Ozempic really could turn back the clock on your biological age

The type 2 diabetes drug Ozempic has been linked to slower rates of ageing, and now we have good-quality evidence that this really does occur.

GLP-1 drugs like Ozempic and Wegovy, both of which contain the medication semaglutide, have gained huge prominence for their effects on obesity, but are also being explored for conditions such as cardiovascular disease, addiction and dementia.

Scientists have previously suggested that they might delay biological ageing – the rate at which cells age – largely based on animal studies and observational human data. Now, we have the first clinical trial results providing direct evidence of that, says Varun Dwaraka at diagnostics company TruDiagnostic in Lexington, Kentucky.

One way to assess a drug’s effect on biological ageing is through epigenetic clocks. These identify patterns of DNA methylation, the chemical tags added or removed from DNA that affect gene activity. These patterns shift with age and can be sped up or down by lifestyle choices, such as our diet, meaning our biological age can be younger or older than our chronological age.

Dwaraka and his colleagues studied the epigenetic clocks of 108 people with HIV-associated lipohypertrophy, a condition that causes excess fat and accelerated cellular ageing. In a randomised-controlled trial, half were given Ozempic once a week for 32 weeks and the other half a placebo.

Using blood taken before and after the trial, the team identified the biological age of 84 of these individuals. “Those on semaglutide became, on average, 3.1 years biologically younger by the end of the study,” says Dwaraka. Those in the placebo group showed no significant change. “Semaglutide may not only slow the rate of ageing, but in some individuals partially reverse it,” he says.

The researchers also found biological ageing was slowed in several organs and systems, including the heart and kidneys, with the most pronounced effects seen in the inflammatory system and brain – where the drug appeared to delay biological ageing by almost 5 years.

Dwaraka believes the effects stem from semaglutide’s influence on fat distribution and metabolic health. Excess fat around organs can trigger the release of pro-ageing molecules, which alter DNA methylation in key ageing-related genes. Semaglutide also prevents low-grade inflammation, another driver of epigenetic ageing.

Although the results were in people with HIV-associated lipohypertrophy, many of the biological pathways affected by semaglutide weren’t specific to HIV pathology. “Therefore, it is plausible that similar effects on epigenetic ageing could be observed in other populations,” says Dwaraka.

It is unsurprising that ageing is slowed by these drugs, says Randy Seeley at the University of Michigan Medical School, since they reduce the metabolic burden on a wide range of cells and lower inflammation. “Both are major drivers of ageing in many different types of cells.” However, he believes much of this benefit stems not from semaglutide’s direct effect on cells, but from broader improvements to overall health.

Whether we should all be taking semaglutide to stay biologically younger remains to be seen. “Prescribing it more broadly as an anti-ageing therapy is premature,” says Dwaraka. But he says this study adds momentum to ongoing efforts to repurpose existing drugs for age-related problems, which speeds up approval processes and reduces the risk of unexpected side effects. “Semaglutide may well emerge as one of the most promising candidates in this space,” says Dwaraka.