"This raises the intriguing possibility that exposure to cold air - or pharmacological stimulation of the cold-sensitive genetic programme - may promote longevity in mammals," said researcher Shawn Xu from University of Michigan Life Sciences Institute.
Researchers have known for nearly a century that cold-blooded animals, such as worms, flies and fish all live longer in cold environments, but have not known exactly why.
They assumed that animals live longer in cold environments because of a passive thermodynamic process, reasoning that low temperatures reduce the rate of chemical reactions and thereby slow the rate of ageing.
"But now, at least in roundworms, the extended lifespan observed at low temperature cannot be simply explained by a reduced rate of chemical reactions. It's, in fact, an active process that is regulated by genes," Xu said in a statement. Xu found that cold air activates a receptor known as the TRPA1 channel, found in nerve and fat cells in nematodes, and TRPA1 then passes calcium into cells.
The resulting chain of signalling ultimately reaches DAF-16/FOXO, a gene associated with longevity. Mutant worms that lacked TRPA1 had shorter life spans at lower temperatures.
Since the mechanisms identified by Xu and his collaborators also exist in a range of other organisms, including humans, the research suggests that a similar effect might be possible.
The study also linked calcium signalling to longevity for the first time and makes a novel connection between fat tissue and temperature response.
Researchers have known that lowering the core body temperature of warm-blooded animals, such as mice, can extend lifespan by 20 per cent, but it hasn't been practical for humans to attempt to lower the core body temperature, Xu said.
"But if some aspects of the ageing process are initiated in skin and fat cells in humans as they are in nematodes, should we go out to embrace some cold air in the winter?" Xu said.
The study was published in the journal Cell.
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