Ken B. Hanscombe

Socioeconomic Status (SES) and Children's Intelligence (IQ): In a UK-Representative Sample SES Moderates the Environmental, Not Genetic, Effect on IQ

Background The environment can moderate the effect of genes - a phenomenon called gene-environment (GxE) interaction. Several studies have found that socioeconomic status (SES) modifies the heritability of childrens intelligence. Among low-SES families, genetic factors have been reported to explain less of the variance in intelligence; the reverse is found for high-SES families. The evidence however is inconsistent. Other studies have reported an effect in the opposite direction (higher heritability in lower SES), or no moderation of the genetic effect on intelligence. Methods Using 8716 twin pairs from the Twins Early Development Study (TEDS), we attempted to replicate the reported moderating effect of SES on childrens intelligence at ages 2, 3, 4, 7, 9, 10, 12 and 14: i.e., lower heritability in lower-SES families. We used a twin model that allowed for a main effect of SES on intelligence, as well as a moderating effect of SES on the genetic and environmental components of intelligence. Results We found greater variance in intelligence in low-SES families, but minimal evidence of GxE interaction across the eight ages. A power calculation indicated that a sample size of about 5000 twin pairs is required to detect moderation of the genetic component of intelligence as small as 0.25, with about 80% power - a difference of 11% to 53% in heritability, in low- (−2 standard deviations, SD) and high-SES (+2 SD) families. With samples at each age of about this size, the present study found no moderation of the genetic effect on intelligence. However, we found the greater variance in low-SES families is due to moderation of the environmental effect – an environment-environment interaction. Conclusions In a UK-representative sample, the genetic effect on intelligence is similar in low- and high-SES families. Childrens shared experiences appear to explain the greater variation in intelligence in lower SES.

First Genome-Wide Association Study on Anxiety-Related Behaviours in Childhood

Background Twin studies have shown that anxiety in a general population sample of children involves both domain-general and trait-specific genetic effects. For this reason, in an attempt to identify genes responsible for these effects, we investigated domain-general and trait-specific genetic associations in the first genome-wide association (GWA) study on anxiety-related behaviours (ARBs) in childhood. Methods The sample included 2810 7-year-olds drawn from the Twins Early Development Study (TEDS) with data available for parent-rated anxiety and genome-wide DNA markers. The measure was the Anxiety-Related Behaviours Questionnaire (ARBQ), which assesses four anxiety traits and also yields a general anxiety composite. Affymetrix GeneChip 6.0 DNA arrays were used to genotype nearly 700,000 single-nucleotide polymorphisms (SNPs), and IMPUTE v2 was used to impute more than 1 million SNPs. Several GWA associations from this discovery sample were followed up in another TEDS sample of 4804 children. In addition, Genome-wide Complex Trait Analysis (GCTA) was used on the discovery sample, to estimate the total amount of variance in ARBs that can be accounted for by SNPs on the array. Results No SNP associations met the demanding criterion of genome-wide significance that corrects for multiple testing across the genome (p<5×10−8). Attempts to replicate the top associations did not yield significant results. In contrast to the substantial twin study estimates of heritability which ranged from 0.50 (0.03) to 0.61 (0.01), the GCTA estimates of phenotypic variance accounted for by the SNPs were much lower 0.01 (0.11) to 0.19 (0.12). Conclusions Taken together, these GWAS and GCTA results suggest that anxiety – similar to height, weight and intelligence − is affected by many genetic variants of small effect, but unlike these other prototypical polygenic traits, genetic influence on anxiety is not well tagged by common SNPs.

