Can Cold Water Cure Dementia?

If you took part in a polar plunge to clear the cobwebs and ring in the New Year feeling refreshed and ready, you might want to consider adding some more chilly splashes the rest of the year. It might not all be in your head—or maybe that brand-new feeling is in the very cells of your brain itself.

It seems there could be a connection between swimming in cold water and a healthier brain, according to new research led by Giovanna Mallucci, a professor of clinical neurosciences and associate director of the UK Dementia Research Institute at the University of Cambridge. Her team has recently produced some compelling evidence that cold water swimming could slow age-related cognitive decline and maybe even hold the key to a future cure for dementia.

Although the science is still in its infancy, Mallucci and her team have discovered a potentially promising “cold-shock” protein in the blood of winter swimmers who engage in the practice regularly at London’s Parliament Hill Lido, a 60-meter-long, unheated, outdoor pool that’s open year-round. The protein, called RBM3, is also found in hibernating mammals, such as bears and bats.

Inducing a controlled state of hypothermia has a lengthy history in clinical settings and is often used to help people survive and recover from cardiac procedures and head injuries. That’s because it’s long been understood that being cold offers survival advantages to someone facing a traumatic injury or surgery. Why exactly cold helps protect the body isn’t entirely clear.

In terms of brain health, we know that when the body is cool, that can slow destruction of cells and protect synapses, the connection points between brain cells that transfer chemicals and electrical impulses. Healthy synapses are critical to keeping your brain firing, thinking, and functioning as it should.

In the earliest stages of neurodegenerative diseases such as Alzheimer’s and other forms of dementia, however, the synapses become damaged and connections between brain cells become less reliable. This can trigger a series of symptoms starting with memory loss, confusion, and mood swings. Over time, the brain continues to deteriorate, ultimately resulting in death.

The odd thing is that those synaptic connections are also lost when hibernating animals take their long winter’s nap. Research has shown that about 20 percent to 30 percent of animals’ synapses shut down as their bodies preserve resources for the long period of inactivity and lack of regular caloric intake.

But when the animal awakens in the spring, the connections reform, and the animal can resume normal brain function. This, after many months of having had a brain state that mimics that of moderate dementia.

Thus, Mallucci and her team decided to investigate what was happening and conducted studies inducing hypothermia in three groups of mice—a healthy group, a group with Alzheimer’s disease, and another group with a neurodegenerative prion disease.

After rewarming the mice, the researchers found that only the healthy mice could regenerate synapses. The mice with Alzheimer’s and prion disease could not. They also noted that levels of RBM3 were very high in the healthy mice, but not in the other two groups, which suggested that RBM3 was the key to regenerating synapses. A subsequent experiment, published in the journal Nature, more clearly demonstrated that boosting RBM3 levels in mice could prevent brain cell death.

This spurred the researchers to move toward trying to develop a drug that could promote production of RBM3 to slow or possibly even reverse progression of neurogenerative diseases in humans. The first step was to find out whether humans—mammals that don’t hibernate—even had RBM3 to begin with. But medical ethics prevented the team from developing a study that would induce hypothermia in people.

However, it turns out there’s already a group of people who are regularly doing that to themselves in the name of fun, fitness, and swimming all across Britain. And thus, Mallucci and her team had found some willing test subjects at the local lido.

Over the winters of 2016, 2017, and 2018, the researchers tested a group of winter swimmers for RBM3. Members of a tai chi club that practice near the pool but don’t swim in the cold water served as the control group. After three seasons, the results were clear—the winter swimmers had significantly higher levels of RBM3 than the tai chi group.

Although there’s no definitive answer yet as to whether regularly inducing a reduced body temperature or hypothermia can actually stave off neurodegenerative decline, there seems to be a clear connection between swimming in cold water and higher levels of protective RBM3. Work continues to determine the exact mechanisms at play, how much cold-water swimming or hypothermia one must endure to achieve benefits, and whether the protein can be synthesized into a game-changing drug that could be administered to people without the risks cold water swimming can carry.

In the meanwhile, if you’re a winter swimmer, enjoy your swims. If you’re curious, reach out to a veteran to learn the ropes for safe cold-water swimming. It might just do wonders for your brain.