Using MR, a one allele increase in smoking volume genetic risk score was associated with higher odds of COPD in ever smokers, (OR = 4.32 95%CI:3.37-5.54 P<1×10−15), but no association was seen in IPF (OR=0.55 95%CI: 0.17-1.81 P=0.33). We performed analyses using one-sample MR to test for inferred smoking causality in ever smokers using genetic variants that have a previously demonstrated association with smoking heaviness.Strong associations between disease status and ever having smoked were found in both IPF (OR = 1.52 95%CI:1.32-1.74 P=2.4×10−8) and COPD (OR= 5.77 95%CI:5.48-6.07 P<1×10−15). Here, we used data from the UK Biobank (UKBB) and the well-established genetic technique of Mendelian randomisation (MR) methods to investigate whether smoking is causal for IPF compared with COPD, where causality is established.We looked at observational associations in unrelated Europeans, with 871 IPF cases, 11,413 COPD cases and 366,942 controls. Smoking is a recognised risk factor for IPF but the question of causality remains unanswered.
#Robin on general hospital weight gain 2017 full
Full text.ĪbstractIn a normal year, the fatal lung disease Idiopathic Pulmonary Fibrosis (IPF) accounts for ∼1% of UK deaths. This work demonstrates that for any level of maternal FPG, fetal genetics has a major impact on fetal growth and acts predominantly through independent mechanisms. Similar results were seen for HAPO participants of non-European ancestry (n = 2,842 pairs). Unlike maternal glucose, the fetal genetic score was not associated with cord insulin or C-peptide. For mothers with FPG in the top tertile, the frequency of large for gestational age (birth weight ≥90th centile) was 31.1% for offspring with the highest tertile genetic score and only 14.0% for those with the lowest tertile genetic score. The fetal genetic score influenced birth weight independently of maternal FPG and impacted growth at all levels of maternal glycemia. We tested the effects of maternal fasting plasma glucose (FPG) and a fetal genetic score for birth weight on birth weight and fetal insulin in 2,051 European mother-child pairs from the Exeter Family Study of Childhood Health (EFSOCH) and the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study. It is not known whether fetal genotype modifies the impact of maternal glycemia or whether it acts through insulin-mediated growth.
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Maternal glycemia is a key determinant of birth weight, but recent large-scale genome-wide association studies demonstrated an important contribution of fetal genetics.
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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. 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. 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. In expanded genome-wide association analyses of own birth weight (n = 321,223) and offspring birth weight (n = 230,069 mothers), we identified 190 independent association signals (129 of which are novel). Birth weight variation is influenced by fetal and maternal genetic and non-genetic factors, and has been reproducibly associated with future cardio-metabolic health outcomes.