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Background Methods Results Conclusions Mental health problems and traits capturing psychopathology are common and often begin during adolescence. Decades of twin studies indicate that genetic factors explain around 50% of individual differences in adolescent psychopathology. In recent years, significant advances, particularly in genomics, have moved this work towards more translational findings.This review provides an overview of the past decade of genetically sensitive studies on adolescent development, covering both family and genomic studies in adolescents aged 10–24 years. We focus on five research themes: (1) co‐occurrence or comorbidity between psychopathologies, (2) stability and change over time, (3) intergenerational transmission, (4) gene–environment interplay, and (5) psychological treatment outcomes.First, research shows that much of the co‐occurrence of psychopathologies in adolescence is explained by genetic factors, with widespread pleiotropic influences on many traits. Second, stability in psychopathology across adolescence is largely explained by persistent genetic influences, whereas change is explained by emerging genetic and environmental influences. Third, contemporary twin‐family studies suggest that different co‐occurring genetic and environmental mechanisms may account for the intergenerational transmission of psychopathology, with some differences across psychopathologies. Fourth, genetic influences on adolescent psychopathology are correlated with a wide range of environmental exposures. However, the extent to which genetic factors interact with the environment remains unclear, as findings from both twin and genomic studies are inconsistent. Finally, a few studies suggest that genetic factors may play a role in psychological treatment response, but these findings have not yet been replicated.Genetically sensitive research on adolescent psychopathology has progressed significantly in the past decade, with family and twin findings starting to be replicated at the genomic level. However, important gaps remain in the literature, and we conclude by providing suggestions of research questions that still need to be addressed. [ABSTRACT FROM AUTHOR]

The article discusses the relationship between school socioeconomic composition and academic outcomes, particularly in Australia, through large-scale assessments. It addresses the debate on whether academic composition mediates the effects of socioeconomic composition on student achievement. The author responds to a critique of their study, arguing that the critique did not engage with the theoretical basis of their research and made erroneous statements about their findings. The study suggests that school socioeconomic compositional effects are substantial and warrant policy reforms, emphasizing the importance of considering academic composition in understanding these effects. [Extracted from the article]

Genotype-phenotype associations between the bovine genome and grazing behaviours measured over time and across contexts have been reported in the past decade, with these suggesting the potential for genetic control over grazing personalities in beef cattle. From the large array of metrics used to describe grazing personality behaviours (GP-behaviours), it is still unclear which ones are linked to specific genes. Our prior observational study has reported associations and trends towards associations between genotypes of the glutamate metabotropic receptor 5 gene (GRM5) and four GP-behaviours, yet the unbalanced representation of GRM5 genotypes occurring in observational studies may have limited the ability to detect associations. Here, we applied a subsampling technique to create a genotypically-balanced dataset in a quasi-manipulative experiment with free ranging cows grazing in steep and rugged terrain of New Zealand's South Island. Using quadratic discriminant analysis, two combinations of eleven GP-behaviours (and a total of fifteen behaviours) were selected to build an exploration model and an elevation model, respectively. Both models achieved ∼ 86% accuracy in correctly discriminating cows' GRM5 genotypes with the training dataset, and the exploration model achieved 85% correct genotype prediction of cows from a testing dataset. Our study suggests a potential pleiotropic effect, with GRM5 controlling multiple grazing behaviours, and with implications for the grazing of steep and rugged grasslands. The study highlights the importance of grazing behavioural genetics in cattle and the potential use of GRM5 markers to select individuals with desired grazing personalities and built herds that collectively utilize steep and rugged rangelands sustainably. [ABSTRACT FROM AUTHOR]

A convergence of trends in assessing the future risk of reoffending could result in morally questionable inputs into the criminal process. Advances in the analysis of DNA and increases in the availability of information about people gleaned from social media might allow for new inferences to be drawn against offenders during the sentencing process. We explore how developments in forensic DNA analysis methods and law enforcement DNA databases in conjunction with information about an offender’s developmental environment could lead the prosecution to postulate a high risk of recidivism and thus argue for a longer sentence. We then consider some reasons why such a prosecution strategy might be troubling. In doing so, we focus on issues related to the inferential process, discrimination, privacy and constitutive luck. [ABSTRACT FROM AUTHOR]

