Reconsidering the Heritability of Intelligence in Adulthood: Taking Assortative Mating and Cultural Transmission into Account

Heritability estimates of general intelligence in adulthood generally range from 75 to 85%, with all heritability due to additive genetic influences, while genetic dominance and shared environmental factors are absent, or too small to be detected. These estimates are derived from studies based on the classical twin design and are based on the assumption of random mating. Yet, considerable positive assortative mating has been reported for general intelligence. Unmodeled assortative mating may lead to biased estimates of the relative magnitude of genetic and environmental factors. To investigate the effects of assortative mating on the estimates of the variance components of intelligence, we employed an extended twin-family design. Psychometric IQ data were available for adult monozygotic and dizygotic twins, their siblings, the partners of the twins and siblings, and either the parents or the adult offspring of the twins and siblings (N = 1314). Two underlying processes of assortment were considered: phenotypic assortment and social homogamy. The phenotypic assortment model was slightly preferred over the social homogamy model, suggesting that assortment for intelligence is mostly due to a selection of mates on similarity in intelligence. Under the preferred phenotypic assortment model, the variance of intelligence in adulthood was not only due to non-shared environmental (18%) and additive genetic factors (44%) but also to non-additive genetic factors (27%) and phenotypic assortment (11%).This non-additive nature of genetic influences on intelligence needs to be accommodated in future GWAS studies for intelligence

Erratum to: Genetic and environmental contributions to the inverse association between specific autistic traits and experience seeking in adults (American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, (2016), 171, 7, 10.1002/ajmg.b.32352)

The above mentioned article was mistakenly omitted from publishing in American Journal of Medical Genetics Part B: Neuropsychiatric Genetics in the Special Issue “Family, Twin and Adoption Studies of Childhood Onset Psychiatric and Neurodevelopmental Disorders,” Volume 171, Issue 7, October 2016, http://onlinelibrary.wiley.com/ doi/10.1002/ajmg.b.v171.7/issueto

Prevalence and predictors of vitamin D deficiency based on maternal mid-gestation and neonatal cord bloods: the Generation R Study

Background Population-based studies have confirmed that the prevalence of vitamin D deficiency is substantial in many societies, and is of particular concern in pregnant women. Vitamin D deficiency during pregnancy is associated with a wide range of adverse maternal and offspring health outcomes. To date, studies of vitamin D deficiency during pregnancy have focused on measurements at one or two time points in isolation. We examined both midgestation and cord blood 25 hydroxyvitamin D (25OHD) concentration and explored the prevalence and correlates of vitamin D deficiency in a large ethnically diverse cohort of pregnant women and their infants in the Netherlands. Methods This study was embedded in the Generation R Study, a population-based prospective cohort from fetal life onwards in Rotterdam, The Netherlands. Using a highly sensitive tandem mass spectroscopy-based assay, we measured 25OHD in 7256 midgestation samples (mean gestation 20.6 weeks) and 5023 neonatal cord blood samples (mean gestation 40.0 weeks). Using a conservative threshold of less than 25 nmol/L to define vitamin D deficiency, we examined the prevalence and socio-demographic correlates of vitamin D deficiency in mothers and infants. We also derived a measure of vitamin D deficiency based on the two time points in order to explore persistent vitamin D deficiency in mother-infant pairs. Results The prevalence of vitamin D deficiency at midgestation was 26%, while in neonates 46% were deficient. 21% of the mother-infant pairs had persistent vitamin D deficiency (i.e., deficient in maternal and cord samples) and an additional 29% were vitamin D deficient in one of the two samples only. Persistent vitamin D deficiency was strongly associated with non-European ancestry and spring birth. Conclusions A sizeable proportion of women and their neonatal offspring in the Generation R cohort were vitamin D deficient. In light of the large body of evidence linking vitamin D deficiency with adverse health outcomes for pregnant women and their offspring, our findings indicate a large unmet need in this population. In particular, women and infants from non-European ethnic background are at high risk of vitamin D deficiency

Dominance Genetic Variation Contributes Little to the Missing Heritability for Human Complex Traits

For human complex traits, non-additive genetic variation has been invoked to explain "missing heritability,'' but its discovery is often neglected in genome-wide association studies. Here we propose a method of using SNP data to partition and estimate the proportion of phenotypic variance attributed to additive and dominance genetic variation at all SNPs (h(SNP)(2) and delta(2)(SNP)) in unrelated individuals based on an orthogonal model where the estimate of h(SNP)(2) is independent of that of delta(2)(SNP). With this method, we analyzed 79 quantitative traits in 6,715 unrelated European Americans. The estimate of delta(2)(SNP) averaged across all the 79 quantitative traits was 0.03, approximately a fifth of that for additive variation (average h(SNP)(2) = 0.15). There were a few traits that showed substantial estimates of delta(2)(SNP), none of which were replicated in a larger sample of 11,965 individuals. We further performed genome-wide association analyses of the 79 quantitative traits and detected SNPs with genome-wide significant dominance effects only at the ABO locus for factor VIII and von Willebrand factor. All these results suggest that dominance variation at common SNPs explains only a small fraction of phenotypic variation for human complex traits and contributes little to the missing narrow-sense heritability problem

Bos taurus strain:dairy beef (cattle): 1000 Bull Genomes Run 2, Bovine Whole Genome Sequence

Whole genome sequence data (BAM format) of 234 bovine individuals aligned to UMD3.1. The aim of the study was to identify genetic variants (SNPs and indels) for downstream analysis such as imputation, GWAS, and detection of lethal recessives. Additional sequences for later 1000 bull genomes runs can be found at partners individual projects including PRJEB9343, PRJNA176557, PRJEB18113, PRNJA343262, PRJNA324822, PRJNA324270, PRJNA277147, PRJEB5462