How much do your genes determine how long you’ll live? It’s a question that fascinates us, and one that’s been debated for decades. For years, the answer seemed settled – genes account for about 20–25% of the variation in human lifespan, with the rest down to lifestyle and environment.
But a new study published in Science has challenged this view, suggesting the genetic contribution might be considerably higher.
The reason, according to the researchers, is that previous estimates failed to account for how the causes of death have changed over time. A century ago, many people died from what scientists call extrinsic causes – accidents, infections and other external threats.
Today, in developed countries at least, most deaths result from intrinsic causes: the gradual wearing out of our bodies through ageing and age-related diseases like dementia and heart disease.
To get a clearer picture, the research team analysed large groups of Scandinavian twins, carefully excluding deaths from external causes. They also studied twins who were raised apart and siblings of centenarians in the US.
When they stripped away deaths from accidents and infections, the estimated genetic contribution jumped dramatically – from the familiar 20–25% to around 50–55%.
The pattern makes sense when you look at individual diseases. Genetics explain much of the variation in dementia risk, have an intermediate effect on heart disease, and play a relatively modest role in cancer. As environments become more favourable, populations age and diseases caused by the ageing process itself become more common, the genetic component naturally appears larger.
Our genes haven’t become more powerful
But here’s where interpretation becomes crucial. A higher estimate doesn’t mean genes have suddenly become more powerful, nor does it mean you can only influence half your chances of reaching old age. What’s changed is the environment, not our DNA.
Consider human height as an example. A hundred years ago, how tall you grew depended heavily on whether you had enough food and whether childhood illnesses stunted your growth.
Today, in wealthy nations, nearly everyone gets adequate nutrition. Because these environmental differences have narrowed, most of the remaining variation in height is now explained by genetic differences – not because nutrition has stopped mattering, but because most people now reach their genetic potential. However, a malnourished child will still fail to grow tall, regardless of their genes.
The same principle applies to lifespan. As we’ve improved vaccination, reduced pollution, enhanced diet and adopted healthier lifestyles, we’ve lessened the overall impact of environmental factors.
When environmental variation decreases, the proportion of remaining variation attributed to genetics – what scientists call “heritability” – increases by mathematical necessity. The earlier estimates weren’t wrong; they simply reflected different historical circumstances.
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This reveals something fundamental: heritability isn’t a fixed biological property but a measure that depends entirely on the population and circumstances you’re looking at. The traditional 20–25% figure described lifespan as it was actually experienced in historical populations, where external threats loomed large.
The new 50–55% estimate describes a different scenario where those threats have been largely removed – essentially describing a different trait.
The headline figure of lifespan being around “50% heritable” risks being misunderstood as meaning genes determine half of a person’s life chances. In reality, the genetic contribution for any given individual can range from very small to very large depending on their circumstances.
There are countless routes to a long life: some people have robust genetic profiles that protect them even in difficult conditions, while others compensate for less favourable genetics through excellent nutrition, exercise and healthcare. Each person represents a unique combination, and many different combinations can result in exceptional longevity.
Which combinations prove most common depends entirely on the population and the conditions in which people live and age. As external causes of death continue to decline in the real world – though they won’t disappear entirely – it will be fascinating to see how these patterns evolve.
The authors of this latest study admit that about half of lifespan variation still depends on environment, lifestyle, healthcare and random biological processes, such as cells dividing out of control in cancer. Their work, they argue, should renew efforts to identify the genetic mechanisms involved in ageing and longevity. Understanding how different genetic factors interact with different environments is probably the key to explaining why some people live much longer than others.
The study offers valuable insights into how different types of mortality have shaped our understanding of lifespan. But its results are best understood as showing how heritability changes across different contexts, rather than establishing a single, universal genetic contribution to how long we live.
In the end, both genes and environment matter. And, perhaps more importantly, they matter together. So whether that feels like good news or bad news, you will probably never get a simple answer to how much of your lifespan is determined by genes alone.
Karin Modig receives funding from Swedish Research Council for Health, Working Life and Welfare and from Karolinska Institutets research funds.