The Twins Early Development Study (TEDS) is a longitudinal study following a cohort of twins born 1994-1996 in England and Wales. Of the 13,759 families who originally consented to take part, over 10,000 families remain enrolled in the study. The current focus of TEDS is on mental health in the mid-twenties. Making use of over 25 years of genetically sensitive data, TEDS is uniquely placed to explore the longitudinal genetic and environmental influences on common mental health disorders in early adulthood. This paper outlines recent data collection efforts supporting this work, including a cohort-wide mental health assessment at age 26 and a multi-phase Covid-19 study. It will also provide an update on data linkage efforts and the Children of TEDS (CoTEDS) project. [ABSTRACT FROM AUTHOR]

Autism spectrum disorder (ASD) is a genetically heterogeneous condition, caused by a combination of rare de novo and inherited variants as well as common variants in at least several hundred genes. However, significantly larger sample sizes are needed to identify the complete set of genetic risk factors. We conducted a pilot study for SPARK (SPARKForAutism.org) of 457 families with ASD, all consented online. Whole exome sequencing (WES) and genotyping data were generated for each family using DNA from saliva. We identified variants in genes and loci that are clinically recognized causes or significant contributors to ASD in 10.4% of families without previous genetic findings. In addition, we identified variants that are possibly associated with ASD in an additional 3.4% of families. A meta-analysis using the TADA framework at a false discovery rate (FDR) of 0.1 provides statistical support for 26 ASD risk genes. While most of these genes are already known ASD risk genes, BRSK2 has the strongest statistical support and reaches genome-wide significance as a risk gene for ASD (p-value = 2.3e-06). Future studies leveraging the thousands of individuals with ASD who have enrolled in SPARK are likely to further clarify the genetic risk factors associated with ASD as well as allow accelerate ASD research that incorporates genetic etiology.

In the article, we review key methodological issues and study results on the heritability of political attitudes. These studies show to what degree the variance of observed attitudes can be explained by genetic variance. We have analysed studies differing in terms of applied methods, techniques and research tools, as well as sample populations of different age and sex structures. Regardless of these differences, the studies show that political attitudes are most likely influenced to some extent by genetic factors. This research suggests that the influence of genes on attitudes is subject to change over the life cycle. It also provides knowledge regarding the mechanisms that may link genes and attitudes. The studies conducted to date offer the opportunity to broaden the culturalism-based explanations of political attitudes with biological aspects; however, they also point to several issues that will require additional attention from the researchers. [ABSTRACT FROM AUTHOR]

Assortative mating is a phenomenon in which romantic partners typically resemble each other at a level greater than chance. There is converging evidence that social behaviours are subject to assortative mating, though less is known regarding social cognition. Social functioning requires the ability to identify and understand the mental states of others, i.e., theory of mind. The present study recruited a sample of 102 heterosexual couples via an online survey to test if theory of mind as measured using facial expressions (Reading the Mind in the Eyes Test) or language (Stiller-Dunbar Stories Task) is associated with assortative mating. Results provide evidence of assortative mating for theory of mind via facial expressions, though there was no such effect for theory of mind via language. Assortative mating for theory of mind via facial expressions was not moderated by length of relationship nor by partner similarity in age, educational attainment, or religiosity, all variables relevant to social stratification. This suggests assortative mating for theory of mind via facial expressions is better explained by partners being alike at the start of their relationship (initial assortment) rather than becoming similar through sustained social interaction (convergence), and by people seeking out partners that are like themselves (active assortment) rather than simply pairing with those from similar demographic backgrounds (social homogamy). [ABSTRACT FROM AUTHOR]

Background: Educational attainment is connected to many important life outcomes, and the previous research has already focused on identifying its genetic and environmental components. However, most of these studies used twin data only and did not incorporate information from other family members. Twin studies typically decompose the phenotypic variance into genetic, shared, and unique environment components. In this study design, the shared environment component encompasses the influence of parents and the shared environments of twins and siblings independent of parents (e.g., teachers, schools, and peers). The classical twin design (CTD) conflates these influences as part of the shared environment. This shortcoming can be overcome using the nuclear twin family design (NTFD), which enables separation of the parental and shared twin/sibling environmental components. Aims: The aim of this study was to broaden the understanding of the aetiology of educational attainment using the nuclear twin family design to provide a detailed account of the genetic and environmental effects on the type of school leaving certificate. Sample: The data of 1,048 monozygotic and 916 dizygotic same‐sex twins, their biological parents, and non‐twin full biological siblings of the German project TwinLife were used in the nuclear twin family design. Methods: Structural equation modelling (SEM) techniques were used to analyse the variance–covariance patterns of the ordinal outcome variable. Results: Genetic influences were found to make up around 60% of variance, whilst environmental influences shared by all siblings, educational influences shared by the twins only, and non‐shared environmental influences explained the remaining variance in equal amounts. Environmental transmission from parent to offspring was found to be negligible. Conclusion: Through its advanced design, our study extends the previous work enabling more detailed and robust estimations of sources of variance and contributes to a better understanding of the complex aetiology of educational attainment. [ABSTRACT FROM AUTHOR]

