London in the wintertime is a place for woolly sweaters and mugs of hot tea, yet those brave enough to take a dip in one of the city’s outdoor swimming spots may be rewarded with certain neurological benefits. According to as yet unpublished research conducted by a team of scientists from Cambridge University, Londoners who regularly swim outdoors during the winter have elevated levels of a protein that plays a key role in the formation of brain connections.
What makes this finding significant is that the protein in question has been found to help protect the brain against neurodegenerative diseases like Alzheimer’s in old age, and could therefore be used to stave off dementia.
The work was presented by Professor Giovanna Mallucci, Associate Director of the UK Dementia Research Institute at the University of Cambridge, in an online lecture, but has not yet been published in a scientific journal.
Throughout a person’s lifetime, their brain continuously rewires itself by culling some connections – known as synapses – and forming new ones. However, a loss of the ability to create new synapses results in an overall loss of brain connections, leading to the sort of cognitive decline experienced by dementia sufferers.
Researchers have known for some time that this process can be influenced by temperature, as hibernating mammals experience a significant loss of synapses when they enter their annual slumber, yet immediately regain these connections when they awake in spring.
A few years ago, a paper published in the journal Nature revealed that this effect is mediated by a “cold shock” protein in the brain called RBM3. The study authors exposed regular mice as well as those that had been bred to develop dementia to freezing temperatures, and found that this caused both groups to experience a loss of synapses as they became hypothermic.
When the rodents were warmed up, levels of RBM3 skyrocketed in the healthy mice, resulting in a restoration of these lost synapses. The same did not occur in the rodents with dementia, though, as insufficient RBM3 was generated and the lost brain connections were therefore not replaced.
These results were then compounded when the study authors artificially induced the formation of RBM3 in the brains of these mice, which caused synapses to reform at the same rate as in healthy mice.
To investigate whether this cold shock chemical plays a similar role in humans, the same researchers measured RBM3 levels in the blood of a group of outdoor swimming enthusiasts who regularly bathed in London’s Parliament Hill Lido during three consecutive winters. Importantly, all of these swimmers became hypothermic during their chilly dips.
Compared to a control group of non-swimmers, the cold water bathers displayed significantly higher levels of RBM3 in their blood, suggesting that hypothermic conditions do indeed trigger the release of this key synapse builder in humans.
While this is clearly very exciting, this is yet to be peer-reviewed research, so it’s far too early to say whether or not swimming in cold water really does protect against dementia. It’s also important to remember that entering icy water and becoming hypothermic can be extremely dangerous.
According to BBC News, the scientists behind this research are keen to stress that older people should not take to outdoor swimming in winter. Instead, they are working on developing new drugs that can stimulate RBM3 production in the brain without requiring anyone to get wet.