Median lifespan rose from 742 to 834 days, about 12 percent, when female mice started semaglutide at 20 months. No human lifespan data exist.
Old female mice that started a daily semaglutide injection at 20 months lived a median of 834 days. Old female mice given saline lived a median of 742 days (1). Median lifespan is the age by which half the animals have died. The gap is 92 days, about 12 percent.
The result comes from a paper published in Nature on 2 September 2026 by a team at the University of California, Berkeley (1). It tests semaglutide, the drug sold as Ozempic and Wegovy, against lifespan. It is also a mouse result. Nobody has tested whether it holds in people, and the authors say that would take long-term clinical studies built around ageing outcomes (1).
Where Semaglutide Comes From
In 1902, William Bayliss and Ernest Starling reported that acid in the gut triggers a chemical that travels in the blood and sets the pancreas secreting digestive juice (2, 8). They named it secretin. It was the first hormone identified (3). In 1905 Starling introduced the term hormone for such chemical messengers (3, 8).
GLP-1 belongs to the same family of gut hormones. Gut cells release it when food arrives. It raises insulin when blood sugar is high and tells the brain to eat less (1). Semaglutide is a lab-made drug that acts on the same receptor.
The drug was built for type 2 diabetes and obesity. Our earlier piece on GLP-1 drugs and longevity covers what it has done in people so far. One large trial found fewer heart attacks and strokes. The cost was lost muscle, and weight that came back when treatment stopped. That evidence is about heart events and weight. It does not test how long people live.
The new study asks a different question. If you start semaglutide late in life, in an animal that is already old, does the animal live longer?
What the Researchers Did
The team used female C57BL/6 mice, a standard laboratory strain, obtained from the National Institute on Aging at 20 months of age (1). The mice were randomly assigned to groups.
Each mouse got a daily injection under the skin. The dose was 10 nanomoles of semaglutide per kilogram of body weight, or an equal volume of saline for the comparison group (1). The paper does not set this dose against the human dose, and we do not either.
There were several separate groups of mice (1):
- The lifespan group: 39 mice on saline and 40 on semaglutide, treated until they died.
- The 3-month groups: mice treated for 3 months, then tested and killed for tissue study. These were 10 pairs for physiology tests, 5 pairs for brain stem cell work and 6 pairs for other lab measures.
- The calorie restriction group: 10 mice on saline, 10 on semaglutide and 10 on calorie restriction, followed for 5 months.
The researchers who ran the tests did not know which treatment each mouse had received (1). The exception was the calorie restriction mice, whose feeding schedule gave them away.
The Lifespan Result in Numbers
Median lifespan was 742 days in the saline group and 834 days in the semaglutide group (1). The 92-day gap is 12.4 percent of 742.
The authors tested the difference with a log-rank test, which compares the two survival curves across the whole follow-up rather than just at one age. Its P value was 5.7 x 10^-6, read from the survival figure (1).
A P value is the chance of seeing a gap at least this large if the drug genuinely had no effect on lifespan. Here that chance is about 6 in a million. That makes the difference statistically significant, and it says nothing yet about how large or useful the difference is. The 92 days is the size.
The saline mice lived within the range reported for this strain (1). That matters because an unusually short-lived comparison group can make a drug look better than it is.
In the survival curves, a mouse counted as a death if it died or was put down because it was too ill to continue. No mouse was removed for reasons unrelated to age (1).
The kinds of illness at the end of life, tumours included, showed no statistically significant difference between groups (1). Age at death also appeared later in the semaglutide group for several causes unrelated to tumours (1). The authors read that as a broad delay in decline, not the removal of one disease.
We do not quote a maximum lifespan. The paper gives none.
What Changed in the Mice's Bodies
Semaglutide cut how much the mice ate by 24 percent (1). The weight they lost was mostly fat, and the share of lean tissue rose (1). Movement, oxygen use and energy expenditure showed no statistically significant change once body weight was taken into account (1).