PurposeTo investigate the association between social isolation and loneliness, how they relate to depression, and whether these associations are explained by genetic influences.MethodsWe used data from the age-18 wave of the Environmental Risk Longitudinal Twin Study, a birth cohort of 1116 same-sex twin pairs born in England and Wales in 1994 and 1995. Participants reported on their levels of social isolation, loneliness and depressive symptoms. We conducted regression analyses to test the differential associations of isolation and loneliness with depression. Using the twin study design, we estimated the proportion of variance in each construct and their covariance that was accounted for by genetic and environmental factors.ResultsSocial isolation and loneliness were moderately correlated (r = 0.39), reflecting the separateness of these constructs, and both were associated with depression. When entered simultaneously in a regression analysis, loneliness was more robustly associated with depression. We observed similar degrees of genetic influence on social isolation (40 %) and loneliness (38 %), and a smaller genetic influence on depressive symptoms (29 %), with the remaining variance accounted for by the non-shared environment. Genetic correlations of 0.65 between isolation and loneliness and 0.63 between loneliness and depression indicated a strong role of genetic influences in the co-occurrence of these phenotypes.ConclusionsSocially isolated young adults do not necessarily experience loneliness. However, those who are lonely are often depressed, partly because the same genes influence loneliness and depression. Interventions should not only aim at increasing social connections but also focus on subjective feelings of loneliness.

Mammalian and fish pineals play a key role in adapting behaviour to the ambient light conditions through the release of melatonin. In mice, light inhibits nocturnal locomotor activity via the nonvisual photoreceptor Melanopsin. In contrast to the extensively studied function of Melanopsin in the indirect regulation of the rodent pineal, its role in the intrinsically photosensitive zebrafish pineal has not been elucidated. Therefore, it is not evident if the light signalling mechanism is conserved between distant vertebrates, and how Melanopsin could affect diurnal behaviour. A double knockout of melanopsins (opn4.1-opn4xb) was generated in the diurnal zebrafish, which manifests attenuated locomotor activity during the wake state. Transcriptome sequencing gave insight into pathways downstream of Melanopsin, implying that sustained repression of the melatonin pathway is required to elevate locomotor activity during the diurnal wake state. Moreover, we show that light induces locomotor activity during the diurnal wake state in an intensity-dependent manner. These observations suggest a common Melanopsin-driven mechanism between zebrafish and mammals, while the diurnal and nocturnal chronotypes are inversely regulated downstream of melatonin. [ABSTRACT FROM AUTHOR]

The last 2 decades have seen the collection of increasingly rich bodies of genetic data, opening up a multitude of new research avenues. These data have made undeniable contributions to health research, but have they equally contributed to the population sciences? This article critically surveys the assumptions underlying sociogenomics, a new field that explores the links between genetics and human behaviour. While sociogenomics as such is new, these links have long been debated, as seen for example in the writings of Alfred Jacquard and Daniel Courgeau. [ABSTRACT FROM AUTHOR]

The rapid development of genetic research, determined, among others, by the requirements of The Human Genome Project, and a gradual reorientation in the perception of the role of nature and culture in the process of shaping complex networks of human relations by some political scientists, result in the increasing application of genetic data and methods in research regarding political behaviours. One of the key philosophical objections against the studies of the genetic foundations of political behaviours is that of excessive reductionism. This is supposed to manifest itself in the inadequate selection of the level of analysis for the explained phenomenon, the incompleteness of explanations and their low utility. My findings show that this objection is not sufficiently supported by contemporary science. Both studies using classical behavioural genetic methodologies and studies using DNA-based methods show that genes most likely play a role in political behaviours. Emphasising the significance of genetic influences in the midst of multiple extra-genetic interactions generates highly idealised explanations. Using the conceptual apparatus of the deformational concept of culture, I have demonstrated that the omission of a number of important extra-genetic influences by researchers is a consequence of focusing on specific causal patterns. This omission, however, does not entail negating the influence of non-genetic factors and, importantly, it may not have to be permanent. Following this approach, if correct, the reductionism of research into the genetic foundations of political behaviours is a standard cognitive procedure applied in science. [ABSTRACT FROM AUTHOR]