In search of genes associated with risk for psychopathic tendencies in children: a two‐stage genome‐wide association study of pooled DNA

BACKGROUND Quantitative genetic data from our group indicates that antisocial behaviour (AB) is strongly heritable when coupled with psychopathic, callous-unemotional (CU) personality traits. We have also demonstrated that the genetic influences for AB and CU overlap considerably. We conducted a genome-wide association scan that capitalises on these findings in an attempt to identify quantitative trait loci (QTLs) that may increase risk for psychopathic tendencies (AB+/CU+). METHODS Teacher ratings at age 7 were used to screen 8374 twins with available DNA samples for individuals that were high vs. low on both AB and CU. In Stage 1, we screened for allele frequency differences in 642,432 autosomal single-nucleotide polymorphisms (SNPs) using the Affymetrix 6.0 GeneChip with pooled DNA for high-scoring (AB+/CU+) versus low-scoring children (N = approximately 300/group). In Stage 2, we tested the 3000 most strongly associated SNPs from Stage 1 for association in the same direction in a second sample of high- versus low-scoring children from the same twin study (18% co-twins). RESULTS Using allele frequencies estimated from pooled DNA, we found suggestive evidence for enrichment of association in the second stage of our two-stage genome-wide association design and focus on reporting the 30 top-ranking SNPs nominally associated with psychopathic tendencies. These SNPs include neurodevelopmental genes such as ROBO2. CONCLUSIONS Although none of the SNPs reached genome-wide statistical significance we have generated a list of SNPs that are potentially associated with psychopathic tendencies, which we believe warrant verification and replication in large independent and clinical samples.

The correlation between reading and mathematics ability at age twelve has a substantial genetic component

Dissecting how genetic and environmental influences impact on learning is helpful for maximizing numeracy and literacy. Here we show, using twin and genome-wide analysis, that there is a substantial genetic component to children’s ability in reading and mathematics, and estimate that around one half of the observed correlation in these traits is due to shared genetic effects (so-called Generalist Genes). Thus, our results highlight the potential role of the learning environment in contributing to differences in a child’s cognitive abilities at age twelve.

Chaotic Homes and Children’s Disruptive Behavior A Longitudinal Cross-Lagged Twin Study

Chaotic home lives are correlated with behavior problems in children. In the study reported here, we tested whether there was a cross-lagged relation between children’s experience of chaos and their disruptive behaviors (conduct problems and hyperactivity-inattention). Using genetically informative models, we then tested for the first time whether the influence of household chaos on disruptive behavior was environmentally mediated and whether genetic influences on children’s disruptive behaviors accounted for the heritability of household chaos. We measured children’s perceptions of household chaos and parents’ ratings of children’s disruptive behavior at ages 9 and 12 in a sample of 6,286 twin pairs from the Twins Early Development Study (TEDS). There was a phenotypic cross-lagged relation between children’s experiences of household chaos and their disruptive behavior. In genetically informative models, we found that the effect of household chaos on subsequent disruptive behavior was environmentally mediated. However, genetic influences on disruptive behavior did not explain why household chaos was heritable.

Chaotic homes and school achievement: a twin study

Background Chaotic homes predict poor school performance. Given that it is known that genes affect both childrens experience of household chaos and their school achievement, to what extent is the relationship between high levels of noise and environmental confusion in the home, and childrens school performance, mediated by heritable child effects? This is the first study to explore the genetic and environmental pathways between household chaos and academic performance. Method Childrens perceptions of family chaos at ages 9 and 12 and their school performance at age 12 were assessed in more than 2,300 twin pairs. The use of child-specific measures in a multivariate genetic analysis made it possible to investigate the genetic and environmental origins of the covariation between childrens experience of chaos in the home and their school achievement. Results Childrens experience of family chaos and their school achievement were significantly correlated in the expected negative direction (r = −.26). As expected, shared environmental factors explained a large proportion (63%) of the association. However, genetic factors accounted for a significant proportion (37%) of the association between childrens experience of household chaos and their school performance. Conclusions The association between chaotic homes and poor performance in school, previously assumed to be entirely environmental in origin, is in fact partly genetic. How childrens home environment affects their academic achievement is not simply in the direction environment → child → outcome. Instead, genetic factors that influence childrens experience of the disordered home environment also affect how well they do at school. The relationship between the child, their environment and their performance at school is complex: both genetic and environmental factors play a role.