In the 3-month groups, treated old mice differed from untreated old mice on many measures (1):
- Movement and curiosity: they moved more in an open arena and entered open arms of a raised maze more often, which the paper reads as more exploratory activity.
- Memory: in a maze with a hidden escape hole they spent more time in the right quadrant, searched more of the right holes and found the exit faster.
- Strength and endurance: they stayed on a rotating rod and a hanging screen longer, and ran longer and farther on a treadmill.
- Blood sugar: they cleared a sugar dose from the blood faster.
Under the microscope, the old treated mice had fewer blood-forming stem cells in the bone marrow but similar marrow cell counts. The authors read that as each stem cell doing more work. They had more new brain cells in a memory region called the dentate gyrus. Markers of inflammation and of worn-out (senescent) cells were lower. A marker of DNA damage was lower, and measures of cell energy production were higher (1).
These are tissue findings from a few groups of 5 to 10 mice, and they are measurements of ageing markers, not of lifespan. They fit the idea that the drug slowed something general. They do not prove it. Our hallmarks of aging article explains why these markers are used.
Semaglutide Next to Calorie Restriction
Calorie restriction means eating less without going short of nutrients. The paper describes it as slowing ageing and extending lifespan across species (1), and it is hard to keep up. That is why researchers look for drugs that copy it, called calorie restriction mimetics.
The team put the idea to a direct test. They gave 20-month-old female mice saline, semaglutide, or a diet cut by 24 percent for 5 months. The 24 percent was chosen to match the average drop in food intake that semaglutide produced, and it was not adjusted afterward (1). Treated and restricted mice lost similar amounts of body weight and fat (1).
The two groups ate in very different ways. Restricted mice ate their ration soon after it arrived and then fasted, and they grew restless before the next feeding. Semaglutide mice ate gradually through the day, as you would expect when appetite is dulled (1). So the same calorie cut came with different behaviour and different body rhythms.
On the function tests, mice on either treatment held their ground while untreated mice declined over the 5 months (1):
- About the same as restriction: movement in the open arena and the raised maze, the rotating rod, the hanging screen and treadmill endurance.
- Better than restriction: time spent in the centre of the open arena, performance in the memory maze and blood sugar clearance. Mice on restriction stayed near where they started on these. Semaglutide mice improved above their starting point.
The authors read this as semaglutide copying many benefits of calorie restriction and adding some that reduced intake alone does not explain (1). Two cautions apply. The paper itself calls the centre-of-arena result a measure of exploratory drive, a behaviour test and not a health outcome. And the comparison lasted 5 months with 10 mice per group. It did not follow the animals to death, so it cannot tell us whether semaglutide lengthens life more than calorie restriction does.
Why Only Female Mice
The authors give a practical reason: female mice were chosen "to minimize confounding effects of male aggression and injury", as in earlier long-term ageing studies (1). Male mice housed together fight, and injuries from fights can end a life early for reasons that have nothing to do with the drug.
The cost is that we know nothing here about males. Sex differences in lifespan drugs can be large.
In the National Institute on Aging's Interventions Testing Program, a different diabetes drug, canagliflozin, lengthened median lifespan in male mice by 14 percent (5). It showed no detectable lifespan effect in females, even though it improved blood sugar in both. Our article on SGLT2 inhibitors and longevity goes through that result. It is a reminder that the sex of the mouse can decide the answer. Here the answer is known for females only.
Why a Mouse Result Is Not a Human Result
Mouse lifespan gains often shrink in longer-lived animals. Calorie restriction is the clearest case. It lengthens life in rodents, but in rhesus monkeys two large studies disagreed. The Wisconsin study found a survival benefit. The National Institute on Aging study found no significant survival effect (6, 7).
The 2017 paper points to differences in study design that could contribute, such as when restriction started and what the monkeys ate. It concludes that the health benefits of restriction carry over to monkeys (7).
So a 12 percent gain in mouse median lifespan does not translate into a 12 percent gain in people, or into any specific number. The authors take the same view. They write that whether the drug changes ageing or lifespan in people "will require long-term clinical studies designed to evaluate ageing-related outcomes in older populations" (1).
