Somewhere between the ancestral DNA test and the biological age clock, a familiar question takes hold: if your genes determine lifespan, what exactly are you optimizing for?
Jordan Weiss has spent his career trying to answer it. An assistant professor at the NYU Grossman School of Medicine, his research focuses on what separates people who thrive in old age from those who decline.
When a landmark study published in Science this January put a number on how much lifespan variation comes down to genetics—roughly 50 percent—it was one of the most significant updates to longevity science in years. We asked Weiss to break down what it means.
The 50 percent figure is easy to misread. “When scientists say lifespan is 50 percent heritable, they aren’t saying your DNA determines half of how long you will personally live,” Weiss says. “Heritability is a population statistic. It describes how much of the variation between individuals in a group can be traced to genetic differences, within a specific environment and at a specific time.”
What makes this particular study notable is what the researchers—a team from the Weizmann Institute of Science and collaborators across Sweden, China, and the Netherlands—stripped out. Previous heritability estimates were pulled down by extrinsic mortality: deaths from accidents, infections, and environmental hazards that reflect bad luck rather than biology.
“When you strip away the randomness of a 19th-century typhoid death or a workplace accident,” Weiss says, “the underlying biological pace of aging becomes much clearer. This reconciles a long-standing puzzle: why human lifespan seemed far less heritable than what we observed in animal models or in virtually any other human trait.”
It’s also worth knowing that the science here is still active. A 2018 study put heritability as low as 7 percent, arguing that earlier estimates were inflated by assortative mating, or the tendency for people to choose partners with similar lifestyles, which can mimic genetic inheritance. Weiss doesn’t dismiss that work. “The honest answer,” he says, “is that this science is still being worked out.”
The same study that attributes roughly half of lifespan variation to genetics leaves the other half unaccounted for by DNA. “The same study that says genetics explains about half the variation also says the other half is not genetic,” Weiss says. “That is an enormous space in which what researchers now call the exposome—the totality of environmental exposures across a lifetime—shapes health outcomes. This includes everything from the food you eat and the air you breathe to the stress you carry and the relationships you maintain.”
The near-doubling of human life expectancy over the past century makes the point clearly. “That also came from factors like sanitation, vaccination, antibiotics, and improved living conditions, not from changes in our genome,” Weiss says. “So this paper should not be read as a permission slip to skip the walk.”
So, what about the half that is modifiable? Weiss is direct. “Regular cardiovascular exercise is arguably the single most powerful intervention we have for living healthy longer,” he says. From there, the list is short and familiar: adequate sleep with preserved deep and REM phases, strength training, sensible nutrition rather than any single named diet, and social connection. “These behaviors likely account for far more healthspan variance than any supplement, peptide, or biohack on the market.”
That’s also where Weiss pushes back on a particular strain of wellness messaging. Some people carry variants that meaningfully raise their risk for heart disease or certain cancers. Others ignore every guideline and make it to 105. Genetics helps explain that variance.
“There should be caution against the implication that if you do everything ‘right’ and still get sick, you somehow failed,” he says.
His own approach, he says, amounts to something between a Golden Retriever and a Mediterranean grandmother. “Move around a lot, eat real food, rest, and be happy to see people.”