Abstract Aims Here we report the results of the first systematic investigation of genetic and environmental influences on 57 psychological traits covering major issues in emerging adulthood such as aspirations, thoughts and attitudes, relationships and personality. We also investigate how these traits relate to physical and mental health, educational attainment and wellbeing. Materials & Methods We use a sample of nearly 5000 pairs of UK twins aged 21–25 from the Twins Early Development Study. We included 57 measures of traits selected to represent issues in emerging adulthood (EA) such as aspirations, thoughts and attitudes, life events, relationships, sexual and health behaviour and personality. We also included measures related to what are often considered to be the core functional outcomes even though here we refer to the data collected at the same time: adverse physical health, adverse mental health, wellbeing, and education. Results All 57 traits showed significant genetic influence, with an average heritability of 34% (SNP heritability ~10%). Most of the variance (59% on average) was explained by non‐shared environmental influences. These diverse traits were associated with mental health (average correlation 0.20), wellbeing (0.16), physical health (0.12) and educational attainment (0.06). Shared genetic factors explained the majority of these correlations (~50%). Together, these emerging adulthood traits explained on average 30% of variance in the outcomes (range = 8% to 69%), suggesting that these traits relate to the outcomes additively. Discussion & Conclusions We conclude that even as the majority of individual differences in EA traits is explained by non‐shared environmental factors, genetic influence on these traits is still substantial; the environmental uncertainties of emerging adulthood in the 21st century do not diminish the importance of genetics. As adolescents travel down long and winding roads to adulthood, their trip is substantially influenced by genetic proclivities that nudge them down different paths leading to different destinations.

Bullying‐victimisation has been associated with sleep disturbances. This study investigated the degree to which subtypes of bullying‐victimisation in adolescence are linked with sleep disturbances. Genetic and environmental contributions underlying bullying‐victimisation and sleep disturbances were investigated. Participants (3,242–5,076 pairs) from a longitudinal community twin study reported on their bullying‐victimisation at the age of 14 years, and sleep quality and insomnia symptoms at age 16. Regression analyses were used, accounting for the role of individual and family factors. Structural equation twin model fitting was conducted. Bullying‐victimisation was modestly associated with sleep quality and insomnia symptoms (r = 0.22–0.23) and a similar strength of associations was found across bullying‐victimisation subtypes (r = 0.11–0.22). Bullying‐victimisation, sleep quality and insomnia symptoms were predominantly influenced by genes (25–59%) and non‐shared environments (40–62%). The association between bullying‐victimisation and sleep quality was explained by genetic and non‐shared environmental influences. For insomnia symptoms and sleep quality, the association with bullying‐victimisation was in part explained by a genetic overlap. Associations between bullying‐victimisation and sleep disturbances are not limited to specific aspects of bullying‐victimisation but appear to exist for all subtypes. These findings stimulate research questions regarding the mechanisms underlying these links. For example, could certain heritable traits, such as temperament, increase vulnerability to experiencing sleep disturbances and being bullied? Research on bullying and sleep should aim to take the role of genetic predisposition into account, while also noting that it is not the only causal influence. Understanding more about these pathways could strengthen the development of techniques to prevent these difficulties from occurring. [ABSTRACT FROM AUTHOR]

Subjective well-being is a construct that was examined within numerous psychological research and its popularity has been growing over the last thirty years. It is defined as a combination of cognitive evaluation of one’s life and affective tendencies. However, there are certain inconsistencies and differences in its operationalization in the literature, which will be discussed in this paper. After presenting the definition of subjective well-being, this paper will focus on two main goals. First will be presented findings about the sources of individual differences in subjective well-being, based on the studies that used a behavioural genetic methodology. Results of those studies suggest a moderate heritability of subjective well-being, ranging from 30-40%. Secondly, the main aim is to report the findings of the associations between subjective well-being and personality traits. Numerous studies indicate a strong phenotypic association of subjective well-being with neuroticism, extraversion, and, to a lesser extent, with conscientiousness. Finally, these phenotypic correlations will additionally be interpreted from a behavioural genetic perspective, i.e., with the presentation of studies that have examined the aetiology of these correlations. Namely, different studies showed that subjective well-being and personality share genetic variance but it is not yet clear whether there is a genetic effect of subjective well-being that is independent of personality. [ABSTRACT FROM AUTHOR]

