Coffee doesn’t just perk up your brain, it might be flipping important switches inside your cells, too. While known for boosting alertness and offering some health perks, caffeine also tinkers with cellular behavior.
One key player it may influence is TORC1, a kind of biological traffic light signal that tells cells, “grow now!” or “hold off,” depending on energy and nutrient levels. This signal has been controlling energy and stress responses in living things for over 500 million years.
Some studies suggest caffeine can slow down this growth signal, possibly explaining its link to longer cell life. But here’s the mystery: it’s still unknown if caffeine hits the brakes directly on TORC1 or if it gets there through backroads.
A recent study from the Cellular Ageing and Senescence laboratory at Queen Mary University of London’s Centre for Molecular Cell Biology found that caffeine doesn’t directly shut down TORC1 (the cellular growth switch) as once thought. Instead, it activates AMPK, an ancient cellular fuel sensor that’s like a biological battery meter, conserved from yeast to humans.
AMPK gets switched on when cells sense low energy. When caffeine flips this switch, AMPK naturally dials down TORC1, slowing growth and potentially promoting longevity.
Metformin, a widely used drug for type 2 diabetes, activates AMPK, helping cells improve their energy balance. It's being explored for life-extending effects beyond blood sugar control.
Scientists used yeast (a favorite model for studying cells) to discover how caffeine affects AMPK. In cells with mutations in the AMPK pathway, caffeine seems to increase sensitivity to DNA damage, but not because of its effects on cell division (mitosis), as you might expect. Instead, the researchers found that caffeine works together with other DNA-damaging agents to make this effect stronger.
Interestingly, caffeine also speeds up how quickly cells divide and helps extend their lifespan (known as chronological lifespan, or CLS), and this benefit is linked to the AMPK pathway.
"These findings help explain why caffeine might be beneficial for health and longevity," says John-Patrick Alao, the postdoctoral research scientist leading this study. "And they open up exciting possibilities for future research into how we might trigger these effects more directly – with diet, lifestyle, or new medicines."
"Direct pharmacological targeting of AMPK may serve towards healthspan and lifespan benefits beyond yeasts, given the highly conserved nature of this key regulatory cellular energy sensor,” the researchers add.
The study is published in the journal Microbial Cell.
Source: Queen Mary University of London