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Rivadeneira, F.

Publications and source records attributed to Rivadeneira, F..

6 recordsLinked to original sources

Variants in the fetal genome near pro-inflammatory cytokine genes on 2q13 are associated with gestational duration

The duration of pregnancy is influenced by fetal and maternal genetic and non-genetic factors. We conducted a fetal genome-wide association meta-analysis of gestational duration, and early preterm, preterm, and postterm birth in 84,689 infants. One locus on chromosome 2q13 was associated with gestational duration; the association was replicated in 9,291 additional infants (combined P = 3.96 x 10-14). Analysis of 15,536 mother-child pairs showed that the association was driven by fetal rather than maternal genotype. Functional experiments showed that the lead SNP, rs7594852, alters the binding of the HIC1 transcriptional repressor. Genes at the locus include several interleukin 1 family members with roles in pro-inflammatory pathways that are central to the process of parturition. Further understanding of the underlying mechanisms will be of great public health importance, since giving birth either before or after the window of term gestation is associated with increased morbidity and mortality.

genetics

Machine Learning to Predict Osteoporotic Fracture Risk from Genotypes

BackgroundGenomics-based prediction could be useful since genome-wide genotyping costs less than many clinical tests. We tested whether machine learning methods could provide a clinically-relevant genomic prediction of quantitative ultrasound speed of sound (SOS)--a risk factor for osteoporotic fracture.\n\nMethodsWe used 341,449 individuals from UK Biobank with SOS measures to develop genomically-predicted SOS (gSOS) using machine learning algorithms. We selected the optimal algorithm in 5,335 independent individuals and then validated it and its ability to predict incident fracture in an independent test dataset (N = 80,027). Finally, we explored whether genomic pre-screening could complement a UK-based osteoporosis screening strategy, based on the validated tool FRAX.\n\nResultsgSOS explained 4.8-fold more variance in SOS than FRAX clinical risk factors (CRF) alone (r2 = 23% vs. 4.8%). A standard deviation decrease in gSOS, adjusting for the CRF-FRAX score was associated with a higher increased odds of incident major osteoporotic fracture (1,491 cases / 78,536 controls, OR = 1.91 [1.70-2.14], P = 10-28) than that for measured SOS (OR = 1.60 [1.50-1.69], P = 10-52) and femoral neck bone mineral density (147 cases / 4,594 controls, OR = 1.53 [1.27-1.83], P = 10-6). Individuals in the bottom decile of the gSOS distribution had a 3.25-fold increased risk of major osteoporotic fracture (P = 10-18) compared to the top decile. A gSOS-based FRAX score, identified individuals at high risk for incident major osteoporotic fractures better than the CRF-FRAX score (P = 10-14). Introducing a genomic pre-screening step into osteoporosis screening in 4,741 individuals reduced the number of required clinical visits from 2,455 to 1,273 and the number of BMD tests from 1,013 to 473, while only reducing the sensitivity to identify individuals eligible for therapy from 99% to 95%.\n\nInterpretationThe use of genotypes in a machine learning algorithm resulted in a clinically-relevant prediction of SOS and fracture, with potential to impact healthcare resource utilization.\n\nResearch in ContextO_ST_ABSEvidence Before this StudyC_ST_ABSGenome-wide association studies have identified many loci associated with risk of clinically-relevant fracture risk factors, such as SOS. Yet, it is unclear if such information can be leveraged to identify those at risk for disease outcomes, such as osteoporotic fractures. Most previous attempts to predict disease risk from genotypes have used polygenic risk scores, which may not be optimal for genomic-prediction. Despite these obstacles, genomic-prediction could enable screening programs to be more efficient since most people screened in a population are not determined to have a level of risk that would prompt a change in clinical care. Genomic pre-screening could help identify individuals whose risk of disease is low enough that they are unlikely to benefit from screening.\n\nAdded Value of this StudyUsing a large dataset of 426,811 individuals we trained and tested a machine learning algorithm to genomically-predict SOS. This metric, gSOS, had performance characteristics for predicting fracture risk that were similar to measured SOS and femoral neck BMD. Implementing a gSOS-based pre-screening step into the UK-based osteoporosis treatment guidelines reduced the number of individuals who would require screening clinical visits and skeletal testing by approximately 50%, while having little impact on the sensitivity to identify individuals at high risk for osteoporotic fracture.\n\nImplications of all of the Available EvidenceClinically-relevant genomic prediction of heritable traits is feasible using the machine learning algorithm presented here in large sample sizes. Genome-wide genotyping is now less expensive than many clinical tests, needs to be performed once over a lifetime and could risk stratify for multiple heritable traits and diseases years prior to disease onset, providing an opportunity for prevention. The implementation of such algorithms could improve screening efficiency, yet their cost-effectiveness will need to be ascertained in subsequent analyses.

genomics

Genomic analysis of diet composition finds novel loci and associations with health and lifestyle

We conducted genome-wide association study (GWAS) meta-analyses of relative caloric intake from fat, protein, carbohydrates and sugar in over 235,000 individuals. We identified 21 approximately independent lead SNPs. Relative protein intake exhibits the strongest relationships with poor health, including positive genetic associations with obesity, type 2 diabetes, and heart disease (rg {approx} 0.15 - 0.5). Relative carbohydrate and sugar intake have negative genetic correlations with waist circumference, waist-hip ratio, and neighborhood poverty (|rg| {approx} 0.1 - 0.3). Overall, our results show that the relative intake of each macronutrient has a distinct genetic architecture and pattern of genetic correlations suggestive of health implications beyond caloric content.

