Investigating the genetic pathways of insomnia in Autism Spectrum Disorder.
Maria Niarchou, Emily V Singer, Peter Straub and 2 others
PMID 35820265WHAT IT FOUND
Genetic risk scores for insomnia and autism did not predict insomnia in people with autism.
Rare circadian variants showed no robust association. These scores did not identify insomnia risk in autism.
Key findings
01Genetic risk scores for insomnia did not predict insomnia in either sample or in the combined analysis.
02Genetic risk scores for autism did not predict insomnia in the combined analysis.
03Rare variants in BHLHE41 showed nominal evidence in MSSNG, p = 0.03, but did not survive correction and were not significant after combining samples, p = 0.39.
STILL TO COME
How it was doneWhat they found
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What it does not show
The study had less than 80% power to detect genetic score effects that explained less than 1% of variation. Small genetic effects could have been missed. Sleep problems were not objectively measured. They came from parent reports, self reports, or clinician notes. Participants were selected for primarily European ancestry. Results may not apply to other genetic backgrounds. The BioVU sample was older than the MSSNG sample. The study could not test whether child and adult insomnia genetics differ. The rare BHLHE41 finding did not survive multiple testing and disappeared when samples were combined. The authors note that sleep problems may have multiple causes, such as environment. This study did not test those causes.
Declared interests
The supplied text does not report funding or conflicts of interest.
The easy way to misread this
Do not read the nominal BHLHE41 result as evidence that this gene causes insomnia in autism. It did not survive correction for multiple testing and was not significant when the samples were combined.