in my article on geroscience and longevity medicine. I also discuss GLP-1 drugs and anti-aging in a separate article.
The bottom line on genetics and longevity
The Weizmann study suggests a new direction: understanding which biological differences contribute to longevity once the researchers filter out the effect of external risks. If further studies confirm the finding, researchers will be able to pinpoint protective mechanisms more precisely. They will also be able to develop ways to help all of us live more years in good health. Overall, genes matter more than we thought, but they alone do not decide how long we will live.
Frequently asked questions
My parents lived long lives. Will I live a long time too?
A family history of longevity is a good sign, but not a promise. Heritability describes a population; it does not set the age at which a particular person will die.
My genes are “not good.” Is there any point in a healthy lifestyle?
Absolutely. Large studies link habits such as not smoking, physical activity, a high-quality diet and a healthy weight to many extra years of life. At the same time, the new study neither tested nor ruled out that effect.
Should I get a genetic test to find out how long I’ll live?
The study did not examine such tests and offers no basis for recommending them. Instead, it’s better to talk with your doctor about your family history.
Sources
Rethinking longevity: genes matter more than we thought (Weizmann Institute, in Hebrew)
Heritability of intrinsic human life span is about 50% when confounding factors are addressed
Integrating the environmental and genetic architectures of aging and mortality
Impact of Healthy Lifestyle Factors on Life Expectancies in the US Population
Misclassification of heritable mortality undermines estimates of intrinsic life span heritability