genetics

Low-frequency variation in TP53 has large effects on head circumference and intracranial volume

Cranial growth and development affects the closely related traits of head circumference (HC) and intracranial volume (ICV). Here we model the developmental genetic architecture of HC, showing this is genetically stable and correlated with genetic determinants of ICV. Investigating up to 46,000 children and adults of European descent, we identify association with final HC and/or final ICV+HC at 9 novel common and low-frequency loci, illustrating that genetic variation from a wide allele frequency spectrum contributes to cranial growth. The largest effects are reported for low-frequency variants within TP53, with 0.5 cm wider heads in increaser-allele carriers versus non-carriers during mid-childhood.

genetics

Consortium genome-wide meta-analysis for childhood dental caries traits

Prior studies suggest dental caries traits in children and adolescents are partially heritable, but there has been no large-scale consortium genome-wide association study (GWAS) to date. We therefore performed GWAS for caries in participants aged 2.5-18.0 years from 9 contributing centers. Phenotype definitions were created for the presence or absence of treated or untreated caries, stratified by primary and permanent dentition. All studies tested for association between caries and genotype dosage (imputed to Haplotype Reference Consortium or 1000 Genomes phase 1 version 3 panels) accounting for population stratification. Fixed-effects meta-analysis was performed weighted by inverse standard error. Analysis included up to 19,003 individuals (7,530 affected) for primary teeth and 13,353 individuals (5,875 affected) for permanent teeth. Evidence for association with caries status was observed at rs1594318-C for primary teeth (intronic within ALLC, Odds Ratio (OR) 0.85, Effect Allele Frequency (EAF) 0.60, p 4.13e-8) and rs7738851-A (intronic within NEDD9, OR 1.28, EAF 0.85, p 1.63e-8) for permanent teeth. Consortium-wide estimated heritability of caries was low (h2 of 1% [95% CI: 0%:7%] and 6% [95% CI 0%:13%] for primary and permanent dentitions, respectively) compared to corresponding within-study estimates (h2 of 28%, [95% CI: 9%:48%] and 17% [95% CI:2%:31%]) or previously published estimates. This study was designed to identify common genetic variants with modest effects which are consistent across different populations. We found few single variants associated with caries status under these assumptions. Phenotypic heterogeneity between cohorts and limited statistical power will have contributed; these findings could also reflect complexity not captured by our study design, such as genetic effects which are conditional on environmental exposure.\n\nAuthor summaryDental caries (tooth decay) is a common disease in children. Previous studies suggest genetic factors alter caries risk, but to date there is a gap of knowledge in identifying which specific genetic variants are responsible. We undertook analysis in a consortium including around 19,000 children and investigated whether any of 8 million common genetic variants were associated with risk of caries in primary (milk) or permanent teeth. If identified, these variants are used as tags to highlight genes which may be involved in a disease. We identified variants in two loci associated with caries status; in the primary (rs1594318) and permanent dentition (rs7738851). The former is intronic in ALLC, a gene with poorly understood function. The latter is an intronic variant within NEDD9, a gene which has several known functions including a role in development of craniofacial structures. To gain a more comprehensive understanding of genetic effects which influence caries larger studies and a better understanding of environmental modifiers or interactions with genetic effects are required.

genetics

Maternal and fetal genetic contribution to gestational weight gain

BackgroundClinical recommendations to limit gestational weight gain (GWG) imply high GWG is causally related to adverse outcomes in mother or offspring, but GWG is the sum of several inter-related complex phenotypes (maternal fat deposition and vascular expansion, placenta, amniotic fluid and fetal growth). Understanding the genetic contribution to GWG could help clarify the potential effect of its different components on maternal and offspring health. Here we explore the genetic contribution to total, early and late GWG.\n\nParticipants and MethodsA genome-wide association study was used to identify maternal and fetal variants contributing to GWG in up to 10,543 mothers and up to 16,317 offspring of European origin, with replication in 10,660 mothers and 7,561 offspring. Additional analyses determined the proportion of variability in GWG from maternal and fetal common genetic variants and the overlap of established genome-wide significant variants for phenotypes relevant to GWG (e.g. maternal BMI and glucose, birthweight).\n\nResultsWe found that approximately 20% of the variability in GWG was tagged by common maternal genetic variants, and that the fetal genome made a surprisingly minor contribution to explaining variation in GWG. We were unable to identify any genetic variants that reached genome-wide levels of significance (P<5x10-8) and replicated. Some established maternal variants associated with increased BMI, fasting glucose and type 2 diabetes were associated with lower early, and higher later GWG. Maternal variants related to higher systolic blood pressure were related to lower late GWG. Established maternal and fetal birthweight variants were largely unrelated to GWG.\n\nConclusionWe found a modest contribution of maternal common variants to GWG and some overlap of maternal BMI, glucose and type 2 diabetes variants with GWG. These findings suggest that associations between GWG and later offspring/maternal outcomes may be due to the relationship of maternal BMI and diabetes with GWG.

genetics