Two details of the mouse study also limit how far it travels:
- The mice began at 20 months, which is old for a mouse. The result says the drug did something when started late in these animals. It does not say when in a human life, if ever, a similar start would help.
- The study looked for harm only within the end points it monitored. The authors report no adverse effects they could attribute to semaglutide within those end points (1). That is a statement about 79 mice in one laboratory, not a safety record for older people.
What the Human Evidence Shows So Far
The best human evidence on semaglutide is about specific diseases. The SELECT trial enrolled 17,604 adults aged 45 or older who had heart disease and overweight but no diabetes (4). They were assigned to 2.4 milligrams of semaglutide weekly or a placebo and followed for a mean of 39.8 months.
A heart attack, stroke or death from heart disease happened in 569 of 8,803 people on semaglutide (6.5 percent) and 701 of 8,801 on placebo (8.0 percent). The hazard ratio was 0.80 (4).
A hazard ratio compares how fast events piled up in the two groups, and it is not a count of people. Here, 0.80 means events accumulated more slowly on the drug. In absolute terms that is 1.5 fewer events per 100 people over a mean follow-up of about 3.3 years.
Stopping the drug also had costs. In SELECT, adverse events led 1,461 people on semaglutide (16.6 percent) to stop the drug for good, against 718 on placebo (8.2 percent) (4).
SELECT counted heart events in people who already had heart disease. It did not measure whether anyone lived longer, and it was not designed to. No trial has randomized healthy older adults to semaglutide and followed them for ageing outcomes. That gap is why this mouse study draws attention, and also why it should not be read as advice.
What You Can Do Now
Nothing in this paper is a reason to start semaglutide, stop it, or change a dose. The drug is approved for diabetes and for weight management in people who meet clinical criteria, and its use belongs in a conversation with a doctor who knows your history.
If you already take it, the study does not change your plan. If you are weighing it for weight or blood sugar, the decision rests on those benefits and risks, which are better understood than any effect on ageing.
If you want to follow this research, watch for a trial that measures ageing outcomes in older adults. That is exactly what the authors say is missing.
Frequently Asked Questions
Does semaglutide extend lifespan in humans?
Nobody knows. In a 2026 Nature study, old female mice that started semaglutide lived a median of 834 days against 742 on saline. No human trial has measured lifespan. The authors say that would take long-term studies built around ageing outcomes in older people.
How much longer did the mice live?
Median lifespan rose by 92 days, from 742 to 834, about 12 percent. The study followed 39 saline mice and 40 semaglutide mice from 20 months of age. The gap was statistically significant (P = 5.7 x 10^-6).
Is semaglutide a calorie restriction mimetic?
The authors say it copies many effects of calorie restriction. Over 5 months, semaglutide matched a 24 percent diet cut on most function tests and beat it on memory and blood sugar. That comparison did not measure lifespan, so the claim is about function in mice, not about living longer.
Why did the study use only female mice?
The authors say it was to avoid male aggression and injury, which can end lives early in group-housed males. The cost is that the paper says nothing about males. Another diabetes drug, canagliflozin, lengthened life in male mice and not in females, so sex can change the result.
Should I take Ozempic or Wegovy to slow aging?
No evidence supports taking it for that purpose. The mouse result is a reason for human trials, not for personal use. Semaglutide is a prescription drug with known side effects, and whether it is right for you is a decision for you and your doctor.
How is this different from the canagliflozin mouse study?
Canagliflozin was tested in a large multi-site program using genetically varied mice and extended life in males only. The semaglutide study used one inbred strain, one laboratory and females only. Both are mouse results, and neither shows a human lifespan effect.
