GLP-1 may slow biological aging

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GLP-1 may slow biological aging

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June 11, 2026
Susanne Clara Bard, UC San Diego

A set of three blue GLP-1 pens

Semaglutide, a extensively used importance defeat medication sometimes sold as Ozempic or Wegovy, slowed biologic aging throughout multiple epigenetic clocks in a randomized, double-blind, placebo-controlled medicinal trial.

Credit: iStock/Eduardo Monroy Husillos

Beyond the general notice GLP-1 narcotics are receiving for treating obesity, lowering lifeblood sugar and decreasing the hazard of cardiovascular disease, emerging investigation is examining their another possible impacts — including their effects on aging.

Now, a new study provides the archetypal randomized, placebo-controlled medicinal evidence that semaglutide, a extensively used GLP-1 drug, slows downward the gathering of biologic aging markers in the DNA of adults alongside HIV. The study is published in Nature Communications.

Researchers at the University of California, San Diego and multiple partner institutions analyzed data from a earlier published clinical trial of 108 adults alongside HIV‑associated lipohypertrophy, a circumstance in which excess fat builds up about the abdomen. About fractional of the participants received weekly injections of semaglutide, alongside the remainder receiving placebo injections.

The squad used a set of biologic “epigenetic clocks” to track cellular aging complete the 32-week care period. These clocks detect DNA methylation, chemic marks on DNA that assistance control how genes are turned on or off without changing the familial sequence itself. By measuring changes in these marks, the squad could measure whether the care was connected alongside a slower or faster biologic aging pattern.

People alongside HIV frequently cognition accelerated aging, equal if it is well-controlled alongside antiretroviral therapy, according to archetypal author Michael Corley, Ph.D., affiliate prof at UC San Diego School of Medicine and the Stein Institute for Research on Aging. However, the study established compared to the placebo group:

  • Participants treated alongside semaglutide exhibited a broad form of slower biologic aging throughout epigenetic clocks connected to inflammation and blood, brain, heart, kidney, liver and metabolic health.

  • The medication slowed the gait of biologic aging by 9 %, as measured by the DunedinPACE epigenetic clock.

  • The medication considerably slowed biologic processes connected alongside the hazard of all‑cause mortality and age-related disease, as measured by the PCGrimAge epigenetic clock.

Research suggests there are multiple mechanisms by which semaglutide may power biologic aging. By reducing inflammation and metabolic stress, GLP-1 narcotics decreased chronic immune activation, a chief controller of accelerated aging in group alongside HIV. They additionally decrease visceral and ectopic fat that accumulates about the abdomen and organs, which may assistance curb the inflammatory and metabolic signals that advance aging.

“Emerging data additionally propose that GLP-1 narcotics may reprogram certain cells in distinct organs, which could assistance explain why we see effects throughout multiple aging clocks,” stated Corley.

While the study focused on group alongside HIV‑associated lipohypertrophy, Corley says it may additionally recommendation lessons for the wider population.

“Many of the biologic processes we study in HIV are additionally chief to aging in the broad population,” he said. “Because these processes can appear before or be additional pronounced in group alongside HIV, this community can assistance us acknowledge interventions that may enhance healthspan additional broadly.”

We are not saying that semaglutide reverses aging or makes group younger. What we are seeing is a indication that it may dilatory several of the biologic processes connected alongside aging.

Michael Corley, Ph.D.

In a connected aviator study published in npj Aging final month, Corley and another squad of researchers established that taking semaglutide for 24 weeks:

  • Reduced the charge of biologic aging for 42% of participants alongside HIV and metabolic dysfunction-associated steatotic liver sickness (MASLD) — additionally known as fatty liver sickness — as measured by the DunedinPACE epigenetic clock. Those participants additionally had a greater decrease in liver fat compared alongside participants whose gait of aging sped up.

  • Slowed aging connected alongside the hazard of all‑cause mortality in 34% of participants as measured by the PCGrimAge epigenetic clock.

  • Increased the dimension of telomeres — repetitive DNA sequences at the ends of chromosomes that defend familial matter — in nearly 49 % of participants as measured by the PCDNAmTL epigenetic clock. Those participants additionally tended to stroll faster following treatment, suggesting improved bodily function.

Together, these studies add to expanding evidence that GLP-1 narcotics may power pathways engaged in biologic aging.

“We are not saying that semaglutide reverses aging or makes group younger,” stated Corley. “What we are seeing is a indication that it may dilatory several of the biologic processes connected alongside aging. With newer GLP-1–based therapies now emerging, the site has an chance to test whether distinct narcotics in this category have distinct effects on aging existence discipline and to acknowledge which patients may advantage most.”

Larger medicinal trials are needed to verify the findings, decide how lengthy care effects last, and established optimal dosing and care duration for the two group alongside HIV and the broader population. Future studies volition additionally be needed to test whether the effects of GLP-1 effects on aging existence discipline are enhanced whenever blended alongside manner interventions specified as diet, exercise and sleep optimization.

The Stein Institute for Research on Aging plans to translate these results into individualized “aging dashboards” to track biologic aging alongside epigenetic clocks, enabling clinicians to scheme personalized therapies that mark the underlying mechanisms of aging and assistance forestall age‑related diseases.

Additional co-authors on the Nature Communications study include: Alina P. S. Pang at UC San Diego;  Varun Dwaraka and Ryan Smith at TruDiagnostic; Danielle Labbato and Grace A. McComsey at University Hospitals Cleveland Medical Center; Allison Ross Eckard at the Medical University of South Carolina; and Grace A. McComsey at Case Western Reserve University. The study was funded, in part, by the National Institutes of Health (grants P30 AI036214, R01DK121619 and UM1TR004528) and the James B. Pendleton Charitable Trust.

Additional co-authors on the npj Aging study include: Alina P. S. Pang at UC San Diego; Douglas W. Kitch and Amy Kantor at Harvard T.H. Chan School of Public Health; Fred Sattler at University of Southern California Keck School of Medicine; Pablo F. Belaunzaran‑Zamudio at the National Institute of Allergy and Infectious Diseases. Todd T. Brown at Johns Hopkins University School of Medicine; Alan Landay at the University of Texas Medical Branch; Jordan E. Lake at UTHealth Houston; and Kristine M. Erlandson at University of Colorado Anschutz Medical Campus. The study was funded, in part, by the National Institutes of Health (grants P30 AI036214, UM1 AI068634, UM1 AI068636, UM1 AI106701) and the James B. Pendleton Charitable Trust.

Corley serves as a specialized adviser for TruDiagnostic.

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