Ozempic really could turn back the clock on your biological age

Type 2 ozempic was linked to slower aging rates, and now we have good quality evidence that it really happens.

GLP-1 drugs such as Ozempic and Wegovy, which both contain the semaglutide of drugs, have acquired great importance for their effects on obesity, but are also explored for conditions such as cardiovascular disease, dependence and dementia.

Scientists previously suggested that they could delay biological aging – the speed at which cells age – largely based on animal studies and observational human data. Now we have the first results of clinical trials providing direct evidence of this, explains Varun Dwaraka in the Trudiagnostic diagnostic company in Lexington, Kentucky.

One way to assess the effect of a drug on organic aging consists of epigenetic clocks. These identify DNA methylation models, chemical labels added or removed from DNA that affect gene activity. These models move with age and can be accelerated or lowered by lifestyle choices, such as our diet, which means that our biological age can be younger or older than our chronological age.

Dwaraka and his colleagues studied the epigenetic clocks of 108 people with lipohypertrophy associated with HIV, a condition that causes excess fat and accelerated cell aging. In a randomized controlled trial, half received the ozempic once a week for 32 weeks and the other half of a placebo.

Using blood taken before and after the trial, the team identified the biological age of 84 years of these individuals. “Those of Sémaglutide became, on average, 3.1 years biologically younger at the end of the study,” explains Dwaraka. Those of the placebo group have shown no significant change. “The semaglutide can not only slow down the aging rate, but in some people partially,” he said.

Researchers also found that biological aging had been slowed down in several organs and systems, including the heart and kidneys, with the most pronounced effects observed in the inflammatory system and the brain – where the drug seemed to delay biological aging of almost 5 years.

Dwaraka believes that the effects arise from the influence of the semaglutide on the distribution of fats and metabolic health. An excess of fat around the organs can trigger the release of pro-aging molecules, which modify the methylation of DNA in key genes linked to age. The semaglutide also prevents inflammation of low grade, another engine of epigenetic aging.

Although the results were in people with lipohypertrophy associated with HIV, many biological paths affected by the semaglutide were not specific to the pathology of HIV. “Consequently, it is plausible that similar effects on epigenetic aging can be observed in other populations,” explains Dwaraka.

It is not surprising that aging is slowed down by these drugs, explains Randy Seeley at the Faculty of Medicine of the University of Michigan, because they reduce the metabolic load on a wide range of cells and lower inflammation. “The two are the main engines of aging in many different types of cells.” However, he thinks that a large part of this advantage does not result from the direct effect of semaglutide on cells, but from the broader improvement in overall health.

It remains to be seen if we must all take semaglutide to remain biologically younger. “Prescribe it more widely as anti-aging therapy is premature,” explains Dwaraka. But he says that this study adds momentum to continuous efforts to reuse existing drugs for age -related problems, which accelerates approval processes and reduces the risk of unexpected side effects. “The semaglutide may well become one of the most promising candidates in this space,” says Dwaraka.