Why do spatial abilities predict mathematical performance

Abstract Spatial ability predicts performance in mathematics and eventual expertise in science, technology and engineering. Spatial skills have also been shown to rely on neuronal networks partially shared with mathematics. Understanding the nature of this association can inform educational practices and intervention for mathematical underperformance. Using data on two aspects of spatial ability and three domains of mathematical ability from 4174 pairs of 12‐year‐old twins, we examined the relative genetic and environmental contributions to variation in spatial ability and to its relationship with different aspects of mathematics. Environmental effects explained most of the variation in spatial ability (~70%) and in mathematical ability (~60%) at this age, and the effects were the same for boys and girls. Genetic factors explained about 60% of the observed relationship between spatial ability and mathematics, with a substantial portion of the relationship explained by common environmental influences (26% and 14% by shared and non‐shared environments respectively). These findings call for further research aimed at identifying specific environmental mediators of the spatial–mathematics relationship. Research highlights About a third of the variation in spatial ability at age 12 is explained by genetic factors; a little less than half of the variation in mathematics at this age is genetic. We find no sex differences in the genetic and environmental influences (either in magnitude or type) on mathematical and spatial variation at age 12. The observed overlap between spatial ability and mathematics is substantial (r > .40). Approximately 60% of this overlap is explained by common genetic effects, with 40% of the overlap due to environmental experience.

Genetic variation at 16q24.2 is associated with small vessel stroke

Genome‐wide association studies (GWAS) have been successful at identifying associations with stroke and stroke subtypes, but have not yet identified any associations solely with small vessel stroke (SVS). SVS comprises one quarter of all ischemic stroke and is a major manifestation of cerebral small vessel disease, the primary cause of vascular cognitive impairment. Studies across neurological traits have shown that younger‐onset cases have an increased genetic burden. We leveraged this increased genetic burden by performing an age‐at‐onset informed GWAS meta‐analysis, including a large younger‐onset SVS population, to identify novel associations with stroke.

Understanding the science-learning environment: A genetically sensitive approach

Previous studies have shown that environmental influences on school science performance increase in importance from primary to secondary school. Here we assess for the first time the relationship between the science-learning environment and science performance using a genetically sensitive approach to investigate the aetiology of this link. 3000 pairs of 14-year-old twins from the UK Twins Early Development Study reported on their experiences of the science-learning environment and were assessed for their performance in science using a web-based test of scientific enquiry. Multivariate twin analyses were used to investigate the genetic and environmental links between environment and outcome. The most surprising result was that the science-learning environment was almost as heritable (43%) as performance on the science test (50%), and showed negligible shared environmental influence (3%). Genetic links explained most (56%) of the association between learning environment and science outcome, indicating gene–environment correlation.

Trajectories of Callous-Unemotional Traits in Childhood Predict Different Forms of Peer Victimization in Adolescence

Callous-unemotional (CU) traits (e.g., lack of empathy and guilt) differentiate a group of children at particularly high risk for engaging in aggressive behavior, notably bullying. However, little is known about whether youths with CU traits are at risk for being victimized by their peers. We examined the associations between trajectories of CU traits in childhood (between 7 and 12 years old) and peer victimization in adolescence (14 years old). The participants were drawn from the Twins Early Development Study, a longitudinal population-based study of twins born in England and in Wales. The trajectories of CU traits (i.e., stable high, increasing, decreasing and stable low) were identified through general growth mixture modeling. Four forms of peer victimization were considered: physical victimization, verbal victimization, social manipulation, and attacks on property. We found that youths with stable high levels, increasing levels, and decreasing levels of CU traits in childhood had higher levels of physical victimization in adolescence, not explained by other predictors at age 7 (e.g., conduct problems). Youths with increasing levels of CU traits, compared with the ones with stable low levels, also had higher levels of verbal victimization, social manipulation, and attacks on property. Our findings highlight the importance of distinct trajectories of CU traits in accounting for the experience of different forms of peer victimization. Youths with CU traits may benefit from bullying prevention programs, as they are likely to be the targets of peer victimization.