Marit Naess1,2, Erik R Sund1,2,3, Gunnhild Å Vie4, Johan H Bjørngaard3,4, Bjørn Olav Åsvold1,5,6, Turid Lingaas Holmen1, Kirsti Kvaløy1,2,7. 1. HUNT Research Centre, Department of Public Health and Nursing, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway. 2. Nord-Trøndelag Hospital Trust, Levanger Hospital, Levanger, Norway. 3. Faculty of Nursing and Health Sciences, Nord University, Levanger, Norway. 4. Department of Public Health and Nursing, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway. 5. Department of Endocrinology, St. Olav's University Hospital, Trondheim University Hospital, Trondheim, Norway. 6. K.G. Jebsen Center for Genetic Epidemiology, Department of Public Health and Nursing, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway. 7. Centre for Sami Health Research, Department of Community Medicine, UiT The Arctic University of Norway, Tromsø, Norway.
Abstract
OBJECTIVE: This study examined the relationship between parental obesity polygenic risk and children's BMI throughout adolescence. Additionally, from a smaller subsample, the objective was to assess whether parental polygenic risk score (PRS) may act as a proxy for offspring PRS in studies lacking offspring genetic data. METHODS: A total of 8,561 parent-offspring (age 13-19 years) trios from the Trøndelag Health Study (the HUNT Study) were included, of which, 1,286 adolescents had available genetic data. Weighted parental PRSs from 900 single-nucleotide polymorphisms robustly associated with adult BMI were constructed and applied in linear mixed-effects models. RESULTS: A positive association between parental PRS and offspring sex- and age-adjusted BMI (iso-BMI) throughout adolescence was identified. The estimated marginal effects per standard deviation increase in parental PRS were 0.26 (95% CI: 0.18-0.33), 0.36 (95% CI: 0.29-0.43), and 0.62 kg/m2 (95% CI: 0.51-0.72) for maternal, paternal, and combined parental PRS, respectively. In subsample analyses, the magnitude of association of the parental PRS versus offspring PRS with iso-BMI in adolescents was similar. CONCLUSIONS: Parental PRS was consistently associated with offspring iso-BMI throughout adolescence. Results from subsample analyses support the use of parental PRS of obesity as a proxy for adolescent PRS in the absence of offspring genetic data.
OBJECTIVE: This study examined the relationship between parental obesity polygenic risk and children's BMI throughout adolescence. Additionally, from a smaller subsample, the objective was to assess whether parental polygenic risk score (PRS) may act as a proxy for offspring PRS in studies lacking offspring genetic data. METHODS: A total of 8,561 parent-offspring (age 13-19 years) trios from the Trøndelag Health Study (the HUNT Study) were included, of which, 1,286 adolescents had available genetic data. Weighted parental PRSs from 900 single-nucleotide polymorphisms robustly associated with adult BMI were constructed and applied in linear mixed-effects models. RESULTS: A positive association between parental PRS and offspring sex- and age-adjusted BMI (iso-BMI) throughout adolescence was identified. The estimated marginal effects per standard deviation increase in parental PRS were 0.26 (95% CI: 0.18-0.33), 0.36 (95% CI: 0.29-0.43), and 0.62 kg/m2 (95% CI: 0.51-0.72) for maternal, paternal, and combined parental PRS, respectively. In subsample analyses, the magnitude of association of the parental PRS versus offspring PRS with iso-BMI in adolescents was similar. CONCLUSIONS: Parental PRS was consistently associated with offspring iso-BMI throughout adolescence. Results from subsample analyses support the use of parental PRS of obesity as a proxy for adolescent PRS in the absence of offspring genetic data.