https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 Associations of autozygosity with a broad range of human phenotypes https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45256 1.4 million individuals, we show that FROH is significantly associated (p < 0.0005) with apparently deleterious changes in 32 out of 100 traits analysed. These changes are associated with runs of homozygosity (ROH), but not with common variant homozygosity, suggesting that genetic variants associated with inbreeding depression are predominantly rare. The effect on fertility is striking: FROH equivalent to the offspring of first cousins is associated with a 55% decrease [95% CI 44–66%] in the odds of having children. Finally, the effects of FROH are confirmed within full-sibling pairs, where the variation in FROH is independent of all environmental confounding.]]> Wed 26 Oct 2022 20:06:39 AEDT ]]> Trans-ethnic association study of blood pressure determinants in over 750,000 individuals https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42468 Wed 24 Aug 2022 11:40:43 AEST ]]> Genetic analysis of over 1 million people identifies 535 new loci associated with blood pressure traits https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44073 Wed 22 Mar 2023 15:46:47 AEDT ]]> 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 ]]> Genome-wide analysis in over 1 million individuals of European ancestry yields improved polygenic risk scores for blood pressure traits https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55383 Fri 24 May 2024 10:35:40 AEST ]]>