Can a diabetes medication slow down agin

The mechanism of action of the drug is based on a kind of deception of the cell: metformin creates an illusion of energy deficiency for it — a state similar to what occurs during fasting or calorie restriction. This triggers the activation of AMPK — a key sensor of cellular energy. As a result, the cell activates processes for clearing damaged components, known as autophagy, as well as repair support mechanisms. Thus, the effect of metformin goes beyond simple glucose level correction and affects the basic mechanisms underlying many age‑related changes.

The effectiveness of metformin in the context of aging has been studied in various model organisms, and the results have proved promising. On microscopic C. elegans worms, the drug increased life expectancy by 36-40% due to a condition similar to calorie restriction. In experiments on mice, the average life expectancy increased by 5.8–20.1%, while slowing the appearance of some tumors was also observed. In monkeys, after 40 months of taking the drug, tissues became biologically younger, and the brain showed signs of rejuvenation equivalent to about 6 years, which, by human standards, is comparable to 18 years. Observational studies in humans show that patients taking metformin may have a biological age up to 3.43 years younger, and people with diabetes who received the drug lived up to 15 % longer compared to their peers without diabetes.

In addition to its effect on carbohydrate metabolism, metformin affects several key processes closely linked to aging. It stimulates autophagy and maintains genome stability, helping the cell get rid of accumulated debris and preserve DNA integrity. The effect on epigenetic mechanisms also plays an important role: metformin stabilizes the TET2 enzyme, which is involved in regulating DNA methylation.

Since methylation patterns change with age and this directly affects gene function, the drug’s ability to maintain a more youthful gene regulation profile looks particularly promising. Furthermore, metformin affects the gut microbiome — it promotes the growth of beneficial bacteria that protect the mucous membrane and increases the production of short‑chain fatty acids. This effect may help reduce systemic age‑related inflammation, which is considered one of the main drivers of aging.

The idea of targeting not individual age‑related diseases but the general mechanisms of aging formed the basis of the scientific field of geroscience. In this context, metformin is particularly interesting because it simultaneously affects many fundamental processes associated with aging and has the potential to delay the development of several chronic diseases at once. Nevertheless, the available evidence cannot yet be considered conclusive.

The results of studies on cells, animals, and humans often contradict each other. Most of the data on humans were obtained through observational studies, where it is difficult to separate the effect of the drug itself from the influence of diabetes and its comprehensive treatment. Moreover, one of the well‑known studies linking metformin use to improved survival was later criticized due to the inability to reproduce its results.

Today, the main gap in the science of longevity is the lack of large‑scale, rigorous studies of metformin in healthy adult individuals without diabetes. This task is intended to be addressed by the TAME project (Targeting Aging with Metformin), the goal of which is to test whether the drug can delay the onset of several age‑related chronic diseases in humans. If the results of this study are convincing, they could become an important step towards recognizing approaches aimed at slowing down the aging process itself.