Novo Nordisk and Lilly Report GLP-1 Drugs Slowed Aging Clocks, but Data Are Unreviewed

Novo Nordisk and Eli Lilly told the Aging Research & Drug Discovery conference in Boston in early October 2026 that their GLP-1 drugs slowed molecular measures of biological aging, with Novo reporting a 2-to-4-year effect on heart "age" across 10,052 trial participants. None of the human results has been peer reviewed: Novo's analysis is a preprint, and Lilly's was presented by a company executive at the meeting.

What did the companies report?

According to MIT Technology Review, Novo analysed blood samples from 10,052 people, half of them on semaglutide (sold as Ozempic and Wegovy) and half on placebo, using "proteomic clocks" that estimate age and mortality risk from protein levels. Nikolaj Roed, a Novo project leader, put the overall difference at "two to three years", and Novo's Alejandro Aguayo-Orozco said the effect reached as much as four years on a clock built from heart proteins. Harvard biologist Vadim Gladyshev assisted with the molecular measurements.

CNN's report, carried by CP24 on 14 October, adds that the semaglutide work is posted as a preprint, meaning it has not been through peer review. The preprint, titled "Semaglutide reduces proteomic organ-specific biological age across randomized clinical trials", is hosted on Research Square. CNN said heart biological age fell by two to four years against placebo, while lung, kidney, brain and pancreas clocks fell by one to four years. The researchers said weight loss, blood sugar control and inflammation did not fully account for the shift.

Lilly's data are smaller. CNN reported that the analysis covered 71 tirzepatide users over age 50 in a substudy of the Surmount V trial, which randomised more than 700 adults with overweight and without diabetes to tirzepatide or semaglutide for 72 weeks. Epigenetic clocks, which count accumulated chemical changes to DNA, advanced between 0.7 and 1.1 years over the study period, against an expected 1.38 years, and some clocks ran backward. There was no placebo group and follow-up was short. Kevin Duffin, Lilly's vice president of aging research, told MIT Technology Review the effect is "significant" but that nobody should expect a 30-year reduction.

How strong is the evidence?

Three tiers of evidence are in play, and they should not be blended.

The first is peer reviewed, but it is in mice. A paper in Nature, led by Danica Chen of UC Berkeley, found that semaglutide given to 20-month-old female mice slowed aging and extended lifespan. According to News-Medical's reprint of the NIH release, treated mice had a median lifespan nearly 100 days longer than untreated ones, and the benefits went beyond what a 24% calorie-restricted diet produced. The same release stresses that the work does not imply the same result in humans.

The second tier is the Novo preprint. It draws on five placebo-controlled trials and so has the strongest design of the human data, since a placebo arm separates the drug from the passage of time. But a preprint can change substantially, or fail, in review.

The third tier is the Lilly substudy: a conference presentation of a company analysis with no placebo group and 71 people. Duffin attributed the effects mostly to blood sugar reduction and weight loss, according to CNN. The MIT report did not give a sample size for Lilly's study, and CNN's account of Duffin's estimate (a reduction of about three to six years in biological age) sits uneasily with the 0.7-to-1.1-year averages it also reports, so the exact claim should be checked against the presentation when it is published.

Why do the caveats matter?

Aging clocks are measurements of biomarkers, not of how long anyone lives. Steve Horvath, the UCLA researcher who developed the first epigenetic clocks, told MIT Technology Review that "two years is a pretty strong effect, in my book", and that the data could suggest the drugs are geroprotectors. He added that he had not yet seen sufficient evidence that the drugs would benefit thin people, and noted side effects such as muscle loss. Gladyshev said that in a healthy population "no one knows".

James Kirkland of Cedars-Sinai warned CNN against overinterpreting the findings, particularly for lean people without diabetes taking the drugs. He noted that the biomarker tests many companies sell to consumers are still in development and vary widely from day to day within the same person. Weight-loss surgery, CNN also noted, slows biological aging by these measures too, which fits the possibility that the clocks partly track weight loss and metabolic health rather than a distinct anti-aging mechanism.

Aguayo-Orozco, asked by MIT Technology Review whether a reasonable person should start semaglutide for this purpose, replied: "I am not a physician. I cannot answer that question."

What happens next?

The commercial stakes are large. MIT Technology Review reported that tirzepatide earned Lilly more than $36 billion last year, with semaglutide a close second, so a credible longevity indication would extend the market for drugs already prescribed to millions. The regulatory route for an anti-aging indication is still being worked out. In January, the US agency ARPA-H committed $38 million to a Texas study testing whether semaglutide slows aging in healthy people over 60, measuring cognition, mobility and sensory acuity, with the aim of helping define a regulatory path for anti-aging drugs, MIT Technology Review reported.

That trial, rather than clock readouts, is likely to carry the most weight. Clocks are a fast proxy that lets companies and academics screen interventions in months instead of decades. Whether a two-year difference on a proteomic clock translates into fewer strokes, fractures or dementia diagnoses in people who are not obese or diabetic is exactly the question the existing data cannot answer.

What we don't know yet

Several material points remain unconfirmed. Neither company has published the Lilly data in a journal. The Novo preprint has not been peer reviewed. It is unclear whether the apparent slowing reflects weight loss, glucose control or a drug effect on aging biology, and the sources disagree on how large Lilly's effect was. No study reviewed here followed participants long enough to show an effect on disease or death from aging. Until peer-reviewed human data and the ARPA-H-funded trial report, the headline figures are best read as hypothesis-generating signals from company-led work.