What past selection pressures have shaped human traits and their variation and covariation across individuals? These are key questions in the evolutionary social sciences. Recent advances in the field of human genomics have yielded a wealth of evidence that sheds light on these questions, yet the findings and their implications seem to be little known in the evolutionary social sciences. In this paper I aim to bring together these findings while explaining the conceptual and technical background that is often assumed knowledge for reading the primary reports. First, I outline the genomics methodologies that have enabled the relevant findings, such as genomewide association studies and DNA-based heritability estimation. I describe how these methodologies reveal the genetic architecture of traits, and then how this information in turn enables inferences about past selection. The findings show pervasive evidence that the genetic architecture of complex traits has been shaped by negative (purifying) selection, implying that the extant genetic variation in the traits has been maintained by mutation-selection-drift balance. On the other hand, there is no evidence that balancing selection has substantively shaped complex traits, and strong evidence that it has not. Finally, I discuss the implications of these findings for issues such as the dimensional structure of personality variation and the plausibility of psychological life history theory. [ABSTRACT FROM AUTHOR]

Background: The heritability of language and literacy skills increases from early‐childhood to adolescence. The underlying mechanisms are little understood and may involve (a) the amplification of genetic influences contributing to early language abilities, and/or (b) the emergence of novel genetic factors (innovation). Here, we investigate the developmental origins of genetic factors influencing mid‐childhood/early‐adolescent language and literacy. We evaluate evidence for the amplification of early‐childhood genetic factors for vocabulary, in addition to genetic innovation processes. Methods: Expressive and receptive vocabulary scores at 38 months, thirteen language‐ and literacy‐related abilities and nonverbal cognition (7–13 years) were assessed in unrelated children from the Avon Longitudinal Study of Parents and Children (ALSPAC, Nindividuals ≤ 6,092). We investigated the multivariate genetic architecture underlying early‐childhood expressive and receptive vocabulary, and each of 14 mid‐childhood/early‐adolescent language, literacy or cognitive skills with trivariate structural equation (Cholesky) models as captured by genome‐wide genetic relationship matrices. The individual path coefficients of the resulting structural models were finally meta‐analysed to evaluate evidence for overarching patterns. Results: We observed little support for the emergence of novel genetic sources for language, literacy or cognitive abilities during mid‐childhood or early adolescence. Instead, genetic factors of early‐childhood vocabulary, especially those unique to receptive skills, were amplified and represented the majority of genetic variance underlying many of these later complex skills (≤99%). The most predictive early genetic factor accounted for 29.4%(SE = 12.9%) to 45.1%(SE = 7.6%) of the phenotypic variation in verbal intelligence and literacy skills, but also for 25.7%(SE = 6.4%) in performance intelligence, while explaining only a fraction of the phenotypic variation in receptive vocabulary (3.9%(SE = 1.8%)). Conclusions: Genetic factors contributing to many complex skills during mid‐childhood and early adolescence, including literacy, verbal cognition and nonverbal cognition, originate developmentally in early‐childhood and are captured by receptive vocabulary. This suggests developmental genetic stability and overarching aetiological mechanisms. [ABSTRACT FROM AUTHOR]

Twin studies of insomnia exhibit heterogeneity in estimates of heritability. This heterogeneity is likely because of sex differences, age of the sample, the reporter and the definition of insomnia. The aim of the present study was to systematically search the literature for twin studies investigating insomnia disorder and insomnia symptoms and to meta‐analyse the estimates of heritability derived from these studies to generate an overall estimate of heritability. We further examined whether heritability was moderated by sex, age, reporter and insomnia symptom. A systematic literature search of five online databases was completed on 24 January 2020. Two authors independently screened 5644 abstracts, and 160 complete papers for the inclusion criteria of twin studies from the general population reporting heritability statistics on insomnia or insomnia symptoms, written in English, reporting data from independent studies. We ultimately included 12 papers in the meta‐analysis. The meta‐analysis focussed on twin intra‐class correlations for monozygotic and dizygotic twins. Based on these intra‐class correlations, the meta‐analytic estimate of heritability was estimated at 40%. Moderator analyses showed stronger heritability in females than males; and for parent‐reported insomnia symptoms compared with self‐reported insomnia symptoms. There were no other significant moderator effects, although this is likely because of the small number of studies that were comparable across levels of the moderators. Our meta‐analysis provides a robust estimate of the heritability of insomnia, which can inform future research aiming to uncover molecular genetic factors involved in insomnia vulnerability. [ABSTRACT FROM AUTHOR]

