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.
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.
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.
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.
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.
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 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. 61 positions are linked to this page; the ones this page's own text discusses are shown first.
Databases, guidelines and references
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.
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.
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.
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.
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.