Could GLP-1 drugs become the first longevity medications? Scientists think it’s possible

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For years, billionaire biohackers and longevity entrepreneurs have promoted the idea that an “anti-aging drug” could slow — or even reverse — aging, often promising results well beyond what science supports. 

But behind the hype, researchers in the burgeoning field of geroscience — which seeks to understand the biology of aging — have been investigating whether GLP-1 drugs like Ozempic and Zepbound do more than treat obesity and diabetes. Although experts caution the research is still in its infancy, a growing body of evidence suggests these weight-loss drugs may slow biological aging. Now, a new study conducted in humans offers promising results. 

Nir Barzilai, a geroscientist and professor of genetics and medicine at the Albert Einstein College of Medicine, said GLP-1 drugs are among a handful of medications that appear to influence the “hallmarks of aging,” making them promising candidates for longevity therapy. 

“We have promising evidence today,” said Daniel Belsky, an associate professor of epidemiology at Columbia University’s Aging Center. “We’ll have more rigorous evidence in a few years, and then you know, perhaps within the next five to 10 years, we’ll actually have the capacity to say definitively yes, this drug is intervening on the biology of aging in a way that is going to give us a more healthy lifespan.”

There are currently no FDA-approved longevity drugs, in part because the agency does not recognize aging as a disease. Instead, physicians, including Barzilai, prescribe medications approved for specific conditions that may also have broader effects on aging. At the same time,  the federal government has invested millions of dollars through programs like the National Institute on Aging and the Advanced Research Projects Agency for Health to discover drugs that target the biology of aging. Some geroscientists say GLP-1 drugs have emerged as one of the most promising candidates yet — raising the possibility that medicine may be approaching its first gerotherapeutic. 

The golden age of aging 

Over the past two decades, scientists have transformed the study of aging. Advances in genetics, molecular biology and biotechnology have given researchers new tools to understand why we age and to measure the mechanisms driving the process. Rather than viewing aging as an inevitable part of life, many geroscientists now see it as a condition that could one day be slowed or modified, much like other diseases. 

The field has sometimes been overshadowed by outlandish claims promising dramatic life extension, but researchers say that misses the point. 

“Aging and interventions on aging have a certain kind of biohacker flavor. That’s not at all what the real science of aging is about,” Belsky said. “Ultimately, this is a field organized around the idea that we can deliver additional years of healthy life to the average person. Nobody’s trying to make anyone live forever. Nobody’s trying to make older people young again.”

Rather than extending life indefinitely, geroscientists are focused on delaying the biological changes that give rise to chronic diseases and disability. Instead of treating heart disease, cancer, Alzheimer’s disease and other age-related conditions as separate problems, geroscientists argue they are linked by common biological processes, including chronic inflammation, impaired cellular repair, metabolic dysfunction and the accumulation of damaged cells. Researchers refer to these shared processes as the hallmarks of aging and believe drugs capable of modifying several of them could delay multiple diseases simultaneously instead of treating them one at a time. 

“There are ways of doing that that appear within reach that would be affordable to scale and deliver across the population,” Belsky said.

What is a longevity drug? 

Researchers use several benchmarks to determine whether a medication qualifies as a potential longevity drug, or gerotherapeutic, Barzilai explained. 

First, they look for evidence that a drug acts on the biological processes that drive aging, such as inflammation, metabolism or the body’s ability to repair and recycle damaged cells. Next, scientists investigate whether those changes translate into healthier, longer lives in animal studies. Finally, geroscientists look for evidence in people that a drug developed for one condition also reduces the risk of other diseases and, ideally, lowers overall mortality. 

So far, GLP-1 drugs seem to satisfy each of those requirements. 

An analysis of three large weight-loss trials revealed that people taking GLP-1s had 39% to 48% reductions in C-reactive protein, a marker of inflammation, suggesting the drugs might have anti-inflammatory properties. Other studies have found that GLP-1s enhance cell survival, promote tissue regeneration and reduce stem cell death.

Scientists believe some of those benefits result from weight and fat loss, but Barzilai said that cannot fully explain the drugs’ effects. 

“When you analyze the data, we think that the effects through weight loss are maybe a third or half,” Barzilai said. “They’re independent of effects that work mainly through the biology of aging, and that’s why they’ve been so important for us.”