Background: Anorexia nervosa and bulimia nervosa are two severe eating disorders associated with high premature mortality, suicidal risk and serious medical complications. Transition between anorexia nervosa and bulimia nervosa over the illness course and familial co-aggregation of the two eating disorders imply aetiological overlap. However, genetic and environmental liabilities to the overlap are poorly understood. Quantitative genetic research using clinical diagnosis is needed. Methods: We acquired a clinical diagnosis of anorexia nervosa (prevalence = 0.90%) and bulimia nervosa (prevalence = 0.48%) in a large population-based sample (N = 782 938) of randomly selected full-sisters and maternal half-sisters born in Sweden between 1970 and 2005. Structural equation modelling was applied to quantify heritability of clinically diagnosed anorexia nervosa and bulimia nervosa and the contributions of genetic and environmental effects on their overlap. Results: The heritability of clinically diagnosed anorexia nervosa and bulimia nervosa was estimated at 43% [95% confidence interval (CI) (36–50%)] and 41% (31–52%), respectively, in the study population, with the remaining variance explained by variance in unique environmental effects. We found statistically significant genetic [0.66, 95% CI (0.49–0.82)] and unique environmental correlations [0.55 (0.43–0.66)] between the two clinically diagnosed eating disorders; and their overlap was about equally explained by genetic and unique environmental effects [co-heritability 47% (35–58%)]. Conclusions: Our study supports shared mechanisms for anorexia nervosa and bulimia nervosa and extends the literature from self-reported behavioural measures to clinical diagnosis. The findings encourage future molecular genetic research on both eating disorders and emphasize clinical vigilance for symptom fluctuation between them. [ABSTRACT FROM AUTHOR]

The study of political attitudes and behaviours is important from a cognitive point of view and carries considerable practical implications. Therefore, researchers should consider the widest possible spectrum of factors determining the participation of individuals in politics. Their analyses, however, are usually limited to the effects of environmental factors, ignoring or marginalizing the impact of genetic factors. An approach called 'genopolitics' has been trying to fill the resulting knowledge gap for over a decade. The aim of this article is to provide a synthetic description of genopolitics based on institutional, methodological, epistemological and social criteria. The main points of consideration are the assessment of the explanatory utility of genopolitical research, as well as the analysis of the cognitive and non-cognitive conditions and barriers to the development of genopolitics. [ABSTRACT FROM AUTHOR]

Scientific advances in genetic analysis have been made possible in recent years by technical developments in computational biology, or bioinformatics. Bioinformatics has opened up the human genome to diverse analyses involving automated laboratory hardware and machine learning algorithms and software. As part of an emerging field of social genomics, recent educational genetics studies using big data have begun to raise challenging findings linking DNA to predicted life outcomes. Bioinformatic technologies and techniques including 'genome-wide association' and 'polygenic scoring' are producing new kinds of genetic biodata and expert knowledge for rethinking the upbringing and education of children. This article takes as an empirical opening a recent epistemic and ethical controversy over the use of biodata to make genetic predictions about educational, socio-economic and life outcomes, detailing the forms of expert knowledge and technologies involved these predictions, and exploring the social and ethical implications of data-intensive bioinformatics. [ABSTRACT FROM AUTHOR]

Background: The phenotypic and aetiological architecture of depression symptomatology has been mostly studied in Western samples. In this study, we conducted a genetically informed factor analysis to elucidate both the phenotypic and aetiological architectures of self-reported depression among a Japanese adult twin sample. Methods: Depressive symptoms assessed by Zung's Self-rating Depression Scale were self-rated by 425 twin pairs (301 monozygotic and 124 dizygotic twin pairs) in a community sample in Japan. Results: An exploratory factor analysis extracted three symptom domains representing cognitive, affective and somatic symptomatology. A confirmatory factor analysis demonstrated that a bi-factor solution fitted better than the alternative solutions, implying that depression may be defined as a combination of a single general construct and three factors specific to each of the three symptom domains. A multivariate genetic analysis with the bi-factor solution showed that the general factor was substantially heritable (47%), and that only the affective symptom domain was significantly heritable (29%) among the three specific factors, their remaining variance being explained by non-shared environmental influences. Conclusions: Depression symptomatology appears to be adequately captured by a substantially heritable general factor. The heritability of this factor (47%) in a Japanese adult sample is in line with commonly reported heritability estimates for depression. The three specific factors – cognitive, affective and somatic – are mostly explained by non-shared environmental factors, which include measurement error. The extent to which these specific factors are uniquely associated with correlates of depression when the general factor is accounted for should be investigated in future studies. [ABSTRACT FROM AUTHOR]

