Shared genetic architecture underlying sleep and weight in children.

Abstract Meta-analyses suggest shorter sleep as a risk factor for obesity in children. The prevailing hypothesis is that shorter sleep causes obesity by impacting homeostatic processes. Sleep duration and adiposity are both heritable, and the association may reflect shared genetic aetiology. We examined the association between a body mass index (BMI) genetic risk score (GRS) and objectively-measured total sleep time (TST) in a cohort of Norwegian children (enrolled at age four in 2007–2008) using cross-sectional data at age six. The analytical sample included 452 six-year old children with complete genotype and phenotype data. The outcome was actigraphic total sleep time (TST) measured at age six years. Genetic risk of obesity was inferred using a 32-single nucleotide polymorphism (SNP) weighted GRS of BMI. Covariates were BMI-Standard deviation scores (SDS) (which takes into account age and sex) and, in a sensitivity analysis socioeconomic status. Analyses consisted of Pearson's correlations and linear regressions. In our sample, 54% of participants were male; mean (SD) TST, age and BMI were 9.6 (0.8) hours, 6.0 (0.2) years and 15.3 (1.2) kg/m2, respectively. BMI and TST were not correlated, r = −0.003, p = 0.946. However, the BMI GRS was associated with TST after adjusting for BMI-SDS, standardised β = −0.11; 95% confidence interval (CI) = -0.22, −0.01. To our knowledge, this is the first study to establish a relationship between genetic risk of obesity and objective sleep duration in children. Findings suggest some shared genetic aetiology underlying these traits. Future research could identify the common biological pathways through which common genes predispose to both shorter sleep and increased risk of obesity.