This week KENS 5 News in San Antonio asked me about a headline that is everywhere right now: the two biggest makers of GLP-1 drugs say their medications slow biological aging. You can watch the KENS 5 segment above.1 A 90-second news piece leaves room for a sentence or two, so this is the longer version of my answer: what Novo Nordisk and Eli Lilly actually reported, what an aging clock can and cannot tell you, and what it means if you take one of these drugs or are thinking about it.
What Novo Nordisk and Eli Lilly reported
Both companies presented their data in early October at the Aging Research & Drug Discovery meeting in Boston, as first reported by MIT Technology Review.2
- Novo Nordisk (semaglutide, sold as Ozempic and Wegovy). Blood from 10,052 people with overweight or diabetes, half on semaglutide and half on placebo, was drawn at the start and again months later and run through proteomic aging clocks, which estimate age from the levels of many blood proteins. Overall, the semaglutide group came out roughly two to three years younger than the placebo group. One clock built from heart proteins showed a gap of about four years.
- Eli Lilly (tirzepatide, sold as Mounjaro and Zepbound). A smaller study used epigenetic clocks, which read chemical tags (methylation) on DNA. Lilly’s researchers said the clocks mostly told the same story: slower aging on the drug.
Two caveats up front. These were conference presentations by the drugmakers, not peer-reviewed papers yet. And the people studied had obesity or diabetes, so the results say nothing yet about lean, healthy adults.
“Two to three years younger” is not “two to three more years of life”
Some coverage turned the result into people living two to three years longer. That is not what was measured. The studies measured biological age, a statistical estimate built from blood markers. In large population studies, a younger reading goes with a lower risk of disease and death. Nobody has yet shown that pushing the clock down with a drug buys the same amount of extra life. That is the study still to be done, and it takes years.
What an aging clock actually measures
The first widely used aging clock, developed by Steve Horvath at UCLA, estimates age from DNA methylation at a few hundred sites in the genome.3 Newer clocks use blood proteins and can be broken down by organ. A 2023 study in Nature used blood proteins to estimate the age of 11 separate organs, and found that an organ reading “older” than expected predicted disease in that organ and a higher risk of death.4
This is the point I made on KENS 5: the clocks do not all agree, because each one measures something different. The cardiovascular, metabolic, mitochondrial, nervous and reproductive systems each have their own signature. So you would expect variation across clocks and across organs, and that is exactly what the Novo data showed.
Why a GLP-1 would move the clocks
My read is that the benefit comes from what these drugs do to your metabolism, not from something the molecule is magically doing to aging itself. GLP-1 drugs lower blood sugar and insulin, take off visceral fat, lower blood pressure and lower inflammation. Each of those drives the age-related diseases that aging clocks were built to predict. Fix them, and you would expect the readouts to improve.
The outcome trials point the same way. In SELECT, which enrolled 17,604 adults with overweight or obesity and established heart disease but no diabetes, semaglutide cut major cardiovascular events by 20%.5 In FLOW, in people with type 2 diabetes and chronic kidney disease, semaglutide lowered the risk of major kidney events by 24%.6 Heart attacks, strokes, kidney failure and death are hard outcomes, and they matter more than any clock reading. For the wider evidence, see GLP-1s are becoming longevity drugs.
What this means for you
- If you have obesity, type 2 diabetes or high cardiovascular risk, the case for a GLP-1 was already strong on hard outcomes. The aging-clock data is one more reason, not the main one. If you are deciding between the two drugs, see semaglutide vs tirzepatide.
- If you are lean and healthy, there is no evidence yet that a GLP-1 slows your aging. A federally funded ARPA-H study in Texas is now testing semaglutide in healthy adults over 60, looking at cognition, mobility and the senses.2 Until results like that come in, I do not prescribe GLP-1s as an anti-aging drug for people without a metabolic reason to take one.
- Protect your muscle. A meaningful share of the weight lost on these drugs can be lean mass, and muscle is one of the strongest predictors of healthy aging. Strength training and enough protein are not optional; here is how to preserve muscle on a GLP-1.
- Measure what you can act on. A consumer aging-clock test can be interesting, but results vary from one test to the next. I put more weight on markers we can change and re-check: A1c and fasting insulin, ApoB, blood pressure, hs-CRP, liver fat, body composition on a DEXA scan, and VO2 max and grip strength. If those move the right way, your biological age is very likely moving with them.
The bottom line
For people with metabolic disease, GLP-1s increasingly look like they slow the biology of aging, which fits the outcome data we already have. That is real progress. It is not proof that they add years of life, and it is not a reason for healthy people to start injecting. If you want to know whether a GLP-1 fits your own risk profile, and how to use one without giving up muscle, that is what a free discovery call is for; read more about how the longevity program works.
Frequently asked questions
Do GLP-1 drugs slow aging?
Early data suggest they may in people with obesity or diabetes. In October 2026, Novo Nordisk reported that semaglutide lowered biological age on proteomic aging clocks by roughly two to three years versus placebo in 10,052 people, and Eli Lilly reported slower epigenetic aging on tirzepatide. These were drugmaker conference presentations that are not yet peer-reviewed, and no data yet show the same effect in lean, healthy adults.
Will Ozempic or Mounjaro make me live longer?
Not proven. A lower biological-age reading is linked to lower risk of disease and death in population studies, but no trial has shown that a GLP-1 adds a specific number of years of life. What is proven is a reduction in hard outcomes in higher-risk people, such as a 20% cut in major cardiovascular events with semaglutide in the SELECT trial.
What is an aging clock?
An aging clock is an algorithm that estimates biological age from molecular markers in the body, most often DNA methylation (epigenetic clocks) or blood protein levels (proteomic clocks). Different clocks track different systems and organs, so results often vary from one clock to another.
Should I take a GLP-1 for longevity if I am not overweight?
There is no evidence yet that GLP-1s slow aging in lean, healthy people, and they carry side effects including loss of muscle mass. A federally funded ARPA-H study in Texas is testing semaglutide in healthy adults over 60. Until results are in, a GLP-1 makes sense when there is a metabolic reason for it, such as obesity, type 2 diabetes or high cardiovascular risk.
References
Baker J. “Two of the largest GLP-1 drugmakers say their medication could lengthen lives.” KENS 5, October 14, 2026. kens5.com
Regalado A. “Weight-loss drugs show signs of slowing biological aging, say drugmakers.” MIT Technology Review, October 6, 2026. technologyreview.com
Horvath S. “DNA methylation age of human tissues and cell types.” Genome Biology 14 (2013): R115. DOI: 10.1186/gb-2013-14-10-r115
Oh HS-H, Rutledge J, Nachun D, et al. “Organ aging signatures in the plasma proteome track health and disease.” Nature 624 (2023): 164–172. DOI: 10.1038/s41586-023-06802-1
Lincoff AM, Brown-Frandsen K, Colhoun HM, et al. “Semaglutide and cardiovascular outcomes in obesity without diabetes.” New England Journal of Medicine 389, no. 24 (2023): 2221–2232. DOI: 10.1056/NEJMoa2307563
Perkovic V, Tuttle KR, Rossing P, et al. “Effects of semaglutide on chronic kidney disease in patients with type 2 diabetes.” New England Journal of Medicine 391, no. 2 (2024): 109–121. DOI: 10.1056/NEJMoa2403347