How Caffeine May Influence Cellular Aging

A study from the Cellular Ageing and Senescence laboratory at Queen Mary University of London’s Centre for Molecular Cell Biology explores how caffeine may impact the aging process at the cellular level. Published in Microbial Cell, this research investigates caffeine’s effects beyond its well-known role as a stimulant.

Caffeine has been associated with various health benefits, such as a reduced risk of age-related diseases. However, the mechanisms by which it interacts with cellular pathways related to nutrients and stress have remained unclear. To address this, researchers used fission yeast, a single-celled organism that shares key cellular features with human cells.

Previous work by the same team reported that caffeine promotes cell longevity by influencing a growth regulator called TOR (target of rapamycin), which acts as a biological switch controlling cell growth in response to available food and energy. This regulatory system has been present in living organisms for over 500 million years.

The latest findings reveal that caffeine does not act directly on TOR. Instead, it activates AMPK, a cellular energy sensor that is conserved in both yeast and humans. Charalampos (Babis) Rallis, the study’s senior author, explains, “When your cells are low on energy, AMPK kicks in to help them cope. And our results show that caffeine helps flip that switch.”

AMPK is also known as the target of metformin, a diabetes medication being researched for its possible effects on lifespan, alongside rapamycin. By using their yeast model, the researchers demonstrated that caffeine’s activation of AMPK influences cell growth, DNA repair, and responses to stress—processes closely linked to aging and disease.

“These findings help explain why caffeine might be beneficial for health and longevity,” said first author John-Patrick Alao. “And they open up exciting possibilities for future research into how we might trigger these effects more directly—with diet, lifestyle, or new medicines.”