Aims: Humans sleep a third of their life and adequate sleep duration is an important factor in preventing metabolic and psychiatric disorders.

Two GWAS studies in adults have suggested that genetic factors may influence the sleepiness and circadian rhythms. Allembrandt et al. (2011) conducted high-density genome-wide association studies for sleep duration in seven European populations and identified an intronic variant (rs11046205; P=3.99 * 10(-8)) in the ABCC9 gene that explains Approximately 5% of the variation in sleep duration. RNA interference knockdown experiments of the conserved ABCC9 homologue in Drosophila neurons renders flies to sleep less during the first 3 h of the night. ABCC9 encodes an ATP-sensitive potassium channel subunit (SUR2), serving as a sensor of intracellular energy metabolism. Similarity the linkage analysis of sleep by Gottlieb et al. (2007) revealed a linkage peak close to the gene PROK2. Its product is the precursor of prokineticin 2, which is highly expressed in the suprachiasmatic nucleus, regulated by the circadian molecular clock, and believed to be an important output molecule from the suprachiasmatic nucleus, coordinating and transmitting the behavioural circadian rhythm to multiple brain regions (Cheng et al. (2002); Li et al. (2006).

Little is known about the genetic underpinnings sleepiness at distinct childhood growth phases. Through a large-scale meta-analysis of GWAS data for sleep duration, our main aim is to identify genetic mechanisms that underlie sleep duration during childhood.

Hypotheses: We hypothesize that a meta-analysis of GWAS data can identify genetic factors associated with sleep duration.

Outcome variable: Sleep duration during day (night + naps)

Exposure variables: Genetic variants as identified by GWAS genotyping and imputing (1000 Genome Project, release March 2012)

Confounding variables: sex, age, BMI