The makers of the two best-selling GLP-1 drugs, Novo Nordisk and Eli Lilly, presented data at the Aging Research and Drug Discovery (ARDD) meeting in Boston, held October 1 to 3, 2026 at Harvard University, suggesting their medicines shift molecular “aging clocks”25. Novo’s analysis of semaglutide (Ozempic, Wegovy) had been posted as a preprint on September 221. Lilly’s tirzepatide (Mounjaro, Zepbound) results were shown in a conference talk and have not been published4. Neither set of results has been peer reviewed, and aging clocks are estimates built from blood markers, not measures of how long anyone will live4.
What was reported
Novo’s team measured blood proteins with the Olink Explore HT platform in samples from five randomized, placebo-controlled semaglutide trials: SELECT, STEP-HFpEF, STEP-HFpEF DM, FLOW and SOUL, covering 10,052 participants1. The trial populations had overweight or obesity with heart disease, heart failure with preserved ejection fraction, chronic kidney disease, or type 2 diabetes with high cardiovascular risk1. The researchers applied organ-specific “mortality clocks” that had been trained on a separate population, the UK Biobank, to estimate a biological age for each organ1.
According to the preprint, semaglutide lowered the heart clock by roughly 2 to 4 years compared with placebo, and lowered kidney, brain, pancreas, lung and multi-organ clocks by 1 to 4 years, over follow-up of up to 156 weeks1. A proteomic frailty score and protein-based risk scores for cardiometabolic disease also improved1. The heart clock was the most consistent result, falling in all five trials, while other organ effects varied by trial and time point1. Nikolaj Roed, a global project leader at Novo, put the overall difference at around “two to three years”2.
Lilly’s analysis came from SURMOUNT-5, a 72-week trial that randomly assigned more than 700 adults with overweight but without diabetes to tirzepatide or semaglutide3. The aging substudy looked at 71 participants on tirzepatide who were over 50, using epigenetic clocks that read chemical marks on DNA3. Over the period, participants aged 1.38 years by the calendar; across different epigenetic clocks, their measured biological age moved by an average of 0.7 to 1.1 years, and some clocks went backward3.
“All the clocks are telling a consistent story that we’re seeing a reduction in age.” Kevin Duffin, vice president for aging research at Lilly2
How strong the evidence is
The Novo work draws on large randomized trials, which allows a direct comparison between drug and placebo groups. It also has specific weak points that the authors list themselves:
- Selected samples in SELECT. The SELECT protein substudy was enriched for people who had heart events: 781 of 1,641 participants, compared with 1,270 of 17,604 in the full trial. Weighting to correct for this reduced the number of statistically significant organ changes, though the direction stayed similar1.
- Clock artifacts. The adipose (fat tissue) clock rose early in treatment because semaglutide lowers leptin, a protein the model links to worse outcomes. The authors say this likely reflects the clock’s training in weight-stable people, where low leptin can signal frailty or illness1.
- Few proteins doing the work. Several clocks, including the heart clock, depend heavily on a small number of proteins1. The heart clock change was driven in part by NPPB, a marker related to heart strain1.
- Not explained by weight loss alone, statistically. Most heart and kidney clock changes were not statistically mediated by changes in body weight, HbA1c or the inflammation marker hsCRP1. In SOUL, heart-clock change was estimated to account for 34% to 49% of the drug’s effect on selected outcomes, an exploratory analysis1.
The authors conclude that the findings show “reproducible remodeling of mortality-associated proteomic signatures” and support their use as treatment-response readouts “without establishing biological rejuvenation, causal mediation or surrogate validity”1.
Lilly’s data are weaker by design. CNN reported that Duffin acknowledged there was no placebo group and that follow-up was relatively brief3. Asked whether the effect came from weight loss or the drug itself, Duffin said the drugs work through blood sugar reduction and weight loss, and “the effects we’re seeing are mostly due to that”3.
What it does not show yet
None of the data show that GLP-1 drugs make people live longer because of an effect on aging itself. The trials enrolled people with obesity, diabetes, heart or kidney disease, so the results say nothing directly about lean, healthy people13.
“In an unhealthy population, I do think it’s an anti-aging drug. But in a healthy population, no one knows.” Vadim Gladyshev, Harvard biologist who worked with Novo on the measurements2
Steve Horvath of UCLA, who developed early epigenetic clocks, called a two-year shift “a pretty strong effect,” but added that he had not yet seen “sufficient evidence that they will benefit skinny people”2. James Kirkland of Cedars-Sinai told CNN that the clocks are still in development and can “vary tremendously from day to day within a person,” and warned that “people could overread some of this stuff”3. Several people quoted by MIT Technology Review also cautioned that the drugs have side effects, including muscle loss2.
Who is behind it
Most of the preprint’s 12 authors are current or former Novo Nordisk employees who hold company shares, and the last two authors, listed as equal contributors, are from Novo1. Outside authors include Helen Colhoun of the University of Edinburgh, who declares advisory roles for Novo Nordisk and other drugmakers and stock in Eli Lilly and Roche, and Gladyshev, who declares advisory roles for companies including Retro Biosciences and Thorne1. The Lilly data were presented by a Lilly executive2. The ARDD meeting is organized by Insilico Medicine, whose founder Alex Zhavoronkov said at the event that he takes both tirzepatide and semaglutide although he is not overweight25. When he asked whether a reasonable person should start taking semaglutide, Novo’s Alejandro Aguayo-Orozco replied that he is not a physician and could not answer2.
How it fits the field
Semaglutide has already shown cardiovascular and kidney benefits and lower all-cause mortality in high-risk populations, which is why researchers have asked whether it acts on aging more broadly12. Aging-clock researchers have long sought tests of whether their measures move with drugs that have proven benefits; Yuge Ji, founder of the startup Reflector Bio, told MIT Technology Review that “the clock people have been pushing for a decade to get this kind of study done”2.
Animal work points in a similar direction, but it is animal work. CNN described a Nature study from the University of California, Berkeley in which mice started on semaglutide at 20 months old lived an average of 834 days versus 742 days on placebo; mice on a 25% calorie-restricted diet also lived longer3.
What to watch next
- Peer review of the Novo preprint and a full publication of Lilly’s SURMOUNT-5 substudy14.
- Longer follow-up. Lilly hopes to follow people for longer in its next trial; Duffin said it would be interesting to see results four or five years after starting treatment3.
- Healthy older adults. In January 2026 the US agency ARPA-H committed $38 million to a Texas study testing whether semaglutide has anti-aging effects in healthy people over 60, measuring cognition, mobility and sensory function2.
- Clinical outcomes, not just clocks. The authors stress that organ clocks are not yet surrogate endpoints and must still be shown to predict preserved function or less disease1.