Evidence from animal studies, while still limited, points in the same direction. Researchers at Novo Nordisk, the pharmaceutical company that makes Wegovy and Ozempic, reported that mice treated with a GLP-1 drug lived about 20% longer than mice of the same weight and caloric intake. This suggests that the survival benefit could not be explained by weight loss alone, Barzilai said.

More recently, independent researchers also reported that a GLP-1 drug reversed age-related molecular changes across multiple organs in aging mice and improved several measures of physical function, even at doses that produced little change in body weight. 

The most compelling evidence comes from human clinical trials. In one landmark trial that followed more than 17,000 people for more than six years, GLP-1 drugs reduced the risk of heart attack, stroke and cardiovascular death by 20% among adults with overweight or obesity and cardiovascular disease. Participants taking GLP-1s were also 19% less likely to die from any cause during nearly 40 months of follow-up. Other large clinical trials have found the drugs reduce the risk of chronic kidney disease progression and improve outcomes in several other age-related conditions, suggesting their benefits extend well beyond diabetes and weight loss. 

“When it comes to clinical study, you have to show that a drug that was designed for one thing also has effects on other diseases that seem not connected  and also has an effect on overall mortality, not a disease-specific mortality,” said Barzilai. “That’s what we’re showing with GLP-1 agonists again and again and again.”

Slowing aging

Until recently, much of the evidence that GLP-1 drugs influenced aging came indirectly, by measuring improvements in various diseases and biological pathways associated with aging. A new study in people with HIV offered one of the first opportunities to measure whether the drugs appear to slow biological aging itself. 

A group of researchers from institutions across the U.S. conducted a 32-week clinical trial involving 84 adults with HIV and lipohypertrophy, a common condition where fat deposits form under the skin. Participants were randomly assigned to receive either a drug or a placebo, and neither they nor the researchers knew who received which until after the study.

This type of study — a randomized, double-blind, placebo-controlled trial — is considered the gold standard for testing new treatments.  

Researchers chose people living with HIV because the infection is associated with accelerated biological aging. On average, their biological age is about 10 years older than that of people the same chronological age who do not have HIV, according to Barzilai.

Compared with participants who received a placebo, those treated with GLP-1s showed slower biological aging as measured by “epigenetic clocks”  — research tools that analyze chemical changes to DNA to estimate a person’s biological age or the pace at which their body is aging.

“It’s like a speedometer for your own personal rate of aging,” said Belsky, who helped develop several epigenetic clocks. Epigenetic clocks are well validated as research tools and have consistently been shown to predict how many healthy years people are likely to live, as well as their risk of chronic disease, disability and death. Still, Belsky said scientists will need decades-long studies to prove whether changing these biomarkers through an intervention will ultimately translate into longer, healthier lives.

Even with those limitations, epigenetic clocks remain the best tools scientists have for measuring biological age and the pace of aging in humans. 

In the HIV trial, treatment with weight-loss drugs slowed the rate of biological aging by about 9% compared with the placebo. Belsky said the finding suggests that instead of accumulating one year of biological aging for every calendar year, participants appeared to be aging at roughly 90% of the usual pace.

“If you were able to maintain that slow pace of aging over a decade, it would deliver an additional year of health span,” Belsky explained. 

Barzilai explained the research findings in a different way: “If I’m 70 years old now and half of the people die at age 80 and I’m now 9% younger, I’m 63. That means my mortality is now 17 years and not 10 years away,” he said.

Belsky, Barzilai and other geroscientists said they were encouraged by the trial’s results. Barzilai called the study an important milestone because it began measuring the outcome geroscientists ultimately care about: whether a treatment can slow biological aging in humans. 

Still, researchers cautioned against overinterpreting the findings. The trial enrolled just 84 participants, followed them for a short time, and only included people living with HIV. 

“One way of looking at this result is: Here’s an especially challenging setting in which to move the needle on human aging, and isn’t it impressive that this drug has achieved it?” Belsky said. “On the other hand, you might think there are very particular ways in which this disease is affecting biology and physiology that the drug is addressing, and therefore its effect that we observe in this setting may not translate into a healthy patient setting.” 

Little evidence currently exists on whether GLP-1 drugs slow biological aging in people who are metabolically healthy or who do not have obesity, diabetes or another underlying condition. Researchers say larger, longer studies in broader populations are also needed to determine whether the changes captured by epigenetic clocks translate into more years of healthy life.

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