Most of us are more or less divided into two categories: early birds and night owls. Morning people rise with the sun, while night people stay up well into the wee hours. Researchers at The Rockefeller University suggest some night owls adopt different sleep patterns due to a genetic mutation that slows down the the 24-hour circadian clock.

The variant of the gene CRY1 was found to delay the circadian clock, which determines when we go to sleep at night and wake up in the morning. The CRY1 genetic mutation has been linked to a sleeping disorder known as delayed sleep phase disorder (DSPD), where the internal clock runs behind, meaning night owls wake up later than normal, and go to bed later than normal. People who self-identify as night owls are often diagnosed with DSPD, and now this is the first variant linked to the sleep disorder, according to researchers.

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“Compared to other mutations that have been linked to sleep disorders in just single families worldwide, this is a fairly impactful genetic change,” said Michael W. Young, senior author of the study and head of Rockefeller’s Laboratory of Genetics, in a statement.

In the study, published in Cell, researchers collaborated with sleep researchers at Weill Cornell Medical College where participants spent two weeks in a lab apartment isolated from all cues of time of day, so they could eat and sleep whenever they felt inclined. Skin cells were also collected. This would help determine whether mutations in any circadian genes were linked to DSPD.

One participant stood out; a DSPD patient possessed the CRY1 mutation. She not only stayed up late, but also had a circadian cycle that lasted about 30 minutes longer. The patient also experienced changes in body temperature and hormones that are linked to the circadian clock, like melatonin, which helps regulate sleep. Typically, melatonin levels begin to rise between 9 or 10 at night, but in this DSPD patient, this didn't occur until 2 or 3 in the morning.

In a normal circadian clock, genes are turned on and off over a 24-hour cycle, where CRY1 is responsible for suppressing some of these genes throughout specific times. However, in the DPSD patient, the CRY1 protein was more active, and kept other clock genes off for much longer. This compelled the researchers to reach out to other members of the patient's family, where they discovered five relatives who also shared the variant. These family members all had signs of DSPD, or had a history of sleep problems.

Young and his colleagues used large genetic databases from around the globe to determine the incidence of CRY1 mutations. A total of 70 people from six families were found to have the genetic mutation who also had DSPD. Their midpoint of sleep fell between 6 a.m. and 8 a.m., when those without the mutation fell around 4 a.m. Interestingly, members of the same families without DSPD did not have the mutation.

"Carriers of the mutation have longer days than the planet gives them, so they are essentially playing catch-up for their entire lives," said Alina Patke, the lead author of the study and a research associate in the Laboratory of Genetics at The Rockefeller University.

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It's important to note not all DSPD cases are linked with the CRY1 genetic mutation. Although the exact cause of this disorder is unknown, it's believed to be linked with the lack of morning sunlight exposure or overexposure to bright light in the night. For example, using electronic devices at night can increase alertness levels, and suppress melatonin production.

Patke believes identifying one genetic mutation linked to the sleep disorder could help us gain a better understanding of how our circadian rhythms are controlled.

"[I]t’s not inconceivable that one might develop drugs in the future based on this mechanism," she said.

In other words, researchers could potentially develop a drug that can manipulate the clock of night owls to coincide with normal sleep patterns.

In the meantime, DSPD patients are advised to gradually scale back sleeping times, until they achieve a desired time frame. This can be effective, but maintaining the new schedule is essential, according to the American Sleep Association, because it can reset if patients divert from it with just one late night.

The reality is some of us are really not morning people, and our genes are most likely to blame.

Source: Patke A, Murphy PJ, Onat OE et al. Mutation of the Human Circadian Clock Gene CRY1 in Familial Delayed Sleep Phase Disorder. Cell. 2017.

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