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Novo Nordisk and Eli Lilly presented early findings at the Aging Research & Drug Discovery conference suggesting their GLP-1 medicines may affect molecular measures of biological aging. Novo reported signals in proteomic data from a large participant group; Lilly’s tirzepatide findings came from a small, uncontrolled sub-study. Neither presentation establishes that the drugs slow aging or extend life.
Novo Nordisk and Eli Lilly presented early findings at the Aging Research & Drug Discovery (ARDD) conference suggesting that their GLP-1 medicines may shift molecular measures associated with biological aging. The results, involving semaglutide and tirzepatide, are signals from different types of analyses—not proof that either drug slows aging, prevents age-related disease or extends life.
Novo’s presentation drew on blood samples from 10,052 participants, about half of whom received a GLP-1 drug and half a placebo, with samples collected at baseline and later follow-up. The company used proteomic clocks, which estimate age and mortality risk from protein levels. Novo reported lower biological-age estimates across cardiovascular outcome trials, with changes appearing within 13 to 20 weeks and either persisting or growing through 150 weeks. A heart-protein clock showed a shift of as much as four years, according to the presentation.
Novo research leaders described the findings as evidence that semaglutide may affect molecular aging measures. Global Project Leader for Research and Development Nikolaj Roed said the company had observed “improved biological age in our patients across trials and across different tissues,” describing an overall difference of around two to three years. Senior scientific director Alejandro Aguayo-Orozco said semaglutide “actually move[s] the clocks in any direction” and answered, “yes,” based on the company’s data. These are company interpretations of biomarker results, not established clinical measures of how many years a person will live.
Eli Lilly’s results came from an epigenetic sub-study within SURMOUNT-5, its head-to-head trial of tirzepatide and semaglutide. The analysis included 82 participants after quality checks, with paired baseline and week-72 samples for 71. All 15 age-unit clocks showed less aging than the 1.38 years of calendar time that had passed, but only two reached statistical significance. Lilly said median gains on those two clocks were 1.1 and 0.7 years. Its vice president for aging research, Kevin Duffin, characterized the work as a small pilot to test methods and consistency, rather than a definitive result.
Aging Clocks Are Not Lifespan Evidence
The presentations matter because they put biological-aging measures alongside the established clinical research on GLP-1 medicines, which are used for diabetes and weight management. If clock changes are reproducible and tied to meaningful health outcomes, they could help researchers investigate whether benefits extend beyond changes in weight or blood sugar. For now, the findings offer a research lead, not a basis for prescribing these medicines to people seeking to slow aging.
The distinction between a biomarker and a clinical outcome is central. Aging clocks estimate biological features from proteins or DNA methylation; they do not directly measure future lifespan or prove that a person will avoid disease. Novo also presented modeled estimates of 1.9 additional remaining life-years overall, based on SELECT trial effect estimates applied to a UK real-world semaglutide cohort of 19,117 people. That figure is a projection, not observed added survival in that cohort.
Lilly’s presentation included multiple clock and protein signals, but its own caveats limit what can be concluded. The study was small and lacked a placebo group, while some measures were discordant and certain predicted protein changes did not match direct measurements. The results need replication before they can support claims about a general anti-aging effect.
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Two Drugs, Different Aging Measures
The two companies reported different kinds of evidence. Novo’s analysis used proteomic clocks across cardiovascular outcome trials and included a placebo comparison in the reported sample. Its researchers said the clock changes appeared quickly and continued over longer follow-up. The presentation also described proteomic signatures related to vitality and locomotion. The source material does not establish that these clock shifts themselves caused improvements in those functions.
Lilly’s analysis examined DNA methylation in blood from tirzepatide-treated SURMOUNT-5 participants. Zymo Research and TruDiagnostic generated separate methylation datasets, allowing the researchers to compare patterns across providers. Lilly reported that DunedinPACE, a pace-of-aging measure, fell from a median of 1.13 to 1.08 in the Zymo data, with the direction replicated in TruDiagnostic results. The analysis also reported predicted age shifts in immune, kidney, liver and cardiovascular measures, alongside changes in methylation-based protein predictions.
Both presentations took place at ARDD and concern early-stage questions about how GLP-1 medicines may affect aging-related biology. Aging researcher Steve Horvath, credited with inventing aging clocks, said the emerging data could provide “evidence that these GLP-1 drugs are actually what is known as geroprotectors.” He also cautioned that he had not seen enough evidence to take the drugs himself. The remarks reflect a possible interpretation of early findings, not a settled scientific conclusion.
““Improved biological age in our patients across trials and across different tissues.””
— Nikolaj Roed, Novo Nordisk Global Project Leader for Research and Development
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Study Limits Leave Aging Claims Open
Neither presentation proves that semaglutide or tirzepatide slows the biological aging process in a way that improves health or extends life. Clock estimates are indirect measures, and the source material does not report a validated link between the observed changes and longer survival. Novo’s projections of life-years gained are modeled estimates, not outcomes recorded in a trial designed to test lifespan.
Lilly described its sub-study as preliminary and hypothesis-generating. It had no placebo or control group, only 82 unique participants after quality control, and follow-up of 72 weeks—a short interval relative to the measurement error of some clocks. Some clock signals were unresolved or inconsistent, and predicted changes in proteins including VCAM1, SHBG and TNFRSF1B did not match actual measurements. Lilly also noted that the clocks were not trained on randomized controlled trial or longitudinal data.
The reported findings do not establish whether results apply to people who do not have obesity or diabetes, how the medicines compare with one another on aging measures, or whether any changes persist after treatment ends. The source material also does not supply full peer-reviewed reports for both presentations, so details and methods may be further clarified as the work is published.
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Larger Trials Must Test the Signals
Lilly said it plans to expand its work to semaglutide and other chronic weight-management studies. The key next step is replication in larger studies, ideally randomized trials with suitable controls and follow-up long enough to assess whether clock changes track with clinical outcomes. Researchers will also need to establish how reliable the clocks are for detecting treatment effects over the periods studied.
For both companies, the field will need to connect molecular signals to outcomes such as disease incidence, physical function and survival before an anti-aging benefit can be claimed. Until then, these presentations should be read as early research findings about possible biological effects—not as evidence that GLP-1 drugs are established treatments for aging.
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Key Questions
What did Novo Nordisk report?
Novo said proteomic-clock analyses across cardiovascular outcome trials showed lower biological-age estimates among participants receiving GLP-1 medicines, with changes reported as early as 13 to 20 weeks. The company described shifts of up to four years on a heart-protein clock; these are clock estimates, not years added to life.
What did Eli Lilly report about tirzepatide?
Lilly presented early DNA-methylation findings from a small SURMOUNT-5 sub-study. All 15 age-unit clocks showed less aging than the 1.38 years of calendar time in the study, but only two reached statistical significance. The analysis had no control group.
Do the results prove GLP-1 drugs slow aging?
No. The findings are preliminary changes in biological-aging measures. They do not establish that the medicines slow aging in a clinically meaningful way, prevent age-related disease or extend lifespan.
What further evidence is needed?
Researchers need larger studies, preferably randomized and controlled, that replicate the clock findings and test whether they correspond to meaningful health outcomes over time. Lilly said it plans to expand its analyses to semaglutide and other weight-management studies.
Source: hn
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