Here’s what you’ll learn when you read this story:

• Genetics may determine about half of human lifespan, double what scientists previously estimated, new research finds.
• Researchers used twin simulations and real-world data to isolate genetic influence from environmental causes of death.
• The findings could redirect aging research toward identifying the specific genetic variants that govern how long we live.

The internet is crawling with clickbait that flashes the newest superfood, supplement, or “weird old trick” (we’ve all seen that one before) to add years to your life. Scammers take advantage as scientists struggle to figure out what really lies at the core of longevity. It turns out that at least one thing guaranteed to make you live longer isn’t attached to an introductory offer of $19.99 per month and has no questionable fine print. You were already born with it.

Genetics were long considered a secondary factor in determining human lifespans. Scientists used to think that there wasn’t much of a link between molecular biology and birthday candles, with the randomness of environment and chance playing the main role in determining whether you would make it through another year. But recently, biologists Uri Alon and Ben Shenhar from the Weizmann Institute of Science in Rehovot, Israel, analyzed extensive data and used mathematical models to determine that genetic heritability could account for at least half of what influences human lifespan—about double what previous estimates suggested.

“Understanding the heritability of human lifespan is fundamental to aging research,” they said in a study recently published in Science. “However, quantifying the genetic contribution to human life span remains challenging. Although specific lifespan–related alleles have been identified, environmental factors appear to exert a strong effect on lifespan. Clarifying the heritability of lifespan could direct research efforts on the genetic determinants of life span and their mechanisms of action.”

Human lifespan depends on both intrinsic and extrinsic mortality. While extrinsic mortality includes deaths caused by everything outside the body—accidents, infections, homicides, environmental hazards, and so on—intrinsic mortality is associated with processes inside the body such as genetic mutations, along with diseases or decline related to age. In their analysis, Alon, Shenhar, and their research team wanted to see how heavily these intrinsic factors influence lifespan once extrinsic factors are eliminated. But they also needed to account for another variable that differs across studies: the cutoff age, or the minimum age at which individuals must be alive to be included. To their knowledge, neither extrinsic mortality nor cutoff age had been systematically investigated for their effect on lifespan heritability estimates.

The researchers looked into three separate twin studies, which followed twins raised both together and apart, to see how heritability estimates were affected by cutoff age and extrinsic mortality. The data they examined was influenced by a number of historical factors. As medical knowledge improved and technology advanced during the 19th and 20th centuries, extrinsic mortality experienced a significant decline. Unfortunately, older datasets were often biased toward extrinsic factors and tended to leave out details about an individual’s cause of death, making it more difficult to separate intrinsic from extrinsic causes. The researchers created mathematical models based on the twin studies, along with virtual simulations, to account for these factors.

To isolate the genetic contribution to lifespan, Shenhar and Alon used computer simulations of both identical and fraternal twins, incorporating genetically distinct groups and systematically removing extrinsic mortality. As extrinsic mortality decreased in the simulations, lifespan correlations between twins increased until heritability plateaued at about 50%, roughly double previous estimates. Data from a Scandinavian twin study validated these results. When the researchers compared birth cohorts with progressively lower extrinsic mortality, measured heritability rose accordingly. Raising the cutoff age also increased heritability in historical cohorts by excluding early deaths that were predominantly extrinsic. Finally, to confirm the findings extended beyond Scandinavian twins, the team analyzed siblings of U.S. centenarians and found they had dramatically higher odds of reaching 100 themselves, consistent with the same 50% heritability estimate.

The researchers think that extrinsic mortality keeps getting associated with age because of frailty, which causes injuries or infections that often end up being fatal to the elderly. But there are still some aspects of mortality that elude them. These are mostly related to lifestyle, healthcare, socioeconomic factors, and random biological phenomena.

“Correcting for extrinsic mortality raises the estimate for the heritability of human lifespan in twin and sibling studies to [about] 55%, more than twice previous estimates and in line with heritability of most human traits,” Alon and Shenhar concluded. “Identifying the genetic variants underlying this heritability would help us to understand the fundamental mechanisms of human aging.”