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Not medical advice. The Atlas is not a substitute for a clinician who can examine you.

Clock-Gene Variants

PER3, CLOCK, CRY1 · The Genetics of Timing

Evidence grade 4 of 5, Strong. Read how the Atlas grades evidence.

0 human trials, about 300 studies, 697,828 participants (largest chronotype GWAS). The written rationale for this grade is still being prepared.

FDA
Genetic variants
WADA
Not prohibited

Reference only. Not medical advice.

What can go wrong

Consumer single-gene or small-panel 'chronotype DNA' reports overstate actionable precision: the trait is highly polygenic (351 loci, ~13.7 percent SNP heritability), so a single marker explains very little, and the older PER3 and CLOCK single-variant claims do not replicate across populations. Rare high-penetrance mutations that genuinely flip a schedule are diagnosed through clinical evaluation and pedigree, not wellness kits. Sleep timing that causes distress or daytime impairment, and any decision about sleep duration or a suspected familial sleep disorder, should be evaluated by a qualified sleep clinician rather than acted on from a direct-to-consumer genetic report.

The genetics of sleep timing splits cleanly into two findings the evidence supports and one it does not. First, a handful of rare high-penetrance mutations can flip an entire schedule: PER2 and CK1-delta variants cause familial advanced sleep phase (extreme larks), DEC2 and ADRB1 variants cause familial natural short sleep, and a CRY1 splice deletion causes familial delayed sleep phase (extreme owls). These are confirmed in family pedigrees and reproduced in mice. Second, ordinary chronotype is highly polygenic: the largest study, nearly 700,000 people, found 351 associated regions that together explain only a modest fraction of variation, with the most-morning and most-evening genetic extremes separated by roughly 25 minutes of actual sleep timing. What the evidence does not support is the older single-gene story (PER3 length variant, CLOCK T3111C), which fails to replicate across populations, or consumer single-gene tests that promise to read your true chronotype from one or a few markers.

A few rare variants flip your whole schedule. Most chronotype is hundreds of small ones.

What people take it for

What it is taken for. Approval, where it exists, covers only some of these.

  • Understanding heritable, familial patterns in sleep timing
  • Explaining clinically diagnosed familial sleep-phase disorders (advanced and delayed)
  • Context for the limits of consumer single-gene chronotype testing
  • Research framing for chronopharmacology and circadian-period biology
  • Distinguishing rare schedule-determining mutations from common small-effect variation

What people get wrong

  • Often saidA DNA test reveals your true chronotype.

    ActuallyThe largest study, 697,828 people, found chronotype spread across 351 genetic regions with SNP heritability near 13.7 percent (Jones et al., Nature Communications 2019). The genetic extremes, the top versus bottom 5 percent of morningness variants, differ by only about 25 minutes of measured sleep timing. No single gene or small panel captures this, and a short questionnaire typically predicts diurnal preference as well or better. Single-gene chronotype reports are not supported by this evidence.

  • Often saidYour PER3 length variant or CLOCK T3111C says whether you are a lark or an owl.

    ActuallyThese two classic single-marker associations failed to replicate consistently. The PER3 VNTR associated with diurnal preference in British samples but showed no association in Japanese, Han Chinese, and Norwegian samples. The CLOCK T3111C eveningness association, first reported in a Japanese sample (Mishima et al. 2005), was not replicated in later Caucasian and Korean studies. Both are best treated as contested, low-evidence markers, not schedule-determining genes.

  • Often saidIf everyday chronotype is mostly genetic, sleep timing is fixed and unchangeable.

    ActuallyCommon-variant heritability of chronotype is modest, near 13.7 percent in the largest analysis (Jones et al. 2019), meaning most variation is non-genetic and responsive to light exposure, age, and routine. Only the rare high-penetrance mutations, such as PER2, DEC2, ADRB1, and CRY1 variants, strongly constrain an individual schedule, and those are clinical findings, not consumer-test outputs.

  • Often saidA short-sleep gene means anyone can train themselves to sleep four to six hours safely.

    ActuallyFamilial natural short sleep traces to specific rare inherited variants (DEC2-P384R; ADRB1-A187V) carried by a very small number of families; carriers appear to function on roughly six hours without the deficits of ordinary sleep restriction (He et al., Science 2009; Shi et al., Neuron 2019). This does not generalize: for the large majority without these variants, curtailing sleep produces the usual impairments. Persistent short sleep or daytime impairment is best discussed with a qualified clinician.

