Do Weight-Loss Drugs Slow Biological Ageing? Early Studies Show Promise, But Experts Urge Caution

At a conference on ageing research and drug discovery, two of the world's biggest drugmakers presented findings that pushed a familiar class of medicines into new territory. Eli Lilly and Novo Nordisk reported that people taking GLP-1 drugs, widely prescribed for diabetes and weight loss, scored lower on measures of biological age than people given a placebo.

The measures are known as ageing clocks. They estimate how old the body appears at a molecular level, either by tracking chemical changes to DNA or by measuring levels of certain proteins. Biological age is distinct from chronological age, which simply counts the years a person has lived. The clocks try to gauge how old cells, tissues or organs look based on those molecular signals. Some read DNA methylation, while newer versions measure proteins linked to ageing, disease and mortality.

Novo Nordisk's work was the larger of the two. The company analysed blood samples from more than 10,000 people taking either semaglutide or a placebo, using protein-based clocks. It reported that several measures pointed toward slower biological ageing in those receiving the drug. Some of the differences appeared across different tissues and organs.

Eli Lilly ran a smaller study of people taking tirzepatide, using epigenetic clocks that look at chemical modifications to DNA. Its results also suggested that molecular ageing slowed during treatment.

The gaps were modest in absolute terms but striking as headlines. Novo Nordisk said the difference in biological age was generally around two to three years, and a clock built on heart-related proteins showed a gap of as much as four years.

Experts, though, are urging restraint. Dr Ashish Gautam, Principal Director of Robotic and Laparoscopic Surgery at Max Super Speciality Hospital in Patparganj, New Delhi, told NDTV that calling these drugs a way to slow biological ageing is premature. In his words, a biological-age clock is a surrogate measure. A change in it does not establish that someone is ageing more slowly, will live longer or will stay healthier for longer, and he said the long-term human evidence needed to link the two is still lacking.

He also separated weight loss from healthy ageing. GLP-1 medicines can produce substantial weight loss, but part of what is lost can be lean muscle. That matters especially for older adults, who are already prone to sarcopenia, frailty and declining physical function. Preserving muscle, Dr Gautam said, should be central to any weight-management plan, which means looking at body composition and physical function rather than only the number on the scale.

The drugs carry risks too. Dr Gautam pointed to recognised adverse effects including gastrointestinal problems, gallbladder disease and, in some patients, pancreatitis. He raised the question of whether benefits are being overstated as the drugs are used for weight loss outside clearly defined medical indications.

None of this undercuts what the drugs are known to do. They are established treatments for type 2 diabetes and obesity, with demonstrated benefits for several metabolic and cardiovascular outcomes. But Dr Gautam argued those benefits should not be relabelled as evidence of anti-ageing effects. Until long-term studies show the drugs reduce age-related disease, preserve physical function and improve healthy life expectancy, he said, calling them anti-ageing drugs is not scientifically justified. That long-term evidence is what to watch for next.