GLP-1 drugs such as semaglutide — the active ingredient in Ozempic and Wegovy — may slow biological aging, a new study suggests. Researchers at the University of California at San Diego found that the medicines appear to reprogramme cells, boosting immune health and reducing inflammation at a level that could delay the body’s decline.
The findings, published this week in Nature Communications, come from a 32-week randomised, double-blind, placebo-controlled trial involving more than 100 adults living with HIV. All participants had excess fat due to a condition called lipohypertrophy, which is common among people receiving injections and develops as a result of inflammation. Some also had metabolic dysfunction-associated steatotic liver disease (MASLD), another condition frequently seen in people with HIV.
Twenty-four weeks into the trial, the UC San Diego team observed that semaglutide slowed the pace of biological aging for 42 percent of participants who had both HIV and steatotic liver disease. Using an epigenetic clock known as DunedinPACE, which measures DNA methylation patterns to estimate biological age, the drug produced a 9 percent reduction in the speed of aging. A second clock, PCGrimAge, showed that the drug also significantly slowed biological processes linked to the risk of all-cause mortality and age-related disease.
“We are not saying that semaglutide reverses aging or makes people younger,” said Michael Corley, an associate professor of medicine at UC San Diego, in a statement. “What we are seeing is a signal that it may slow some of the biological processes associated with aging.”
The scientists stressed that the effects were observed in people with HIV, a population that often experiences accelerated aging even when viral loads are well controlled, due to persistent inflammation and immune activation. “Many of the biological processes we study in HIV are also central to aging in the general population,” Corley added. “Because these processes can emerge earlier or be more pronounced in people with HIV, this community can help us identify interventions that may improve healthspan more broadly.”
How GLP-1s act at the cellular level
The central mechanism behind the apparent slowing of biological aging appears to be a reduction in chronic inflammation and metabolic stress. Inflammation is the body’s natural response to injury and infection, but when it persists it can damage organs and tissue and accelerate cellular aging. GLP-1 drugs help people shed excess fat — particularly visceral and ectopic fat around organs — which itself can trigger inflammatory signals. By reducing that fat load, the drugs may quiet the inflammatory cascade that drives aging at a cellular level.
UC San Diego explained that GLP-1 drugs also appear to reprogramme cells in various organs. Past research from the University of Colorado at Boulder Anschutz had already shown that GLP-1s can boost the body’s immune response by reprogramming cells. Corley noted that similar cellular reprogramming may be at work in the current study. “Emerging data also suggest that GLP-1 drugs may reprogram certain cells in different organs,” he said.
Beyond fat reduction and immune modulation, the research briefing highlights additional cellular effects identified in previous studies. GLP-1 receptor agonists have been shown to improve mitochondrial function, reduce oxidative stress, and enhance autophagic activity — the process by which cells clear out damaged components. In aged mice, semaglutide reduced cellular senescence, meaning fewer cells entered a state of arrested growth that pumps out inflammatory signals. The drugs also appear to influence epigenetic machinery by reversing aberrant DNA methylation and modulating histone-modifying enzymes.
The net effect, the briefing notes, is a broad systemic improvement. The UC San Diego trial observed positive changes across multiple aging-related measures linked to inflammation, blood, brain, heart, kidney, liver, and metabolic health, suggesting the drugs may act on several organ systems simultaneously.
Broader health benefits already established
The new aging findings add to a growing list of benefits already identified for GLP-1 drugs. Around 30 million Americans are taking them to aid weight loss and to manage conditions such as diabetes and cardiovascular disease. Studies have demonstrated that GLP-1s reduce the risk of major heart events — heart attack, stroke, and cardiovascular death — by roughly 13 to 20 percent. They are approved for treating chronic kidney disease in people with type 2 diabetes, easing pressure within the kidneys and calming inflammation. Emerging research also suggests benefits for brain health, including a lower risk of Alzheimer’s disease and improved cognitive function, likely through the same anti-inflammatory pathways.
For people with HIV, the drugs have shown particular promise in tackling lipohypertrophy and MASLD. The UC San Diego trial specifically investigated semaglutide’s effect on these conditions, and the results indicated that reducing liver fat and improving cardiometabolic parameters may in turn slow aging processes.
Inflammation is also a known risk factor for HIV acquisition. Previous research shows that women who have genital inflammation are at an increased risk of sexual HIV infection, because inflammatory signals recruit immune cells to the genital tract, making it more susceptible to the virus. While this is a separate biological mechanism, it underscores the pervasive role of inflammation in driving disease and aging.
Future research and open questions
The UC San Diego team now plans to conduct larger and longer trials to confirm the findings and to determine how long the drugs can sustain a slower pace of biological aging. Such work could inform optimal dosing and treatment duration for people with HIV and, eventually, for the broader population.
Researchers also want to test whether combining GLP-1s with other proven methods — a healthy diet, regular exercise, and adequate sleep — could enhance the anti-aging effect. “With newer GLP-1–based therapies now emerging, the field has an opportunity to test whether different drugs in this class have distinct effects on aging biology and to identify which patients may benefit most,” said Corley.
One caveat that scientists are careful to emphasise is the potential loss of lean muscle mass, particularly in older adults taking GLP-1s for weight loss. Some studies suggest this risk may be attenuated and that muscle function can even improve, but the question remains an active area of investigation.
The findings build on an earlier pilot study in people with HIV and MASLD, published in npj Aging, which also showed reductions in the pace of biological aging. The current randomised controlled trial provides stronger evidence, yet the researchers acknowledge that much remains unknown. Experts have long known that biological aging can be slowed with good diet, regular exercise, and avoidance of alcohol and drugs; GLP-1s may offer an additional pharmacological lever.
Corley concluded: “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.”