Sources
- Feng Y, Barthez M, Wang Y, et al. Late-life semaglutide treatment slows ageing and extends lifespan in female mice. Nature. Published 2 September 2026. PMID: 42686906. DOI: 10.1038/s41586-026-10940-7. Open access. The survival P value is read from the paper's Figure 1a
- Bayliss WM, Starling EH. The mechanism of pancreatic secretion. J Physiol. 1902;28(5):325-353. PMID: 16992627. DOI: 10.1113/jphysiol.1902.sp000920
- Henriksen JH, de Muckadell OB. Secretin, its discovery, and the introduction of the hormone concept. Scand J Clin Lab Invest. 2000;60(6):463-471. PMID: 11129062. DOI: 10.1080/003655100448446
- Lincoff AM, Brown-Frandsen K, Colhoun HM, et al. Semaglutide and cardiovascular outcomes in obesity without diabetes. N Engl J Med. 2023;389(24):2221-2232. PMID: 37952131. DOI: 10.1056/NEJMoa2307563. NCT03574597
- Miller RA, Harrison DE, Allison DB, et al. Canagliflozin extends life span in genetically heterogeneous male but not female mice. JCI Insight. 2020;5(21):e140019. PMID: 32990681. DOI: 10.1172/jci.insight.140019
- Mattison JA, Roth GS, Beasley TM, et al. Impact of caloric restriction on health and survival in rhesus monkeys from the NIA study. Nature. 2012;489(7415):318-321. PMID: 22932268. DOI: 10.1038/nature11432
- Mattison JA, Colman RJ, Beasley TM, et al. Caloric restriction improves health and survival of rhesus monkeys. Nat Commun. 2017;8:14063. PMID: 28094793. DOI: 10.1038/ncomms14063
- Hirst BH. Secretin and the exposition of hormonal control. J Physiol. 2004;560(Pt 2):339. PMID: 15308687. DOI: 10.1113/jphysiol.2004.073056
Funding Transparency
LSD is editorially independent. We receive no funding from pharmaceutical, supplement or longevity companies. These are the funding ties behind each study above, taken from each paper's own funding and conflict statements where we could read them.
- Source 1 (Feng, 2026): Supported by three National Institute on Aging grants (R01AG063404, R01AG063389 and R01AG082105) and the US National Institute of Food and Agriculture, all awarded to the senior author. The paper's competing interests statement says the Regents of the University of California filed a patent application on GLP-1 receptor agonists for healthy ageing (application 64/113,481). It names no drug company funder.
- Source 4 (SELECT, 2023): Funded by Novo Nordisk, the maker of semaglutide, and several authors are listed as Novo Nordisk employees.
- Source 5 (Miller, 2020): The authors declare no conflict of interest. The study ran inside the National Institute on Aging's Interventions Testing Program.
- Source 7 (Mattison, 2017): Funded by National Institutes of Health grants and the Intramural Research Program of the National Institute on Aging. Some authors hold roles at LifeGen Technologies, GeroScience and Prolongevity Technologies. The paper states that none of these activities benefit directly from the research and declares no competing financial interests.
- Source 6 (Mattison, 2012): Supported by the Intramural Research Program of the National Institutes of Health, National Institute on Aging, per the acknowledgements of the author manuscript (PMC3832985). That manuscript carries no competing interests statement.
- Sources 2, 3 and 8: Historical and review papers on the discovery of secretin. We found no funding statement in what we could read, and no commercial interest in the facts we cite.
Related Reading
- GLP-1 Weight Loss Is Up to 40 Percent Muscle and Bone, what semaglutide has done in people so far
- The Diabetes Drug That Extended Lifespan in Males and Did Nothing in Females, another mouse lifespan result where sex decided the answer
- The 12 Hallmarks of Aging, and Exercise Hits Seven, the markers this study measured
- Cellular Senescence Leaves Cells That Will Not Die, the worn-out cells whose markers fell in treated mice
In old female mice, a daily dose of semaglutide added 92 days to the median lifespan. Whether it does anything for lifespan in people has not been tested.
Written with the help of AI tools, shaped and verified by humans. Every result in this article was checked against the study's own paper, abstract or registry entry.
This article is for information only and is not medical advice. Do not start or stop any medicine on the basis of an article.