Earlier this month, Biohack reported that Novo Nordisk and Eli Lilly said their weight-loss and diabetes drugs slowed lab measures of aging, in company analyses not yet reviewed by outside scientists. What is new now is a different kind of evidence: a peer-reviewed analysis from a trial in which people got either the drug or dummy shots, and their DNA was checked for signs of aging. The study, led by researchers at the University of California San Diego, is published in the journal Nature Communications1.
It found that adults with HIV who took semaglutide, the active ingredient in Ozempic and Wegovy, built up DNA markers of biological aging more slowly than those on a placebo2. The researchers stress this is an early signal, in one specific group of people.
What happened
The team went back to data from a previously published trial of 108 adults with HIV-associated lipohypertrophy, a condition in which extra fat builds up around the belly1. About half got weekly semaglutide injections and the rest got placebo injections1. One summary of the paper reports that 45 people received semaglutide and 39 received placebo3.
The researchers used several “epigenetic clocks” to follow aging over the 32 weeks of treatment1. These clocks read DNA methylation: chemical marks on DNA that help control which genes are switched on or off, without changing the genetic code itself1. Blood samples were taken before treatment and again at week 323.
The evidence so far
Compared with the placebo group, people on semaglutide showed a broad pattern of slower biological aging on clocks linked to inflammation and to blood, brain, heart, kidney, liver and metabolic health, according to UC San Diego1. The main numbers reported:
- On one clock that measures the pace of aging, called DunedinPACE, the drug slowed aging by 9%1.
- On a clock tied to the risk of dying from any cause, called PCGrimAge, the drug significantly slowed the related biological processes1.
- A summary of the paper lists differences on other clocks ranging from 2.2 to 4.9 years, depending on the clock used3.
The researchers suggest a few reasons the drug might have these effects. It may calm inflammation and metabolic stress, which could reduce long-running immune activation, a main driver of faster aging in people with HIV1. It also reduces fat stored deep in the belly and around organs, which may cut down on signals that promote aging1.
Lead author Michael Corley, an associate professor at UC San Diego School of Medicine and the Stein Institute for Research on Aging, said:
“We are not saying that semaglutide reverses aging or makes people younger. What we are seeing is a signal that it may slow some of the biological processes associated with aging,”
That quote was reported by News182.
What it does not show yet
The trial was not designed to study aging. Its main goal was to measure changes in deep belly fat, and the aging analysis was added afterward as an exploratory look3. The registry record lists the trial’s main goals as changes in belly fat, total body fat and fat around the heart at week 324. Checks added after a trial can point to effects worth testing, but they are weaker than goals set in advance.
The group was also narrow. Everyone had HIV and abnormal fat buildup, the sample was small and the follow-up lasted only 32 weeks, so the findings cannot be applied directly to the general population3. Epigenetic clocks are lab estimates; this study did not measure how long anyone lived or whether they got fewer age-related diseases.
Corley argues the results may still carry lessons beyond HIV. “Many of the biological processes we study in HIV are also central to aging in the general population,” he said in the university’s release1. The researchers say much larger trials are needed before drawing conclusions about semaglutide and healthy aging2.
Early versions of these findings were presented at the CROI 2025 conference, before peer review, and researchers said then that larger trials were needed to see whether the effects last and apply to other groups5.
Who is behind it
The analysis was run by UC San Diego and several partner institutions1. The underlying trial is a mid-stage (Phase 2) trial sponsored by Case Western Reserve University; it started in May 2019, and its results were first posted on the registry in February 20264. The sources given to Biohack do not say who paid for the aging analysis or whether any authors have ties to Novo Nordisk, which makes semaglutide.
The same researchers also reported a related pilot study in the journal npj Aging, in people with HIV and fatty liver disease who took semaglutide for 24 weeks1. In that study, 42% of participants had a slower pace of aging on the DunedinPACE clock, 34% had slower aging on the death-risk clock, and nearly 49% had longer telomeres, the protective caps at the ends of chromosomes1. Those with longer telomeres also tended to walk faster after treatment1. The UC San Diego release does not describe how that pilot was designed or how many people took part.
Sources do not all describe these studies the same way. One physician’s blog attributes the one-third and nearly-half figures to the Nature Communications trial6, while UC San Diego attributes them to the separate npj Aging pilot1.
How it fits the field
This is the third piece of the Ozempic-and-aging story Biohack has covered in a month. In September, a Nature study found old female mice given semaglutide lived longer: mice treated from 20 months of age until death lived about 100 days longer on average than untreated mice7. That work was funded by the US National Institute on Aging, and its authors said there is no indication the results could be achieved right away in humans7.
Then, at the ARDD aging conference, Novo Nordisk presented modeling that projected about 1.9 extra years of life for a UK group of about 19,000 semaglutide users, along with lower protein-based biological age estimates in its heart trials6. Those life-year figures were modeled, not observed6. The same commentary also noted a limit: Novo’s own Alzheimer’s trials of semaglutide in 3,800 people came back flat6.
Against that backdrop, the HIV trial matters because it compares the drug with dummy shots in people, which mouse studies and company models cannot do. It is still a small, after-the-fact look at lab measures in one group.
What to watch next
Corley said newer drugs in this family give scientists a chance to test whether different molecules affect aging biology in different ways, and to find out which patients might benefit most2. Researchers also want larger, planned trials in different groups of people, and to test whether pairing the drugs with diet, exercise and better sleep changes the results3.
The key questions remain open: whether slower DNA clocks last after people stop the drug, whether they show up in people without HIV, and whether they translate into fewer age-related diseases or a longer life.
