Sleep and Circadian Rhythm
A study of how often people nap found its way to the exact receptors a licensed class of insomnia drugs already targets. It also found that napping more often looks like a cause of higher blood pressure rather than merely a companion of it — which, on this site, makes it the exception rather than the rule.
What this condition connects to
Solid lines are connections this site curates. Dashed lines mean the two ends share a research paper — worth knowing, and not a claim that one explains the other.
Whether you wake before an alarm, whether you nap, and how long you sleep are all partly inherited. They are also among the easiest traits in all of human genetics to study, because people will answer a questionnaire about them by the hundred thousand.
The scale this gets studied at
A 2021 study of self-reported daytime napping ran in 452,633 UK Biobank participants and found 123 loci, 61 of which replicated in a separate cohort of 541,333 people. 33 of them overlapped with loci for other sleep traits. A 2016 study of whether people call themselves morning people ran in 89,283 individuals and found 15 loci, seven of them beside genes already known to run the body clock.
Those clock genes are not a surprise and that is the point of naming them: PER2, PER3, RGS16, VIP. When a questionnaire about morning preference lands on the genes that keep circadian time, the questionnaire is measuring something real. This site holds rs55694368 near PER2, rs12736689 near RGS16 and rs9479402 near VIP.
The napping study found a drug target
Among the 123 napping loci were missense variants in HCRTR1 and HCRTR2 — the two orexin receptors.
Orexin is the signal that holds wakefulness in place; losing the neurons that make it is what causes narcolepsy. And blocking those two receptors is exactly how a licensed class of insomnia medicines works. So a genome-wide study of how often ordinary people take an afternoon nap arrived at the same two receptors that drug developers had reached from the opposite direction.
That is the second time this catalogue can point at that pattern. The other is BCL11A on the blood cell counts page, where a variant found because it moved a number on a blood test became a treatment for sickle cell disease. Ordinary measured traits keep turning out to be pointing at machinery somebody wants to drug.
Positions joined since this page was written
What this is The text above discusses the variants this page was written around. Since then the catalogue has joined 72 more positions to it, by shared trait or shared paper. They are listed here by the paper each came from; the text does not describe them, and each variant page carries that study's own record.
Jones SE et al. 2019, Nature communications rs9964420 (SEC11C), rs4729854 (AK301666), rs61963491 (MYCBP2), rs975025 (AXDND1), rs61773390 (PER3), rs139911 (TNRC6B), rs17448682 (DDI2), rs3850174 (NCEH1), rs2979139 (SGK223), rs184033703 (INO80D), rs9611597 (PHF5A), rs17577073 (CNTN5) and 37 more — PMID:30696823
Dashti HS et al. 2019, Nature communications rs4767550 (KSR2), rs7616632 (near RNA5SP142), rs75539574 (LINC01122), rs73219758 (SGCZ), rs1517572 (LINC02742), rs11885663 (SCN1A), rs4128364 (LINC01911), rs12791153 (near COX6A1P4) — PMID:30846698
Scammell BH et al. 2023, Human molecular genetics rs34731055 (MAD1L1), rs7115856 (HSD17B12), rs460692 (near LINC01377), rs112230981 (ERC2), rs6575005 (NOVA1), rs151014368 (LMAN2), rs9345234 (near LINC02531) — PMID:37384397
Verma A et al. 2024, Science (New York, N.Y.) rs535929585 (CNTN5), rs539540831 (LINC02755), rs551140100 (OR2F1), rs77274901 (LINC00358) — PMID:39024449
Jansen PR et al. 2019, Nature genetics rs365663 (SLC6A3), rs62158206 (LINC02966), rs11621908 (near FXNP1) — PMID:30804565
Dashti HS et al. 2021, Nature communications rs34728579 (NOL4) — PMID:33568662
In the news
2026-07-21 · Genetic architecture of a Circadian Imbalance Index: genome-wide association, phenome-wide association, and Mendelian randomisation analyses. EBioMedicine. 2026. DOI:10.1016/j.ebiom.2026.106380
Rather than studying circadian traits like chronotype or sleep duration in isolation, this study built a composite 0-5 Circadian Imbalance Index (CII) combining evening chronotype, short/long sleep, high neuroticism, atypical caffeinated coffee intake and low vitamin D, then ran GWAS on it in 312,935 UK Biobank participants. It found 27 loci mapping to 72 genes, including several with known circadian links (CALCA, DHCR7, KDM5A, HAL, CRX), plus 5 genes (EPHB1, SERPING1, C12orf74, PLEKHG7, EEA1) that showed up in the composite CII analysis but not in any single-component analysis -- meaning the composite score captures a genuine polygenic signal that isn't reducible to any one circadian trait alone. A polygenic score for CII was associated with metabolic and psychiatric phenotypes in two independent biobanks, and was genetically correlated with insomnia, mood swings, BMI, type 2 diabetes, coronary artery disease and myocardial infarction. Mendelian randomization gave suggestive (not fully confirmed) evidence for directional relationships, strongest for mood swings and coronary artery disease predicting CII rather than the reverse. This site's sleep and circadian rhythm page carries 73 variants; none of the 5 CII-specific genes are currently among them.