• Both genes and environment contribute to individual differences in attachment. • In childhood, important role of the shared environment, might decrease over time. • In adulthood, genetic factors may have increasingly greater influence. • Considerable influence of unshared environment throughout the life cycle. • The findings of molecular genetic studies are suggestive but, overall, inconclusive. In the last two decades, there has been increasing research interest in disentangling the contribution of genetic and environmental factors to individual differences in attachment, and in identifying the genes involved in shaping attachment. Twin studies suggest that as attachment changes during the course of development, genetic factors may play a progressively more important role, while shared environmental effects might decrease. However, most of this literature is limited by low power, measurement issues, and cross-sectional design. The findings of molecular genetic studies are, overall, inconclusive. The literature on main genetic effects and gene-by-environment interactions on attachment is filled with inconsistent and unreplicated findings. Also, most studies are underpowered. Challenges for future research are to identify the unshared environmental mechanisms involved in shaping attachment, and to better elucidate the genes involved and their interaction with the environment. Some pioneer studies suggested that the incorporation of epigenetic processes into G × E interaction models might represent a promising future way for investigating the complex, dynamic interplay between genes, environment, and attachment. [ABSTRACT FROM AUTHOR]

• Starting from middle childhood, studies point to a strong genetic basis in the association between cognitive ability and academic performance. • Over development, genetic influences are amplified by environmental experiences trhigh gene-environment interplay. • The strong stability and heritability of academic performance is not driven entirely by cognitive ability. • Other educationally-relevant noncognitive characteristics contribute to accounting for the genetic variation in academic performance beyond cognitive ability. • Overall, genetic research has provided compelling evidence that has resulted in greatly advancing our knowledge and understanding of the association between cognitive ability and learning. • Considering both cognitive and noncognitive skills as well as their biological and environmental underpinnings will be fundamental in moving towards a comprehensive, evidence-based model of education. Cognitive ability and educational success predict positive outcomes across the lifespan, from higher earnings to better health and longevity. The shared positive outcomes associated with cognitive ability and education are emblematic of the strong interconnections between them. Part of the observed associations between cognitive ability and education, as well as their links with wealth, morbidity and mortality, are rooted in genetic variation. The current review evaluates the contribution of decades of behavioural genetic research to our knowledge and understanding of the biological and environmental basis of the association between cognitive ability and education. The evidence reviewed points to a strong genetic basis in their association, observed from middle childhood to old age, which is amplified by environmental experiences. In addition, the strong stability and heritability of educational success are not driven entirely by cognitive ability. This highlights the contribution of other educationally relevant noncognitive characteristics. Considering both cognitive and noncognitive skills as well as their biological and environmental underpinnings will be fundamental in moving towards a comprehensive, evidence-based model of education. [ABSTRACT FROM AUTHOR]

Our aim was to assess whether infants influence the quantity and quality of their mothers' speech to them and, in turn, whether this maternal speech influences children's later language. As 189 mothers interacted with each of their twins at age 0;5, we calculated the number of utterances, the proportion of sensitive utterances, and the proportion of self-repeated utterances they produced. We later assessed the twins' language comprehension and production when they were 1;6, 2;6, and 5;2. Quantity of maternal speech predicted child language at 5;2, whereas sensitivity predicted child language at 2;6 and 5;2 and partial self-repetition predicted child language at 1;6. Conversely, sensitivity and partial self-repetition in maternal speech at 0;5 were associated with genetic factors from the child, indicating that infant characteristics influence the quality of maternal speech. Overall, our findings stress the importance of considering both directions in the association between maternal speech and child characteristics. [ABSTRACT FROM AUTHOR]

Marla Sokolowski's scientific achievements established her as an internationally recognized leader in behavioural genetics. As a graduate student, she made a significant discovery while observing natural populations of the fruit fly, Drosophila melanogaster: the larvae exhibited a behavioural polymorphism which she traced to alleles of a single gene. Some larvae were 'sitters' which fed in a restricted location, while others were 'rovers' which ranged more widely in feeding. The gene in question, foraging, codes for a cyclic GMP kinase which is expressed in numerous locations throughout larval and adult Drosophila. Building on this foundation, she and her students have elucidated the genetic and environmental factors that account for individual differences in behaviour. In this article, I review significant stages of her scientific career. [ABSTRACT FROM AUTHOR]

