Can’t sleep? A gene mutation might be what’s keeping you awake


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We’ve all stayed awake past our bedtimes at one point or another, but what about those of us who are often up late at night? If you find yourself often staying up until the wee hours and unable to get out of bed the next morning, genetics could be to blame. There are definite benefits to being a night owl, but for some the feeling of perpetual sleepiness and the inability to go to bed early might be the unwanted result of a newly discovered gene mutation.

According to a new study published in Cell Press and appearing on Science Daily, a mutation in genes called CRY1 can disrupt the circadian clock, the part of the body which determines our sleep and wake cycles. Those with the gene mutation are more likely to experience a delay in sleep of up to two and a half hours.

“Carriers of the mutation have longer days than the planet gives them, so they are essentially playing catch-up for their entire lives,” study author Alina Patke, a research associate in the lab of principal investigator Michael Young, Richard and Jeanne Fisher Professor and Head of the Laboratory of Genetics at The Rockefeller University, told Science Daily.

While you may fancy yourself a night owl, there is an official diagnosis of delayed sleep phase disorder (DSPD) and it’s usually discovered when patients undergo treatments at sleep clinics. Not all cases of DSPD are associated with the newly found CRY1 gene mutation, but this study is the first to indicate that a mutation could be to blame for DSPD, which affects up to ten percent of the population. Those diagnosed with DSPD are unable to fall asleep easily at night, and as a result their delayed sleep pattern can make bedtime feel like a series of long naps. Often, DSPD goes hand in hand with anxiety, depression, cardiovascular disease, and diabetes. Due to their erratic sleep schedule, DSPD patients are often unable to attend social events or take on a schedule that requires early morning work.

For the study, researchers looked at the skin cells of those with DSPD, discovering a mutation in CRY1. In those without DSPD, circadian clocks are able to run on a normal cycle. For those with DSPD, the CRY1 protein “inhibits the circadian clock,” and although “just one letter in its genetic instruction is incorrect,” the mutation causes a massive problem—sending the circadian rhythms into overdrive and stretching out one’s daily circadian cycle. Of the participants in the study, 39 were carriers of CRY1 and displayed an inability to fall asleep quickly, as well as disrupted sleep patterns, compared to the 31 participants who were not carriers of CRY1.

Despite the havoc this mutation can have on sleep schedules, experts advise that it is in one’s power to change how their body responds. One participant in the study was able to manage a normal sleep pattern despite the diagnosis by maintaining a regular sleep and wake schedule and getting out into bright light during the day. “An external cycle and good sleep hygiene can help force a slow-running clock to accommodate a 24-hour day,” says Patke. “We just have to work harder at it.”



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