A new study published in Nature Communications provides the first randomized, placebo-controlled clinical evidence that semaglutide, a widely used GLP-1 drug, slows the accumulation of biological aging markers in adults with HIV, according to researchers at UC San Diego and partner institutions.
The study analyzed data from 108 adults with HIV-associated lipohypertrophy, a condition in which excess fat builds up around the abdomen. About half received weekly semaglutide injections over 32 weeks, while the rest received placebos. Researchers used biological “epigenetic clocks” to track cellular aging by measuring DNA methylation—chemical marks on DNA that regulate gene expression without changing the genetic sequence itself.
Compared to the placebo group, participants treated with semaglutide showed multiple benefits: the drug slowed the pace of biological aging by 9% as measured by the DunedinPACE epigenetic clock, and significantly slowed biological processes associated with mortality risk and age-related disease according to the PCGrimAge epigenetic clock. The treatment also exhibited a broad pattern of slower biological aging across epigenetic clocks linked to inflammation and blood, brain, heart, kidney, liver, and metabolic health.
According to first author Michael Corley, associate professor at UC San Diego School of Medicine, people with HIV often experience accelerated aging even when the virus is well-controlled with antiretroviral therapy. The study suggests semaglutide may slow aging by reducing inflammation and metabolic stress, decreasing chronic immune activation—a primary driver of accelerated aging in people with HIV. The drug also reduces visceral and ectopic fat that accumulates around organs, which may help curb inflammatory and metabolic signals promoting aging.
A related pilot study published in npj Aging found similar results in people with HIV and metabolic dysfunction-associated steatotic liver disease: 42% of participants showed reduced biological aging rates over 24 weeks, 34% showed slowed aging associated with mortality risk, and nearly 49% had increased telomere length—protective DNA sequences at chromosome ends. Those with increased telomere length also tended to walk faster after treatment.
Corley cautioned that larger clinical trials are needed to confirm findings and determine optimal dosing and treatment duration. “We are not saying that semaglutide reverses aging or makes people younger,” he said. “What we are seeing is a signal that it may slow some of the biological processes associated with aging.” Future studies will examine whether GLP-1 effects are enhanced when combined with lifestyle interventions like diet and exercise.
Key facts
- Semaglutide slowed biological aging by 9% in adults with HIV over 32 weeks, according to the DunedinPACE epigenetic clock
- The drug showed slower aging patterns across epigenetic clocks linked to inflammation and multiple organ systems
- A related pilot study found 42% of participants with HIV and fatty liver disease showed reduced biological aging rates over 24 weeks
- Researchers emphasize the findings don’t mean the drug reverses aging, but may slow biological aging processes
- Larger clinical trials are needed to confirm findings and test broader population effects