Ask a friend how they’re doing today and you’re likely to hear that they’re tired. In fact, odds are, right now, you’re tired. A flurry of recent articles has detailed America’s problems with not getting enough sleep: 40 percent of Americans yawn their way through their days, says a Gallup poll; sleep is the new social status symbol, according to the New York Times; the Centers for Disease Control and Prevention has declared insufficient sleep a public health problem; and, perhaps most damning: There’s an emoji for that.
At its core, sleep has three main characteristics: the circadian rhythms of morningness or eveningness (chronotype), the length of time it takes a person to fall asleep (latency), and sleep duration and quality. In genetics jargon, sleep is a “complex trait.” Scientists know it’s affected by our environment—such as noise or stimulants—and by the intricate interactions within our cells, orchestrated by a subset of genes, that help regulate our body’s wake-and-rest cycles and how we naturally sleep.
Genetics may also play a role in insomnia, especially if one does not have good sleeping habits. To understand which genes are involved in sleep, scientists use a common study technique called the genome-wide association study, or GWAS (pronounced “g-wahs”).
Like a tool of the mining prospectors of old, the GWAS is a sort of genetics dowsing rod that tells scientists where in the genome certain genetic changes may be affecting observable traits. These studies focus on single nucleotide polymorphisms or SNPs (called “snips”)—common genetic changes that do not cause a genetic condition, but may subtly change the action of a gene’s protein. Advances in genetics and low-cost testing have allowed researchers to quickly identify SNPs related to traits like sleep.
To find sleep-related genes, researchers perform GWAS and remove factors known to alter sleep (age, illness, gender, among others) while also confirming that a gene’s action is somehow involved in sleep. Through this process, many SNPs have been strongly linked to genes that affect sleep. These genes include RBFOX3 (sleep latency); GNβ3 (sleep quality); VRK2 and CLOCK (sleep duration); and RGS16, PER2, and PER3 (chronotype). In fact, people with one particular SNP spelling in the CLOCK gene slept an average of 36 minutes longer than those with two copies of the alternate allele. Put these SNPs together and a picture of a person’s innate sleep preferences begins to emerge.
There is still lots of work to be done to untangle the genetics of sleep. But one key to a getting better sleep rests (pun intended) not only in improving sleep habits—like forgoing that next episode of Stranger Things—but also in understanding how your genes influence your sleep patterns. This knowledge may lead you to change habits, and, ultimately, to naturally sleep better. So, next time you’re lying in the dark struggling to sleep, instead of counting sheep try listing sleep genes. You just might be able to brag about your sleep at the next social event.
About the author:
Kyle W. Davis, ScM, LCGC, is a genetic counselor specializing in pediatrics and neurodevelopmental genetics. His writing has been featured in the NIH/NHGRI’s News Features, the NIH’s Genome Advance of the Month, and Perspectives in Genetic Counseling. He lives in Austin, Texas. Tweet him @kylewalterdavis.