Episode 11 · MAPASGEN · Free

Free

Lark, Owl, or Something in Between: The Genetics of Your Chronotype

In 2017, the Nobel Prize in Physiology or Medicine was awarded to three American scientists — Jeffrey Hall, Michael Rosbash, and Michael Young — for discovering the molecular mechanisms of circadian rhythm. They decoded how cells 'know' what time it is. Inside every cell of your body, molecular clocks are running — feedback loops of proteins and genes that synchronise cellular processes with the daily cycle.

What we call being a 'morning person' or a 'night owl' is not a habit or upbringing. It is a chronotype: the genetically determined phase of your internal clock. People with an early chronotype are biologically comfortable falling asleep and waking earlier. People with a late chronotype — later. And this difference is written into their DNA.

The CLOCK Gene and Its Mutation in 'Eternal Owls'

The CLOCK gene (Circadian Locomotor Output Cycles Kaput) is one of the primary regulators of circadian rhythm. Together with the BMAL1 gene, it forms a transcription complex that initiates the expression of 'clock' genes — PER1, PER2, PER3, CRY1, CRY2. These genes, in turn, suppress CLOCK/BMAL1 activity, creating a feedback loop with a period of approximately 24 hours.

The polymorphism rs1801260 in the CLOCK gene is associated with a later chronotype. Carriers of a particular allele fall asleep on average 30–60 minutes later and experience greater resistance to early rising — not out of laziness, but because their biological clock runs slightly slower.

Historical context: The first 'clock' genes were discovered in the fruit fly Drosophila melanogaster in 1971 by Seymour Benzer and Ronald Konopka. They found mutants with rhythm periods of 19 hours, 29 hours, or no rhythm at all — depending on which version of the period (per) gene the fly carried. This was the first direct genetic evidence of a molecular clock. The 2017 Nobel work grew directly from this discovery.

PER3 and the 'Sleepiness Gene'

The PER3 gene comes in two main variants by VNTR repeat length: short (4 repeats) and long (5 repeats). A study by Derk-Jan Dijk and colleagues at the University of Surrey (2003) found:

GWAS and 351 Chronotype Loci

In 2019, a team from Massachusetts General Hospital published in Nature Communications the largest GWAS of chronotype at the time: 697,828 participants from the UK Biobank. They identified 351 genetic loci associated with morning or evening preference. These included genes affecting retinal light sensitivity, the sleep cycle, metabolism, and even BMI.

The conclusion: chronotype is a highly polygenic trait. No single gene determines whether you are a lark or an owl. It is the result of the combined contribution of hundreds of variants — and simultaneously the interaction with age, light exposure, and routine.

— Continued in PRO Material —

The PRO material contains the checklist 'Your Chronotype': how to determine your chronotype, how to find the key SNPs in your DNA test, and how to adapt your daily schedule to your genetically optimal sleep rhythm.

Premium contains the longreid 'Sleep and DNA': what happens to the genome during sleep, why chronic sleep deprivation accelerates biological ageing, and which genes protect against the consequences of sleepless nights.

MAPASGEN — the podcast about genetics that is already reshaping your life.

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