A 30-nation investigation of lay heritability beliefs.

Lay beliefs about human trait heritability are consequential for cooperation and social cohesion, yet there has been no global characterisation of these beliefs. Participants from 30 countries (N = 6128) reported heritability beliefs for intelligence, personality, body weight and criminality, and transnational factors that could influence these beliefs were explored using public nation-level data. Globally, mean lay beliefs differ from published heritability (h2) estimated by twin studies, with a worldwide majority overestimating the heritability of personality and intelligence, and underestimating body weight and criminality. Criminality was seen as substantially less attributable to genes than other traits. People from countries with high infant mortality tended to ascribe greater heritability for most traits, relative to people from low infant mortality countries. This study provides the first systematic foray into worldwide lay heritability beliefs. Future research must incorporate diverse global perspectives to further contextualise and extend upon these findings.

Scientific clickbait: Examining media coverage and readability in genome-wide association research.

In the present study, we analyzed a large corpus of English-language online media articles covering genome-wide association studies (GWAS), exemplifying the use of computational methods to study science communication in biological sciences. We analyzed trends in media coverage, readability, themes, and mentions of ethical and social issues, in over 5,000 websites published from 2005 to 2018 from 3,555 GWAS publications on 1,943 different traits, identified via GWAS Catalog using a text-mining approach to inform the discussion about genetic literacy and media coverage. We found that 22.9% of GWAS papers received media attention but most were described in language too complex to be understood by the public. Ethical issues are rarely mentioned and mentions of translation are increasing over time. We predicted media attention based on year of publication, number of genetic associations identified, study sample size, and journal impact factor, using a regression model (r2 = 38.7%). We found that chronotype, educational attainment, alcohol and coffee consumption, sexual orientation, tanning, and hair color received substantially more attention than predicted by the regression model. We also evaluated the prevalence of the clickbait "one gene, one disease" headlines (e.g., "Scientists Say They've Found Gene That Causes Breast Cancer") and found that it is declining. In sum, online media coverage of GWAS should be more accessible, introduce more modern genetics terms, and when appropriate, ELSI should be mentioned. Science communication research can benefit from big data and text-mining techniques which allow us to study trends and changes in coverage trends across thousands of media outlets. Results can be explored interactively in a website we have built for this manuscript: https://jjmorosoli.shinyapps.io/newas/.

Uncovering the genetic architecture of broad antisocial behavior through a genome-wide association study meta-analysis.

Despite the substantial heritability of antisocial behavior (ASB), specific genetic variants robustly associated with the trait have not been identified. The present study by the Broad Antisocial Behavior Consortium (BroadABC) meta-analyzed data from 28 discovery samples (N = 85,359) and five independent replication samples (N = 8058) with genotypic data and broad measures of ASB. We identified the first significant genetic associations with broad ASB, involving common intronic variants in the forkhead box protein P2 (FOXP2) gene (lead SNP rs12536335, p = 6.32 × 10-10). Furthermore, we observed intronic variation in Foxp2 and one of its targets (Cntnap2) distinguishing a mouse model of pathological aggression (BALB/cJ strain) from controls (BALB/cByJ strain). Polygenic risk score (PRS) analyses in independent samples revealed that the genetic risk for ASB was associated with several antisocial outcomes across the lifespan, including diagnosis of conduct disorder, official criminal convictions, and trajectories of antisocial development. We found substantial genetic correlations of ASB with mental health (depression rg = 0.63, insomnia rg = 0.47), physical health (overweight rg = 0.19, waist-to-hip ratio rg = 0.32), smoking (rg = 0.54), cognitive ability (intelligence rg = -0.40), educational attainment (years of schooling rg = -0.46) and reproductive traits (age at first birth rg = -0.58, father's age at death rg = -0.54). Our findings provide a starting point toward identifying critical biosocial risk mechanisms for the development of ASB.

Genetic association study of childhood aggression across raters, instruments, and age.

