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Are you an `elite sleeper’?

It means you have a gene that allows you get full night’s sleep in just 4 hours

| THE INDEPENDENT | Are you one of those lucky people who seem to be able to thrive on between four and six hours of sleep per night? You may be what UC San Francisco researchers have dubbed an “elite sleeper,” and a new study reports the same genes associated with healthy short sleep patterns may also slow the onset of neurodegenerative diseases such as Alzheimer’s.

In 2018, the world’s largest sleep study concluded between seven and eight hours of sleep each night is the sweet spot to maintain optimal cognitive performance and general health. For most people, sleeping less than six hours a night can lead to a number of deleterious health outcomes, from increased dementia risk in later life to higher chances of early death.

But some people can comfortably sleep just a few hours a night while maintaining good health, and researchers have been closely studying these “elite sleepers.”

According to a new study from the University of California San Francisco, these short sleepers are blessed with a number of genes that efficiently rejuvenate the body and brain in a shorter time window than most people require.

People who are able to function fully on four to six hours of sleep have what scientists call Familial Natural Short Sleep (FNSS).

Louis Ptacek, a professor of neurology at the University of California San Francisco and lead author of the new study, has been studying people with FNSS for over a decade. Previous studies showed that FNSS runs in the family. Five genes have been identified thus far linked to FNSS.

More than a decade ago UC San Francisco scientists discovered the first gene associated with these rare short sleep behaviors. Since then, the team has found five genes they believe are linked to a condition now named Familial Natural Short Sleep (FNSS).

“There’s a dogma in the field that everyone needs eight hours of sleep, but our work to date confirms that the amount of sleep people need differs based on genetics,” explained co-senior author Louis Ptacek. “Think of it as analogous to height; there’s no perfect amount of height, each person is different. We’ve shown that the case is similar for sleep.”

Ptacek’s research also suggests that people with FNSS have above-average psychological resilience and resistance to neurodegenerative diseases.

The new study set out to investigate whether these short sleep gene variants directly protect against neurodegeneration linked to Alzheimer’s. The researchers bred mice that had both FNSS genes and genes that are known to predispose them to Alzheimer’s.

These mice ended up developing fewer plaques (abnormal clusters of protein fragments that build up between nerve cells) and tangles (made up of twisted strands of another protein), both considered hallmark aggregates of Alzheimer’s disease (AD). Similar results were obtained when the experiment was repeated with mice that had a different short-sleep gene.

“AD is the leading cause of age-related neurodegeneration, accounting for nearly 75% of all dementia cases. AD is incredibly complex, and its etiology is characterised by the interplay between many physiological, genetic, and environmental influences. Great effort has been put forward during the last few decades in seeking cures for AD, yet most of this has focused on deleterious genetic influences over preventive ones. FNSS individuals do not appear to suffer from increased risk of dementia despite lifelong shorter sleep duration, implying a potential protective effect stemming from these mutations,” the authors wrote in the journal Science.

Across several animal experiments the researchers demonstrated both FNSS gene variants slowed the progression of Alzheimer’s pathology in the mice.

The mechanisms by which the gene variants protect from neurodegeneration are still unclear but the researchers do indicate the findings affirm genetic factors do play a role in slowing the progression of Alzheimer’s pathology.

Ptacek’s team investigated the link between Alzheimer’s and short sleep in detail. The researchers hypothesise that the genes linked to FNSS likely make the process of sleep more efficient. This means those carrying these particular variants seem to accomplish all the brain benefits of longer sleep in shorter periods of time to normal people.

Co-senior author Ying-Hui Fu said the findings fit with plenty of observational research associating poor sleep and brain disease.

“Sleep problems are common in all diseases of the brain,” said Fu. “This makes sense because sleep is a complex activity. Many parts of your brain have to work together for you to fall asleep and to wake up. When these parts of the brain are damaged, it makes it harder to sleep or get quality sleep.”

That’s particularly striking because Alzheimer’s has been linked to not getting enough sleep. But if these elite sleepers are any indication, sleep quality seems to be much more important than sleep quantity.

Sleep problems are a common hallmark of brain diseases. “This makes sense because sleep is a complex activity. Many parts of your brain have to work together for you to fall asleep and to wake up. When these parts of the brain are damaged, it makes it harder to sleep or get quality sleep,” Ptacek said, adding that this makes understanding the biological underpinnings of sleep regulation all the more important.

It is very early days but the researchers argue the implications of these genetic sleep studies could be significant. The few genes Ptacek and colleagues have identified thus far could be targeted by drugs that not only help people with sleeping problems but also healthy people maximize the quality of their sleep.

Linking these specific gene variants to healthy sleep behaviors can point scientists in novel directions for new kinds of treatments targeting a variety of brain diseases. Drugs that influence the expression of these short sleep genes could hypothetically be developed to enhance the quality of sleep in older adults and ultimately prevent or slow the onset of neurodegenerative disease.

“This work opens the door to a new understanding of how to delay and possibly prevent a lot of diseases,” added Fu. “Our goal really is to help everyone live healthier and longer through getting optimum sleep.”


The new study was published in the journal iScience.

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