Are you an ”Early Bird” or “Night Owl”? It may not be up to you!

BY MANDY PHYU

Ever wonder why some of your friends are bouncing out of bed at 6am like clockwork while you hit snooze six times, only to come alive after sunset? Don’t feel bad – turns out your morning mojo (or lack thereof) might be written in your DNA.

What about Circadian Rhythms?

Deep inside your brain, about 20,000 nerve cells in a region called the suprachiasmatic nucleus (SCN) control your internal sleep-wake cycle – your circadian rhythm. This internal clock aligns with the natural rhythm of day and night. But not everyone runs on the same schedule. These circadian preferences in sleep timing are known as "chronotypes”.

Chronotypes: The Science of Sleep Personalities

You’ve probably heard of the “early bird” and the “night owl.” These aren’t just metaphors—they reflect actual biological patterns driven by circadian rhythms. Chronotype is largely heritable, with studies estimating that up to 50% of variation in sleep timing can be explained by genetics. 

Thanks to large genome-wide association studies (GWAS) involving hundreds of thousands of people, scientists have discovered more than 350 genetic loci associated with being a morning or evening person.

To start, the CLOCK and BMAL1 genes form a protein complex that attaches to specific areas on your DNA called E-box sequences, where they turn on other clock genes, including PER (PER1, PER2, PER3) and CRY (CRY1, CRY2).

Once activated, the PER and CRY genes produce proteins that begin to build up in the cell’s cytoplasm. Then, after being phosphorylated by enzymes like Casein Kinase 1 epsilon/delta (CK1ε/δ) and GSK3β, they re-enter the nucleus to inhibit their own expression by suppressing CLOCK-BMAL1 activity. Mutations or variations within these genes can shift your body clock earlier or later, affecting your preference. This all works as a negative feedback loop, key to maintaining your 24 hour rhythm. 

Some night owls aren’t just staying up late for fun. A variant in the CRY1 gene has been linked to Delayed Sleep Phase Disorder (DSPD)—a condition where individuals fall asleep and wake up significantly later than usual. One studied mutation results in a CRY1 protein with an internal deletion, weakening its ability to suppress CLOCK-BMAL1 activity. This lengthens the circadian period, making it harder for individuals to fall asleep at socially acceptable times. Sleep deprivation associated with DSPD can impair memory, decision-making, and performance, and may lead to stimulant use to combat the sleepiness, further exacerbating the problem.

On the opposite end of the spectrum, individuals with Familial Advanced Sleep Phase Disorder (FASPD) have earlier sleep/wake times. Researchers have discovered several genes that cause FASPD when it occurs in a variant form like PER2-S662G (PER2 gene), PER3-H415R/P417A (PER3 gene), CRY2-A260T (CRY2 gene), TIM-R1081X (TIM gene), CKId-T44A (CKId gene). Due to the early sleep onset and awakening, individuals may experience reduced sleep duration, leading to fatigue and daytime sleepiness. Similar to DSPD, they create a significant mismatch between an individual's internal clock and the external world.

Then there are the Familial Natural Short Sleepers (FNSS)—people who function optimally on just 4–6 hours of sleep per night, regardless of circumstances. Their short sleep isn’t a result of insomnia or poor habits—it’s genetic. Identified mutations include hDEC2-P384R (hDEC2 gene), ADRB1-A187V (ADRB1 gene), NPSR1-Y206H (NPSR1 gene), GRM1b-R889W, and GRM1-S458A (GRM1 genes) that are associated with this human short sleep phenotype. They wake up feeling refreshed and energetic, indicating efficient sleep despite changes to their schedule.

So, your tendency to wake up early or stay up late isn’t just a personality trait to compare with others. With science uncovering more about these genetic blueprints, we’re learning that optimal sleep is personal, not one-size-fits-all.

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References:

Jones, C. R., et al. (2013). Genetic basis of human circadian rhythm disorders. Experimental neurology, 243, 28–33. https://doi.org/10.1016/j.expneurol.2012.07.012 

Kripke, D. F., et al. (2014, Oct 20). Circadian polymorphisms in night owls, in bipolars, and in non-24-hour sleep cycles. Psychiatry investigation, 11(4), 345–362. https://doi.org/10.4306/pi.2014.11.4.345 

Scutti, S. (2019, January 29). The genes that might decide whether you’re an early bird or night owl. CNN. https://edition.cnn.com/2019/01/29/health/circadian-rhythms-genetic-study/index.html   

Teh, D. (2022, Sep 17). How genetics determine if you’re an early bird or a night owl. HealthMatch. https://healthmatch.io/blog/how-genetics-determine-if-youre-an-early-bird-or-a-night-owl