Childhood aggressive behavior (AGG) has a substantial heritability of around 50%. Here we present a genome-wide association meta-analysis (GWAMA) of childhood AGG, in which all phenotype measures across childhood ages from multiple assessors were included. We analyzed phenotype assessments for a total of 328 935 observations from 87 485 children aged between 1.5 and 18 years, while accounting for sample overlap. We also meta-analyzed within subsets of the data, i.e., within rater, instrument and age. SNP-heritability for the overall meta-analysis (AGGoverall) was 3.31% (SE = 0.0038). We found no genome-wide significant SNPs for AGGoverall. The gene-based analysis returned three significant genes: ST3GAL3 (P = 1.6E-06), PCDH7 (P = 2.0E-06), and IPO13 (P = 2.5E-06). All three genes have previously been associated with educational traits. Polygenic scores based on our GWAMA significantly predicted aggression in a holdout sample of children (variance explained = 0.44%) and in retrospectively assessed childhood aggression (variance explained = 0.20%). Genetic correlations (rg) among rater-specific assessment of AGG ranged from rg = 0.46 between self- and teacher-assessment to rg = 0.81 between mother- and teacher-assessment. We obtained moderate-to-strong rgs with selected phenotypes from multiple domains, but hardly with any of the classical biomarkers thought to be associated with AGG. Significant genetic correlations were observed with most psychiatric and psychological traits (range [Formula: see text]: 0.19-1.00), except for obsessive-compulsive disorder. Aggression had a negative genetic correlation (rg = ~-0.5) with cognitive traits and age at first birth. Aggression was strongly genetically correlated with smoking phenotypes (range [Formula: see text]: 0.46-0.60). The genetic correlations between aggression and psychiatric disorders were weaker for teacher-reported AGG than for mother- and self-reported AGG. The current GWAMA of childhood aggression provides a powerful tool to interrogate the rater-specific genetic etiology of AGG.

The Role of the Environment in Overweight and Eating Behavior Variability: Insights from a Multivariate Twin Study.

Research has emphasized the genetic basis of individual differences in body mass index (BMI); however, genetic factors cannot explain the rapid rise of obesity. Eating behaviors have been stipulated to be the behavioral expression of genetic risk in an obesogenic environment. In this study, we decompose variation and covariation between three key eating behaviors and BMI in a sample of 698 participants, consisting of 167 monozygotic, 150 dizygotic complete same-sex female twins and 64 incomplete pairs from a population-based twin registry in the southeast of Spain, The Murcia Twin Registry. Phenotypes were emotional eating, uncontrolled eating and cognitive restraint, measured by the Three Factor Eating Questionnaire and objectively measured BMI. Variation in eating behaviors was driven by nonshared environmental factors (range: 56%-65%), whereas shared environmental and genetic factors were secondary. All three eating behaviors were correlated with BMI (r = .19-.25). Nonshared environmental factors explained the covariations (Emotional eating-Uncontrolled eating: rE = .54, 95% CI [.43, .64]; BMI-Cognitive restraint: rE = .15, 95% CI [.01, .28]). In contrast to BMI, individual differences in eating behaviors are mostly explained by nonshared environmental factors, which also accounted for the phenotypic correlation between eating behaviors and BMI. Due to the sample size, analyses were underpowered to detect contributions of additive genetic or shared environmental factors to variation and covariation of the phenotypes. Although more research is granted, these results support that eating behaviors could be viable intervention targets to help individuals maintain a healthy weight.

An Update of Twin Research in Spain: The Murcia Twin Registry.

The Murcia Twin Registry (MTR) is the only population-based registry in Spain. Created in 2006, the registry has been growing more than a decade to become one of the references for twin research in the Mediterranean region. The MTR database currently comprises 3545 adult participants born between 1940 and 1977. It also holds a recently launched satellite registry of university students (N = 204). Along five waves of data collection, the registry has gathered questionnaire and anthropometric data, as well as biological samples. The MTR keeps its main research focus on health and health-related behaviors from a public health perspective. This includes lifestyle, health promotion, quality of life or environmental conditions. Future short-term development points to the expansion of the biobank and the continuation of the collection of longitudinal data.

Genetic and environmental influences to low back pain and symptoms of depression and anxiety: A population-based twin study.

BACKGROUND: People suffering from chronic pain are more likely to experience symptoms of depression and anxiety. However, the mechanisms underlying this relationship remain largely unknown. In light of the moderate to large effects of genetic factors on chronic pain and depression and anxiety, we aimed to estimate the relative contribution of genetic and environmental factors to the relationship between these traits. METHODS: Using data from 2139 participants in the Murcia Twin Registry, we employed a bivariate analysis and structural equation modeling to estimate the relative influences of genetics and the environment on the covariation between low back pain and symptoms of depression and anxiety. RESULTS: We have obtained heritability estimates of 0.26 (95% Confidence Interval (CI) 0.11, 0.41) for chronic low back pain and 0.45 (95% CI 0.29, 0.50) for symptoms of depression and anxiety. The phenotypic, genetic, and unique environment correlations in the bivariate analytical model were, respectively, rph=0.26 (95% CI 0.19, 0.33); rG=0.47 (95% CI 0.42, 0.70); rE=0.14 (95% CI -0.04, 0.25). The percentage of covariance between low back pain and symptoms of depression and anxiety attributable to additive genetic factors was 63.6%, and to unique environment 36.4%. CONCLUSIONS: Our findings confirm the relationship between low back pain and symptoms of depression and anxiety in a non-clinical sample. Shared genetic factors affect significantly the covariation between these conditions, supporting the role of common biological and physiological pathways.

