Efforts to extend life may be succeeding, but not equally.
Extending life is only part of the goal in aging research. Scientists also want more people to reach old age in good health, with fewer differences in when individuals die. This ideal outcome is often described as “squaring the survival curve,” where most deaths are pushed into a narrow window late in life rather than spread out across many years.
To test how close current science comes to that goal, University of Sydney researchers revisited a large meta-analysis of studies in vertebrates. They focused on three widely studied interventions: dietary restriction, rapamycin, and metformin. While all are linked to longevity, they work in different ways.
Dietary restriction involves reducing calorie intake without causing malnutrition. It has been known for more than a century to extend lifespan in animals and is thought to act in part by dialing down a key cellular growth pathway called mTORC1, which helps regulate metabolism and aging. Because strict diets are difficult to maintain, scientists have searched for drugs that mimic these effects. Rapamycin directly blocks mTORC1 activity, while metformin, a common diabetes medication, influences the same pathway indirectly by altering how cells sense energy levels.
Overlooked Tradeoff
Although dietary restriction and rapamycin tended to increase average lifespan, all three interventions also increased the spread in ages at death. In practical terms, some individuals benefited far more than others. The overall variation rose by roughly 17 percent, even as average lifespan increased.
The relative level of variation compared to the average lifespan did not shrink. This means the interventions did not make outcomes more uniform. Instead, longer life came with greater unpredictability. Rather than compressing deaths into a tighter age range, the treatments effectively stretched the distribution.
This pattern may reflect how these interventions influence the biology of aging. Evidence suggests they lower both baseline mortality risk and the rate at which risk increases with age, a combination that raises both the average lifespan and its variability at the same time.
Why Outcomes Differ
Differences in genetics, dosage, and treatment conditions likely add another layer of complexity, helping explain why individuals respond so differently.
Dr. Tahlia Fulton explained the implications: “These approaches can make animals live longer, but the benefits aren’t shared equally. Without more information, the outcome looks like a biological lottery. We’re working to understand why, so future longevity science helps everyone.”
Reference: “No evidence for squaring the survival curve: lifespan-extending treatments increase variation in age- at-death” by Tahlia L. Fulton, Erin L. Macartney and Alistair M. Senior, 1 February 2026, Biology Letters.
DOI: 10.1098/rsbl.2025.0651
Funding: Australian Research Council
Never miss a breakthrough: Join the SciTechDaily newsletter.
Follow us on Google and Google News.