27 research outputs found
Proportion of individuals self-reporting as being “definitely a morning person”, average L5 timing, and average of sleep-midpoint across all nights for each genotype group of variants previously reported to be causal for familial advanced sleep phase in the UK Biobank (UKB), Finnish and MESA studies.
Accelerometer-based estimates of sleep timing unavailable in the Finnish studies. Self-reported “morningness” and accelerometer estimates of L5-timing unavailable in MESA.</p
Summary of self-reported sleep duration in UK Biobank (data field 1160) between carriers of variants previously reported to be causal for familial natural short sleep and non-carriers (homozygous reference called by UK Biobank exome-sequencing) who are also non-carriers for any of the other 12 variants described in this article.
Summary of self-reported sleep duration in UK Biobank (data field 1160) between carriers of variants previously reported to be causal for familial natural short sleep and non-carriers (homozygous reference called by UK Biobank exome-sequencing) who are also non-carriers for any of the other 12 variants described in this article.</p
Summary statistics of “eveningness” across genotype groups for variants previously reported as causal for delayed sleep phase.
Data on being “more or definitely an evening person” unavailable in the Finnish studies. (DOCX)</p
P-values from burden testing of rare (MAF < 0.01%) loss-of-function and missense variants in genes previously reported to harbour variants causal for disruptive sleep duration or timing on accelerometer estimates of sleep duration in UK Biobank.
There were no remaining loss-of-function carriers for GRM1, ADRB1 and CRY2 within the subset of individuals from UK Biobank who wore an accelerometer. (DOCX)</p