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 iswhat generally governs our sleep and wake cycles. This 24-hoursleep-wake cycle involves several biological processes governing the rise and fall of certain hormones, but manypeople suffer from disrupted sleep patterns ranging from narcolepsyto chronic insomnia.
One category of sleep disruption islabeled delayed sleep phase disorder (DSPD) and manifests in aninability to get to sleep early in the evening. Those with DSPD arefound to have a disturbed circadian clock, meaning many of the generalhormones that cycle with a regular body clock are delayed.
When studying the melatonin levels of aDSPD patient, researchers noted an oddly specific delay in theirmelatonin levels rising every evening.
"Melatonin levels start to risearound nine or 10 at night in most people," explains Michael W. Young, senior author on the Rockefeller University study. "In this DSPD patient thatdoesn't happen until two or three in the morning."
In studying the DNA of that patient theresearchers noted a specific mutation in a gene called CRY1, which had previously been flagged as being influential in the developmentof normal circadian cycles. This mutation causedmore activity than normal in the production of a protein thatinhibited the body from producing the necessary hormones thattransition one into the sleep phase of their daily cycle.
The researchers found that thosecarrying this gene variant displayed delays in the onset of sleepevery evening, from between 30 minutes to two and a half hours. Instudying 70 individuals from six families they found 38 subjects thatcarried the genetic variant, all of whom reported either delayedsleep onset times or fractured sleep patterns.
While some clinical studies have shownthat up to 10 percent of people could suffer from some form of DSPD,the researchers point out that this gene variant does not account forall cases of this disorder. However, upon scouring a large genetic databasefor the variant, the researchers do estimate that up to one in 75individuals of non-Finnish, European ancestry could carry this genemutation.
"Just finding the cause doesn'timmediately fix the problem," says research associate Alina Patke. "But it's not inconceivable that onemight develop drugs in the future based on this mechanism."
It's suggested that those carrying thegene variant, or suffering from DSPD in general, could still realign theircircadian rhythms to normal cycles by getting strong light exposureduring the day and self-enforcing regular sleep and wake times.
The team's research was published in the journal Cell.