How Much Do Your Genes Determine How Long You’ll Live?

The Big Question

Even though an overwhelming body of evidence supports the concept that a healthier lifestyle, in particular healthy dietary patterns plays a crucial role in healthy longevity, there are numerous examples of people living into their 90s and even hundreds, who have not followed current dietary recommendations, have consumed alcoholic beverages or have practiced regular physical exercise. Similarly, octogenarians seem to cluster in some families, but not in others.

Scientists have long suspected that genetics play a role in how long you live. But for decades, research suggested that genes mattered surprisingly little. Twin studies from the 1990s and 2000s estimated that only about 20–25% of variation in human lifespan could be traced back to genes. Even more recently, large studies of family trees suggested the figure might be as low as 6%. If those numbers are right, there isn’t much point hunting for “longevity genes” – lifestyle and environment are doing almost all the work.

But a new study published in Science in January 2026 argues that those estimates have been wrong all along – not because the science was bad, but because of a subtle and important flaw in the data.

Dying From the Wrong Causes

The researchers, led by Ben Shenhar and Uri Alon of the Weizmann Institute of Science in Israel, identified a critical confounding factor: extrinsic mortality. This is a fancy term for deaths caused by things outside your body – accidents, infections, homicides, and environmental hazards. These causes of death have little or nothing to do with your genes. Whether you get hit by a carriage in 1890 or die of typhoid fever in 1910 is largely a matter of bad luck, not biology.

The problem is that most of the twin studies used to estimate life span heritability relied on people born in the 1800s and early 1900s – a time when extrinsic mortality was extremely high. Back then, a large fraction of deaths happened for reasons completely unrelated to aging or genetics. When you include all those random, non-genetic deaths in your analysis, it naturally makes twins look less similar to each other in lifespan – even identical twins with the exact same DNA. This artificially deflates the apparent role of genetics.

Think of it this way…if you’re trying to measure whether two identical twins have the same “natural” lifespan, but one of them gets killed in a war at age 25, that data point makes twins look genetically different when they’re actually not. Multiply that across thousands of twins born in an era of high infectious disease and frequent accidents, and you’ve systematically hidden the genetic signal.

How the Researchers Fixed It

Shenhar and colleagues developed a mathematical method to correct for this problem. They built computer models of human mortality that separate intrinsic mortality – biological aging from within the body – from extrinsic mortality. They then used data from three different Scandinavian twin studies: Danish twins born between 1870 and 1900, Swedish twins born between 1886 and 1925, and the SATSA cohort (Swedish Adoption/Twin Study of Aging) of twins born between 1900 and 1935. They also analyzed data from siblings of American centenarians – people who lived to 100 – born between 1873 and 1910.

By mathematically removing the influence of extrinsic deaths from the analysis, the researchers asked, if we could strip away all the accidental and infectious-disease deaths, how similar would twins be in their natural lifespans? The answer was striking. Once extrinsic mortality was accounted for, the estimated heritability of lifespan rose to around 55% – more than double the traditional estimates. The same pattern showed up consistently across all the datasets and both mathematical models they tested, lending strong confidence to the result.

Earlier vs. Later Birth Years

The team also found a compelling real-world check on their theory. Over the course of the 20th century, extrinsic mortality dropped dramatically as sanitation, vaccines, and medical care improved. If the theory is correct, heritability estimates should rise for cohorts born in later, safer years – and that’s exactly what they found. When the SATSA twins were split into three groups by birth decade (1900–1910, 1910–1920, and 1920–1935), extrinsic mortality fell by a factor of three across that span – and uncorrected heritability estimates nearly doubled. This real-world trend matched the mathematical predictions, providing strong support for the researchers’ argument.

What 55% Heritability Actually Means

It’s important to understand what “heritability of 55%” does and doesn’t mean. It does not mean that 55% of your lifespan is predetermined by your DNA. Heritability is a population-level statistic – it describes how much of the variation in lifespan between different people in a given environment can be attributed to genetic differences. A heritability of 55% means that, in a population with typical modern living conditions, slightly more than half the variation in how long people live comes from genetic differences, while the rest comes from environment, lifestyle, luck, and other factors.

Importantly, 55% puts human lifespan heritability squarely in line with most other complex human traits like height, intelligence, and blood pressure, which average around 49% heritability. It also matches what scientists have found for lifespan heritability in laboratory mice (38–55%). The old estimates of 6–25% were the true outliers – and now we know why.

Does This Mean Lifestyle Doesn’t Matter?

Absolutely no – and the authors are careful to say so. Even with heritability at 55%, roughly half of lifespan variation is still explained by non-genetic factors: lifestyle choices like diet, exercise, and smoking; socioeconomic circumstances, social interactions and access to health care; random biological variation; and epigenetic effects (changes in how genes are expressed, influenced by environment).

Why It Matters

The implications of this study reach well beyond academic debate. If lifespan heritability is truly around 55%, it means there are meaningful genetic variants out there that influence how long people live – and it’s worth the effort to find them. Such discoveries could point scientists toward the biological mechanisms that drive aging itself, potentially opening doors to drugs, therapies, or interventions that slow the process.

The study also found interesting variation by cause of death: genetic factors appear most powerful for dementia-related deaths (about 70% heritability by age 80), moderately powerful for cardiovascular disease, and consistently moderate for cancer. Understanding these differences could help personalize preventive medicine.

In short, this paper doesn’t say your fate is written in your genes – but it does say your genes matter more than we thought. By correcting a decades-old blind spot in the data, Shenhar and colleagues have put human longevity genetics back on solid scientific footing, and given researchers a clearer target to aim for as they work toward understanding – and perhaps slowing – the aging process.

For further information about this topic, see my podcast episode with longevity expert, Dr. Eric Verdin here.