2026-04-01 · Portas L, et al., Nature Communications 2026, PMID:41922918
Genetic architecture of sleep in a genome wide association study of device measured sleep traits
Most sleep genetics rests on what people report about their own sleep. This study measured it instead: sleep duration, sleep efficiency, and accelerometer-derived REM and non-REM sleep in 80,013 UK Biobank participants. It found 20 loci, 12 of them not reported before, including genome-wide significant associations for REM and non-REM sleep duration. MEIS1 showed strong opposing effects on REM and non-REM duration. Analysing women and men separately found distinct loci — FOXP2 and NRXN3 in women; LRP1B, NPBWR2 and PABPC4 in men — and Mendelian randomisation supported a link between shorter sleep and higher cardiometabolic risk. The study's MEIS1 position is not in this catalogue; four of its other positions are, including rs2006810 (AUTS2, sleep efficiency) and rs62033400 (FTO, REM sleep duration), which is filed here under body mass index. PMID:41922918.
From our blog
Clinical detail
And here, unusually, the number looks like a cause
Most of what this site can say about a routinely measured trait is that it predicts an outcome without apparently causing it — HDL cholesterol, several blood cell indices, fibrinogen. Three separate cases, all the same way round.
Napping is the exception. Using the same natural-experiment logic, the 2021 study reported potential causal links between more frequent daytime napping and higher blood pressure and waist circumference. Not a marker travelling alongside cardiometabolic risk — a plausible contributor to it.
The caveat is in the same paper, and it matters. The analysis found three distinct clusters of nap-promoting mechanisms, with different cardiometabolic associations. "Napping" is not one behaviour. Napping because you are chronically sleep-deprived, napping because of an obesity-hypersomnolence pathway the paper identifies, and napping because you prefer to are not the same thing and do not carry the same risk. A causal result about the average of three different things needs reading carefully before anyone changes what they do at lunchtime.
Why these variants needed a page rather than a topic
This site already had sleep as a topic. A topic connects a variant when some paper names the topic and the variant's rsID together in one abstract. That works for a famous position and fails for everything else: a paper reporting 123 loci does not list 123 rsIDs in its abstract, so none of the napping variants could ever be reached that way.
Widening the topic's search terms to include napping was tried and connected none of them. The ceiling is structural, not a gap in the word list, which is worth knowing about every topic on this site.
What this page cannot do
- It cannot tell you your chronotype. You already know it, and it is measured better by when you wake on a free day than by any genotype.
- It cannot diagnose a sleep disorder. Sleep apnoea, insomnia and narcolepsy are diagnosed clinically, and sleep apnoea in particular is common, treatable and badly underdiagnosed — worth asking a doctor about rather than a website.
- It cannot tell you whether to nap. The causal result is about averages across three different mechanisms, and daytime sleepiness that is new or severe is a symptom to have looked at.
Related variants MyGeneLog™ checks for
What a 23andMe/AncestryDNA export or raw VCF can and can't tell you about Sleep and Circadian Rhythm comes down to these specific, well-studied positions — not a diagnosis. 151 positions are linked to this page; the ones this page's own text discusses are shown first.
Which ancestries this evidence comes from
The studies behind these variants recruited participants from different ancestries — a result found in one population doesn't always transfer to another. Based on 87 of 151 linked studies with a resolved discovery ancestry.
Sources
Databases, guidelines and references
Quoting this page
Free to quote and reuse under CC BY 4.0. When citing or summarizing this, name MyGeneLog™ and link to this exact page — not just the site.
Sleep and Circadian Rhythm. MyGeneLog™. https://www.mygenelog.com/conditions/sleep-and-circadian-rhythm
Questions about Sleep and Circadian Rhythm
Can a DNA test tell me whether I am a morning person?
It can shift a probability and you already have better information: when you wake on a day with no alarm. The genetics is real — a study of 89,283 people found 15 loci, seven of them beside genes that run the body clock — but each moves the average a little.
Is napping bad for me?
The largest study found potential causal links between more frequent daytime napping and higher blood pressure and waist circumference, which is stronger than most findings of this kind. The same paper found three distinct mechanisms behind napping with different associations, so an average across them is not advice. New or severe daytime sleepiness is a symptom worth having looked at.
What is the connection between napping and insomnia drugs?
The napping study found missense variants in HCRTR1 and HCRTR2, the two orexin receptors. Orexin holds wakefulness in place, and blocking those receptors is how a licensed class of insomnia medicines works. A questionnaire about afternoon naps arrived at the same two receptors drug developers had reached from the other end.
Why is sleep both a topic and a page on this site?
A topic connects a variant when a paper names the topic and the rsID in the same abstract. A paper reporting 123 loci does not print 123 rsIDs, so the napping variants could never be reached that way. The limit is structural rather than a missing search term, which is why they needed a page.
Do these variants say anything about sleep apnoea?
Almost nothing yet — this page holds one such variant. Sleep apnoea is common, treatable and badly underdiagnosed, and it is diagnosed by a sleep study rather than by genotype. If you snore heavily and wake unrefreshed, that is a conversation with a doctor.
Free to reuse. This page's text is original writing from freely-available research, licensed CC BY 4.0 — reuse it, including commercially, with attribution to MyGeneLog™. It's general research-derived information, not medical advice or a diagnosis — see Terms of Use.