Your Internal Clock
The circadian-clock genes that decide whether you are wired for early mornings or late nights — and the melatonin receptor that times your nightly wind-down.
Diurnal Preference
CLOCK is a core circadian-clock gene whose 3111 variant in the 3′ untranslated region was the first clock-gene polymorphism linked to human diurnal preference. One allele is associated with a shift toward eveningness—later bedtimes and slower morning wake—while the other supports earlier timing. The effect is modest and strongly shaped by light exposure, meal timing, and social schedule.
Possible results: Earlier chronotype · Intermediate chronotype · Later chronotype
Morningness Tendency
RASD1 encodes Dexras1, a signaling protein in the suprachiasmatic nucleus that helps gate how strongly light exposure resets the body's internal clock each day. A common variant in the gene's 3' untranslated region has been linked, at genome-wide significance in large population studies, to a small shift in self-reported morning-versus-evening preference.
Possible results: Morning-leaning tendency · Intermediate chronotype · Evening-leaning tendency
Morningness
This variant near RGS16 emerged as one of the strongest signals in a genome-wide study of self-reported morningness. RGS16 regulates G-protein signalling in the suprachiasmatic nucleus — the brain's master clock — and influences the length of the circadian period.
Possible results: Baseline timing · Slight morning shift · Morning-associated
Melatonin Timing
MTNR1B encodes the MT2 melatonin receptor, which mediates melatonin signalling in the brain and pancreas. The alternative allele is associated with a later, more prolonged melatonin profile—a slower evening rise and slower morning decline—and separately with higher fasting glucose, since this receptor also regulates insulin secretion in pancreatic β-cells.
Possible results: Typical melatonin profile · Intermediate profile · Shifted melatonin profile