Correction to: Altruistic Behavior among Twins : Willingness to Fight and Self-Sacrifice for Their Closest Relatives.

The original version of this article unfortunately contained a mistake. The presentation of the article title and subtitle was incorrect.

Altruistic Behavior among Twins : Willingness to Fight and Self-Sacrifice for Their Closest Relatives.

According to kin selection theory, indirect reproductive advantages may induce individuals to care for others with whom they share genes by common descent, and the amount of care, including self-sacrifice, will increase with the proportion of genes shared. Twins represent a natural situation in which this hypothesis can be tested. Twin pairs experience the same early environment because they were born and raised at the same time and in the same family but their genetic relatedness differs depending on zygosity. We compared the degree of willingness to fight and sacrifice for the co-twin among monozygotic (MZ) and dizygotic (DZ) pairs in a sample of 1443 same-sex and opposite-sex twins. We also analyzed the effect of the subject's gender and that of the co-twin on those altruistic behaviors. Results partly supported the postulated explanation. MZ twins (who share nearly their entire genome) were significantly more likely than DZ twins (who on average share half of their segregating genes) to self-sacrifice for their co-twins, but zygosity did not affect willingness to fight for him/her. The genders of the subject and of the co-twin, not genetic relatedness, were the best predictors of aggressive altruistic intentions.

Effects of Social Attitude Change on Smoking Heritability.

Societal attitudes and norms to female smoking changed in Spain in the mid-twentieth century from a restrictive to a tolerant, and an even pro-smoking, posture, while social attitudes remained stable for males. We explored whether this difference in gender-related social norms influenced the heritability of two tobacco use measures: lifetime smoking and number of years smoking. We used a population-based sample of 2285 twins (mean age = 55.78; SD = 7.45; 58% females) whose adolescence began between the mid-1950s and the early 1980s. After modeling the effect of sex and year of birth on the variance components, we observed that the impact of the genetic and shared environmental factors varied differently by birth cohort between males and females. For females, shared environment explained a higher proportion of variance than the genetic factors in older cohorts. However, this situation was inverted in the younger female cohorts. In contrast, no birth cohort effect was observed for males, where the impact of the genetic and environmental factors remained constant throughout the study period. These results suggest that heritability is larger in a permissive social environment, whereas shared-environmental factors are more relevant in a society that is less tolerant to smoking.

Genetic and Environmental Contributions to Sleep Quality and Low Back Pain: A Population-Based Twin Study.

OBJECTIVE: The aim of the study was to estimate the extent to which the co-occurrence of poor sleep quality and low back pain is due to the same genetic and/or environmental risk factors or due to a causal association. METHODS: Cross-sectional data on sleep quality (Pittsburgh Sleep Quality index) and low back pain were collected in a population-based sample of adult twins (N = 2134) registered with the Murcia Twin Registry. Bivariate analysis and structural equation modeling were used. RESULTS: The phenotypic correlation between sleep quality and low back pain was 0.23 (95% confidence interval [CI] = 0.17-0.28). The best-fitting bivariate model included additive genetic and unique environmental factors. Genetic factors accounted for 26% (95% CI = 10-40) and 34% (95% CI = 25-43) of the variability of low back pain and sleep quality, respectively. The correlation between the genetic factors underlying each trait was rG of 0.33 (95% CI = 0.03-0.66), and this overlap of genetic factors explained 42.5% of the phenotypic correlation. On the other hand, nonshared environmental factors of each variable were only fairly correlated rE of 0.19 (95% CI = 0.06-0.31), although this overlap explained 57.5% of the phenotypic correlation. In addition, twins in monozygotic pairs with poorer sleep quality presented more often with low back pain than their co-twins (ρ^ = 0.25, p < .0001). CONCLUSIONS: The data are compatible with a causal effect of sleep quality on low back pain (or the reverse effect), because the correlations between the genetic and unique environmental factors for each trait were significant and there was a significant correlation between the monozygotic twins' difference scores. Apart from environmental factors that affect both characteristics, there are many individual-specific events that influence low back pain but differ from those influencing sleep quality.