For some people, waking up in the morning is the ultimate definition of a chore, especially if one tends to be more productive or creative late in the evening. To some, it may seem like personal preference, but a new study suggests that being a “night owl” can be chalked up to gene mutations.
Researchers analyzed a total of 70 subjects from six families, and, as Live Science reported, some of the subjects were found to have a condition called delayed sleep phase disorder, or DSPD. This is a condition where the body clock tends to lag behind that of the average person, causing sufferers to sleep late and wake up similarly late. Based on the research, those with DSPD had a “night owl” gene mutation in the CRY1 gene, one that wasn’t present in family members who didn’t have DSPD.
In order to understand why some people are “night owls,” one has to understand how the body clock, or the circadian clock, works. This is an internal clock of sorts found in all living creatures, telling people, for instance, when they feel sleepy, awake, tired, or hungry. Typically, people strictly adhere to a 24-hour clock, but people with DSPD tend to follow a circadian clock that runs longer than normal.
According to study lead author Alina Patke of the Laboratory of Genetics at the Rockefeller University, people who suffer from DSPD often struggle to keep up with people with normal circadian clocks by having to play “catch-up” for their entire lives. And for those who have this night owl gene mutation, that could either be a good thing or a bad thing, depending on their line of work.
“A person like a bartender, for example, might not experience any problem with the delayed sleep cycle,” Patke said in an interview with Live Science. “But someone like a surgeon who has to be in the (morning) OR in the early morning – that’s not compatible.”
For some individuals, DSPD can be such a burden that they visit sleep clinics in an attempt to get their sleeping habits back to normal. Live Science wrote that this was how Patke and her team discovered the night owl gene mutation.
In 2010, the researchers studied a case of a 46-year-old woman who had visited one of these clinics and had her stay in an apartment for two weeks, with no time cues to guide her actions, meaning no windows, no internet access, and no television. She was then told to “live on her own timeline” and rely on body cues for eating and sleeping.
Patke’s team found that the woman’s circadian clock was one hour longer than the traditional 24-hour cycle and that her sleep was fragmented. Through gene sequencing, the team discovered that she had the CRY1 night owl gene mutation, one where only one “letter” was off in its genetic instructions.
Although this does suggest that late sleepers may have a gene mutation that causes them to prefer to carry on important tasks while most everyone else is sleeping, Patke admitted to Live Science that she herself is a night owl, albeit one that doesn’t have the CRY1 gene mutation. But the mutation could possibly be found in many people who exhibit these nocturnal behaviors.
“Not everybody who had this behavior necessarily has this mutation, but it does seem to have an effect on a large part of the population.”
According to an article on the website Circadian Sleep Disorder, it isn’t clear how many people suffer from DSPD, though it was revealed in the 1990s that the condition affects about one in 600 adults, and is far more common in adolescents, who may or may not overcome the condition later in life. It’s often a lifetime struggle for people, especially for those whose jobs require that they be up in the morning.
While there is no medication for DSPD at the moment, Patke suggested some tools that sufferers can use to reset their body clocks, such as sleeping at night and waking up in the morning at a set time, even on weekends. She added that people should avoid bright lights, including those from electronic gadgets, in the night time, or avoiding exposure to bright sunlight upon waking up in the morning.
The study’s findings on the night owl gene mutation in DSPD sufferers were published Thursday in the journal Cell.
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