Metformin: this old diabetes drug could become the anti-aging “wonder drug”

Metformin: this old diabetes drug could become the anti-aging “wonder drug”
Prescribed against type 2 diabetes, metformin could slow certain markers of aging. In animals, some results are spectacular. In humans, the signals are encouraging, but proof of a real effect remains to be established.

What if a drug that we have known for more than 70 years could also act on certain aging mechanisms? This is the hypothesis that is pushing more and more researchers to take an interest in metformin.

A new review published in August 2026 in Aging
reviews the available data. They paint an attractive scenario: the molecule could act on several mechanisms involved in aging. But between slowing down certain cellular processes and actually extending years of healthy life, there is still an important step to take.

A molecule that acts at the heart of aging mechanisms

Metformin has been used since the 1950s to treat type 2 diabetes. Its interest in aging is based in particular on its ability to modify the energetic functioning of cells.

In particular, it inhibits complex I of mitochondria, which reduces ATP production and activates an enzyme called AMPK. The latter participates in the regulation of cellular energy. Metformin also reduces the production of glucose by the liver, improves insulin sensitivity and inhibits the mTOR pathway.

Another effect studied: the activation of autophagy, a mechanism allowing cells to degrade and recycle certain damaged components. The molecule could also promote mitochondrial biogenesis and reduce oxidative stress.

In other words, metformin would not target a single aging mechanism, but several at the same time.

In animals, the results make you want to believe it

The results obtained in animals partly explain the enthusiasm around the molecule.

At the house of Caenorhabditis elegansa small worm widely used in aging research, metformin has been associated with an increase in the lifespan of 36 to 40%. In mice, studies report more modest extensions of 5.8 to 20.1%as well as a delay in the appearance of certain cancers.

In male cynomolgus macaques treated for 40 months, biological markers even suggested a form of “rejuvenation” of the biological age of the brain, estimated at around six years.

But these results do not allow us to conclude that metformin slows down human aging. The effects observed in animals do not automatically translate to our species.

In humans, the signal is there… but the verdict is still missing

Some observational studies have suggested that people with diabetes taking metformin may live longer than those receiving other treatments. One analysis notably estimated a gain of 15% median survival. But other work has not confirmed this association.

The molecule also appears to influence certain epigenetic markers. In a study of 32 patients, it was associated with a lower biological age of 2.77 to 3.43 years according to several epigenetic “clocks”.

These results are intriguing, but they do not demonstrate that metformin actually slows aging or increases healthy lifespan.

The intestinal microbiota could also play a role, the molecule appearing to modify the composition of intestinal bacteria and the production of certain short-chain fatty acids.

A promising avenue, not yet an anti-aging treatment

This is the difficulty of this research: demonstrating that a drug modifies biological markers is one thing; proving that it allows you to stay healthy longer is another.

In particular, the TAME trial seeks to determine whether metformin can delay several age-related diseases. But the available data remains insufficient to recommend the molecule as a preventive treatment for aging in people who do not have diabetes.

The MeMeMe trial, carried out on more than 1,400 people aged 50 to 79 with metabolic syndrome, showed a reduction in the incidence of type 2 diabetes. On the other hand, it did not demonstrate any preventive benefit on cancers, cardiovascular diseases or mortality.

Metformin is also not without risks. In particular, it can lead to vitamin B12 deficiency and, much more rarely, serious lactic acidosis, particularly when kidney function is impaired.

For researchers, the next steps therefore consist of determining what dose to use, for how long, at what age to start treatment and in which people.

The prospect nevertheless remains fascinating enough to arouse the enthusiasm of the authors of the review. According to them, “By combining clinical, molecular and population data, metformin could be the miracle drug that redefines the boundaries of healthy aging.”.

An attractive formula. But for now, metformin remains primarily a diabetes medication, not a pill that can make us younger.