Can't get to sleep? The reason may be in your genes
If you're naturally inclined to stay awake into the wee hours and have trouble falling asleep at a reasonable hour then your genes may be to blame for your night owl behavior. New research has uncovered a specific gene mutation significantly alters the circadian rhythms of those that carry it.
Our natural in-built circadian clock is
what generally governs our sleep and wake cycles. This 24-hour
sleep-wake cycle involves several biological processes governing the rise and fall of certain hormones, but many
people suffer from disrupted sleep patterns ranging from narcolepsy
to chronic insomnia.
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One category of sleep disruption is labeled delayed sleep phase disorder (DSPD) and manifests in an inability to get to sleep early in the evening. Those with DSPD are found to have a disturbed circadian clock, meaning many of the general hormones that cycle with a regular body clock are delayed.
When studying the melatonin levels of a DSPD patient, researchers noted an oddly specific delay in their melatonin levels rising every evening.
"Melatonin levels start to rise around nine or 10 at night in most people," explains Michael W. Young, senior author on the Rockefeller University study. "In this DSPD patient that doesn't happen until two or three in the morning."
In studying the DNA of that patient the researchers noted a specific mutation in a gene called CRY1, which had previously been flagged as being influential in the development of normal circadian cycles. This mutation caused more activity than normal in the production of a protein that inhibited the body from producing the necessary hormones that transition one into the sleep phase of their daily cycle.
The researchers found that those carrying this gene variant displayed delays in the onset of sleep every evening, from between 30 minutes to two and a half hours. In studying 70 individuals from six families they found 38 subjects that carried the genetic variant, all of whom reported either delayed sleep onset times or fractured sleep patterns.
While some clinical studies have shown that up to 10 percent of people could suffer from some form of DSPD, the researchers point out that this gene variant does not account for all cases of this disorder. However, upon scouring a large genetic database for the variant, the researchers do estimate that up to one in 75 individuals of non-Finnish, European ancestry could carry this gene mutation.
"Just finding the cause doesn't immediately fix the problem," says research associate Alina Patke. "But it's not inconceivable that one might develop drugs in the future based on this mechanism."
It's suggested that those carrying the gene variant, or suffering from DSPD in general, could still realign their circadian rhythms to normal cycles by getting strong light exposure during the day and self-enforcing regular sleep and wake times.
The team's research was published in the journal Cell.