“In sleep we heal” was one of my mother’s favourite sayings: she was convinced a good night’s sleep was the answer to everything thing from a grazed knee to a broken heart. At the age of 91, her mind remained pin sharp while many of her friends drifted off into dementia. It didn’t occur to me to connect the two until I talked to Matthew Walker, the British-born director of the Sleep and Neuroimaging Laboratory at California’s Berkeley University.
My mother’s belief in rest as cure was more than folklore.
The science of sleep has begun to show clear links between lack of sleep and a raft of different ailments – including Alzheimer’s disease. “There really is not a single tissue or organ of the body or process of the mind that doesn’t depend on sleep, and doesn’t implode when you don’t get enough,” says Walker.
Walker’s new book, Why We Sleep: The New Science of Sleep and Dreams, has been among the top ten best-sellers in Britain for nine weeks. It drives home an unwelcome message – that hardly any of us get enough sleep and we’re doing ourselves damage as a result. Sleep has an image problem; rising late or spending lots of time in bed has come to be seen as laziness. Walker meets people all the time who tell him they would like to sleep more but they are just too busy.
In the 1940s, the average British adult was sleeping a little under eight hours a night. Now we make do with 6 hours and 49 minutes. Street lights, electronic devices and cramming family life around long working long hours have conspired to devastate our sleeping and the consequences for a sleep-deprived nation are sobering. He notes that he has always found it curious (in an entirely unscientific way) that both Margaret Thatcher and Ronald Reagan, two world leaders who made a virtue of only sleeping four to five hours a night, both ended up with Alzheimer’s.
We already have more than 850,000 dementia-sufferers in the UK and the Alzheimer’s society estimates that 225,000 people in the UK will develop dementia this year, that’s one every three minutes. Alzheimer’s – named after Aloysius Alzheimer, the German doctor who identified the devastating brain disease in 1901 – is the most common form of dementia, affecting 62% of those diagnosed.
Could sleep offer a way of slowing down the onset of the disease – or help prevent it altogether? Sleep quality generally deteriorates with age, which is linked to a decline in memory and in patients with Alzheimer’s disease the disruption of sleep is far more exaggerated. Walker’s work suggests that sleep and Alzheimer’s could be inextricably linked. “As total sleep has declined across the century, Alzheimer’s rates have increased,” he says.
“Some of that is to do with us living longer but some of it, I believe is to do with us sleeping less. I’m not trying to suggest Alzheimer’s disease is simply a sleep disorder. There are multiple reasons why we develop the disease. Is sleep one of them? Yes.”
Normal, beneficial sleep has two key phases: lighter REM (rapid eye movement) sleep and deeper, non-REM sleep during which our brain produces waves or “spindles” that aid the memory. Information gathered during the day goes into the hippocampus, the short-term memory are of the brain and the deep-sleep spindles essentially hits the save button, moving those information files into long-term storage.
“If you are failing to get sufficient deep sleep you won’t fix those memories in the brain,” he says. “Of course, that may not be a choice. As you get older, your sleep gets worse and it’s especially that deep, non-REM sleep that you lose.”
Walker has been fascinated by dementia ever since he swapped medicine for neuroscience as a student at Nottingham university. He became a sleep researcher almost by accident. His PhD involved a study of the brainwaves of people with differing sorts of dementia and he was frustrated to find them similar.
Then he read a paper describing how some forms of dementia attacked the part of the brain to do with sleep, others did not. He realise he had made a mistake in trying to measure his patients’ brainwaves when they were awake: he allowed them to sleep and discovered there was a clear difference in brain patterns. He wanted to discover whether these varying brainwaves could be an early warning sign of dementia and so, his fledgling sleep laboratory began.
“I would [now] argue that the sleep disruption and memory impairment part of the Alzheimer’s story is increasingly strong, and sleep offers a mechanism for the disease, a possible diagnostic tool, a route for therapy and finally a potential hope for prevention,” he says.
Around six years ago he and his team discovered that beta-amyloid - the sticky, toxic protein which is the hallmark of Alzheimer’s – does not build up all over the brain in a consistent manner, it builds up in specific parts of the brain. The big surprise was that it did not build up at all in the areas of the brain associated with memory, even though loss of memory is most associated with Alzheimer’s.
Instead, they found the protein deposited in the brain region responsible for the generation of deep, non-REM sleep.
In a vicious cycle, the more protein there was in the brain, the less deep sleep the patient had. Which turned out to be critical when Maiken Nedergaard, a fellow sleep scientist working in the US, made a spectacular discovery. Working with mice, she found that there is a network in the brain - known as the glymphatic system – which clears toxins from the brain in the same way the lymphatic system drains toxins from the body.
The fascinating aspect of the discovery for Walker was that this clearing of the metabolic detritus that accumulates as the body uses energy kicks into gear during deep, non-REM sleep. “It is essentially a power cleanse for the brain,” says Walker.
“One of the toxic elements that builds up as we’re awake is beta-amyloid, and what keeps us off the path to Alzheimer’s disease is that the glymphatic system comes to our rescue at night. It washes the brain by bathing it in cerebro-spinal fluid. This pulsing, washing mechanism washes away that sticky, toxic, amyloid protein. And that is what she discovered, that there is this pulsing, washing mechanism, washing away the amyloid protein at night.”
It took just one night of disrupted sleep for beta-amyloid to start building up in the animal brain. “That is a causal demonstration that if you don’t get that deep sleep you get an immediate build-up of that Alzheimer’s-related protein,” says Walker. “If you join it together with our findings it means that if you are not getting sufficient sleep across your lifespan you are going to build up this amyloid protein. The more of it that builds up, the less deep sleep that you are able to generate - and the less deep sleep that you have, the more Alzheimer’s protein you develop. It becomes a self-fulfilling prophecy of disease risk.”
Walker is now starting a new strand of research, aimed at trying to restore deep sleep in dementia patients. Using young, healthy adults - he has shown that it is possible to boost deep sleep brainwaves using electrical impulses. While noone knows whether sleep could become a treatment for dementia patients - an informal experiment on people with sleep apnoea, a disorder which causes disturbed sleep as the patient struggles for breath, suggests it could. Patients who were taught sleep improving strategies found improved their sleep staved off the onslaught of cognitive decline by almost ten years.
“So sleep offers hope from a diagnostic perspective, an understanding of the mechanism, and as a therapy,” says Walker. “If you wanted an insurance policy against Alzheimer’s, prioritising sleep across your lifetime is one of the best things I could advise.”
And it’s never too late.
Walker says some people take his research to mean that if they’ve been too “busy” to sleep for more than a few hours a night and they are in their late forties, their fate is sealed. Not so: “You can’t get back what you’ve lost but it’s never too late to start sleeping better.” So we should all aim to get more and better rest – starting tonight.