Scientifically Speaking: Genes matter more for longevity than previously thought

Research suggested that only 10 to 25% of how long we live is determined by our genes and the rest to lifestyle, environment, and the choices we make

For decades, the scientific consensus has been remarkably comforting for those of us who want to hack our way to a long life. Research suggested that only 10 to 25% of how long we live is determined by our genes. The rest, three-quarters or more, could be attributed to lifestyle, environment, and the choices we make every day.

About two million lives a year are lost to air pollution-related diseases in India. (HT PHOTO)

And why wouldn’t this idea appeal to our sensibilities? It is comforting to believe that we mostly control our own destinies. This belief has fuelled a multibillion-dollar wellness industry, promising that the right diet, exercise regimen, supplement stack, or biohacking protocol can substantially extend lives.

A study published this month in the peer-reviewed academic journal Science suggests this notion may need some revision. Researchers led by Uri Alon at the Weizmann Institute of Science in Israel report that the heritability of human lifespan is actually around half, far higher than previous estimates. This does not mean that healthy practices suddenly stop mattering, but it does force us to confront the extent to which genes may have the upper hand.

So why were we seemingly wrong for so long? The researchers offer a simple explanation. Earlier studies of longevity failed to distinguish between two different ways of dying: intrinsic mortality, which arises from biological aging processes within the body, and extrinsic mortality, which results from external hazards such as accidents, infections, and environmental catastrophes. When someone’s great-grandmother died of typhoid at thirty-two, her death told us nothing about her genetic potential for a long life. Yet earlier studies counted such deaths in much the same way.

This makes intuitive sense. Inherited genes can help shape the trajectory of a person’s life. But they cannot dodge trucks on a busy national highway.

Teasing apart these two components of longevity has not been a trivial matter. In this study, the researchers analysed twin cohorts from Denmark and Sweden. When they mathematically removed extrinsic deaths, the correlation in lifespan between identical twins roughly doubled.

Many earlier longevity studies relied on historical cohorts born at a time when death from external causes was far more common. The world was a much more dangerous place for most people. A young man might have carried genes that could have supported heart health and cognitive resilience into old age, but if cholera or a factory accident killed him at twenty-five, those genetic advantages never had a chance to matter.

The researchers found that as the risk of dying declined across successive birth groups, thanks to sanitation, antibiotics, workplace safety, and modern medicine, the genetic component of lifespan increased.

The study also finds intriguing differences between diseases. Heart disease and dementia showed higher heritability than cancer, at least at earlier old ages. This makes biological sense. Cancer often begins with rare chance events that randomly transform a cell toward malignancy. Heart disease and dementia, by contrast, unfold more predictably from the cumulative wear of genetically influenced biology.

What should we make of this for our daily decisions about diet, exercise, and the latest longevity intervention? The finding does not mean lifestyle is irrelevant. Environment, behaviour, socioeconomic circumstances, health care access, and sheer biological randomness all still matter enormously. So no, this is not an excuse to give up.

But it may be wise to temper expectations about achieving longevity through intervention. If you carry genes that predispose you to robust heart function and efficient cellular repair, healthy living will help you express that potential. If you do not, the same behaviours may shift your trajectory somewhat. But at the end of the day, the uncomfortable truth is that some people who smoke and eat fried food three times a day will outlive others who do everything right. The fault, dear Brutus, lies in our genes, at least in part.

In India, a large population is undergoing a transition from infectious to chronic disease. Much of India’s rise in life expectancy over recent decades reflects fewer deaths from infectious illnesses. But the country now faces a different set of external pressures: air pollution that damages lungs and hearts, diets high in refined carbohydrates and ultra-processed foods, road injuries, and heat stress.

Take pollution as one example. About two million lives a year are lost to air pollution-related diseases in India, according to the State of Global Air report, an increase of more than 40% since 2000. Long-term exposure to fine particulate matter reduces life expectancy by about five years on average across India, according to the Air Quality Life Index, and by as much as 10 years in Delhi.

So, what’s the message? Should we swap palm-reading and horoscopes that claim to tell us how long we will live in favour of genetic determinism? The answer is no. Despite shifting numbers in population studies, we are neither prisoners of our genes nor masters of our destiny. The hand we are dealt matters, but how we play it shapes the outcome. Neither fatalism nor hubris, but a middle path, seems like the best way to live.

Anirban Mahapatra is a scientist and author. His most recent book is When the Drugs Don’t Work. The views expressed are personal