Who profits, and who pushes back

  • Sleep-genetics researchers

    Promotes itAcademic

    Map clock-gene variants to chronotype and sleep disorders; cautious about consumer test utility.

  • Consumer-genomics companies

    Sells this. Has a commercial interest in a product sold as this compound, as of July 2026.

    Promotes itCommercial

    Sell chronotype/sleep gene reports; commercial interest in overstating actionable precision.

  • Michael W. Young

    Pushes backRockefeller University geneticist, 2017 Nobel laureate in Physiology or Medicine for circadian clock work; senior author, CRY1 delayed-sleep-phase study (Patke et al., Cell 2017)

    The CRY1 variant the team described segregates within affected families and lengthens the molecular clock's period; it is a rare, high-penetrance cause of delayed sleep phase identified in specific pedigrees, not a common marker that a population-level test would surface in most people.

  • Samuel E. Jones and Michael N. Weedon

    Pushes backUniversity of Exeter human geneticists; lead and senior authors of the 697,828-participant chronotype GWAS (Nature Communications 2019)

    Even with 351 associated loci, the genetic signal explains a modest share of chronotype: the 5 percent of people carrying the most morningness alleles had measured sleep timing only about 25 minutes earlier than the 5 percent carrying the fewest, underscoring how small each common variant's effect is.

  • Ying-Hui Fu and Louis J. Ptacek

    Pushes backUCSF neuroscientists; discoverers of the PER2, DEC2, and ADRB1 familial sleep variants

    These short-sleep and advanced-phase variants were found in rare families through linkage and sequencing and confirmed in animal models; they are not lifestyle switches and do not imply that the general population can safely adopt the same schedules.

Where the research comes from

Share of published research by country of origin.
PlaceShare of published research
Europe38%
USA34%
Other28%

Research published from: Global.

How we got here

The genetics of circadian timing was illuminated first through families, not populations. In 2001 a University of Utah team studying a Utah family of extreme early risers traced familial advanced sleep phase to a single serine-to-glycine change in the PER2 gene (Toh et al., Science), the first time a point mutation in a clock gene was tied to a human sleep schedule; a partner mutation in casein kinase 1-delta followed in 2005. In 2009 the same lab found a DEC2/BHLHE41 variant in a mother-daughter pair who thrived on about six hours of sleep, the first familial natural short-sleep gene, with a second gene, ADRB1, identified a decade later in 2019. The mirror image, familial delayed sleep phase, was tied to a CRY1 splice deletion in 2017 in several families of Turkish origin (Patke et al., Cell). Only afterward did large genome-wide studies, drawing on UK Biobank and 23andMe data, show that everyday morningness is spread across hundreds of small-effect variants, which is exactly why a single rare mutation can be decisive while a single common variant explains almost nothing.

  1. 2001PER2 S662G mutation identified in a Utah family with familial advanced sleep phase (Toh et al., Science)
  2. 2005Casein kinase 1-delta T44A variant found to act synergistically in advanced sleep phase (Xu et al., Nature)
  3. 2009DEC2/BHLHE41 P384R variant identified as the first familial natural short-sleep gene (He et al., Science)
  4. 2017CRY1 c.1657+3A>C splice deletion (CRY1 delta-11) tied to familial delayed sleep phase across Turkish-origin families (Patke et al., Cell)
  5. 2019ADRB1 A187V identified as a second familial natural short-sleep gene (Shi et al., Neuron)
  6. 2019Largest chronotype GWAS, 697,828 participants, finds 351 loci and confirms chronotype is highly polygenic (Jones et al., Nature Communications)

At a glance

PER3
Sleep-deprivation sensitivity
CLOCK T3111C
Evening preference
CRY1 deletion
Severe delayed sleep phase
Loci
340+ for chronotype

What this entry does not yet cover

What follows is unfinished work on our side, not a finding about Clock-Gene Variants. A short entry is not a safe entry.

  • Cost and market. We have not documented what it sells for or who sells it.
  • Supply chain. We have not mapped where it is made.
  • Who uses it. We have not documented the user groups.
  • What could change. No forward-looking summary yet.
  • How it compares. We have not set it against the alternatives.
  • Children and teenagers. We have not checked what is known about younger people.

Sources