https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 Maternal and fetal genetic effects on birth weight and their relevance to cardio-metabolic risk factors https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48511 n = 321,223) and offspring birth weight (n = 230,069 mothers), we identified 190 independent association signals (129 of which are novel). We used structural equation modeling to decompose the contributions of direct fetal and indirect maternal genetic effects, then applied Mendelian randomization to illuminate causal pathways. For example, both indirect maternal and direct fetal genetic effects drive the observational relationship between lower birth weight and higher later blood pressure: maternal blood pressure-raising alleles reduce offspring birth weight, but only direct fetal effects of these alleles, once inherited, increase later offspring blood pressure. Using maternal birth weight-lowering genotypes to proxy for an adverse intrauterine environment provided no evidence that it causally raises offspring blood pressure, indicating that the inverse birth weight-blood pressure association is attributable to genetic effects, and not to intrauterine programming.]]> Wed 22 Mar 2023 15:25:15 AEDT ]]> Trans-ancestral genome-wide association study of longitudinal pubertal height growth and shared heritability with adult health outcomes. https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54727 Mon 11 Mar 2024 14:11:41 AEDT ]]> Novel loci for childhood body mass index and shared heritability with adult cardiometabolic traits https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41815 Fri 12 Aug 2022 12:45:25 AEST ]]> A trans-ancestral meta-analysis of genome-wide association studies reveals loci associated with childhood obesity https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46943 METTL15). The variant was nominally associated with only the European subgroup analysis but had a consistent direction of effect in other ethnicities. We then utilized trans-ancestral Bayesian analysis to narrow down the location of the probable causal variant at each genome-wide significant signal. Of all the fine-mapped loci, we were able to narrow down the causative variant at four known loci to fewer than 10 single nucleotide polymorphisms (SNPs) (FAIM2, GNPDA2, MC4R and SEC16B loci). In conclusion, an ethnically diverse setting has enabled us to both identify an additional pediatric obesity locus and further fine-map existing loci.]]> Fri 09 Dec 2022 14:01:32 AEDT ]]>