Background: Diverse behaviour problems in childhood correlate phenotypically, suggesting a general dimension of psychopathology that has been called the p factor. The shared genetic architecture between childhood psychopathology traits also supports a genetic p. This study systematically investigates the manifestation of this common dimension across self‐, parent‐ and teacher‐rated measures in childhood and adolescence. Methods: The sample included 7,026 twin pairs from the Twins Early Development Study (TEDS). First, we employed multivariate twin models to estimate common genetic and environmental influences on p based on diverse measures of behaviour problems rated by children, parents and teachers at ages 7, 9, 12 and 16 (depressive traits, emotional problems, peer problems, autism traits, hyperactivity, antisocial behaviour, conduct problems and psychopathic tendencies). Second, to assess the stability of genetic and environmental influences on p across time, we conducted longitudinal twin modelling of the first phenotypic principal components of childhood psychopathological measures across each of the four ages. Third, we created a genetic p factor in 7,026 unrelated genotyped individuals based on eight polygenic scores for psychiatric disorders to estimate how a general polygenic predisposition to mostly adult psychiatric disorders relates to childhood p. Results: Behaviour problems were consistently correlated phenotypically and genetically across ages and raters. The p factor is substantially heritable (50%–60%) and manifests consistently across diverse ages and raters. However, residual variation in the common factor models indicates unique contributions as well. Genetic correlations of p components across childhood and adolescence suggest stability over time (49%–78%). A polygenic general psychopathology factor derived from studies of psychiatric disorders consistently predicted a general phenotypic p factor across development (0.3%–0.9%). Conclusions: Diverse forms of psychopathology generally load on a common p factor, which is highly heritable. There are substantial genetic influences on the stability of p across childhood. Our analyses indicate genetic overlap between general risk for psychiatric disorders in adulthood and p in childhood, even as young as age 7. The p factor has far‐reaching implications for genomic research and, eventually, for diagnosis and treatment of behaviour problems. [ABSTRACT FROM AUTHOR]

The evolutionary origins of advanced eusociality, one of the most complex forms of phenotypic plasticity in nature, have long been a focus within the field of sociobiology. Although eusocial insects are known to have evolved from solitary ancestors, sociogenomic research among incipiently social taxa has only recently provided empirical evidence supporting theories that modular regulation and deeply conserved genes may play important roles in both the evolutionary emergence and elaboration of insect sociality. There remains, however, a paucity of data to further test the biological reality of these and other evolutionary theories among taxa in the earliest stages of social evolution. Here, we present brain transcriptomic data from the incipiently social small carpenter bee, Ceratina calcarata, which captures patterns of cis-regulation and gene expression associated with female maturation, and underlying two well-defined behavioural states, foraging and guarding, concurrently demonstrated by mothers and daughters during early autumn. We find that an incipiently social nest environment may dramatically affect gene expression. We further reveal foraging and guarding behaviours to be putatively caste-antecedent states in C. calcarata, and offer strong empirical support for the operation of modular regulation, involving deeply conserved and differentially expressed genes in the expression of early social forms. [ABSTRACT FROM AUTHOR]

Background: Despite a large body of research that has explored the influence of genetic and environmental factors on educationally relevant traits, few studies have explored teachers' beliefs about, or knowledge of, developments in behavioural genetics related to education. Aims: This study aimed to describe the beliefs and knowledge of UK teachers about behavioural genetics and its relevance to education, and to test for differences between groups of teachers based on factors including years of experience and age of children taught. Sample: Data were gathered from n = 402 teachers from a representative sample of UK schools. Teachers from primary and secondary schools, and from across the state and independent sectors, were recruited. Methods: An online questionnaire was used to gather demographic data (gender, age, years of experience, age of children taught, and state vs. independent) and also data on beliefs about the relative influence of nature and nurture on cognitive ability; knowledge of behavioural genetics; openness to genetic research in education; and mindset. Data were analysed using descriptive statistics, ANOVA, correlations, and multiple regression. Results: Teachers perceived genetic and environmental factors as equally important influences on cognitive ability and tended towards a growth mindset. Knowledge about behavioural genetics was low, but openness to learning more about genetics was high. Statistically significant differences were observed between groups based on age of children taught (openness higher among primary teachers) and state versus independent (more growth‐minded in state sector). Conclusions: Although teachers have a limited knowledge of behavioural genetics, they are keen to learn more. [ABSTRACT FROM AUTHOR]

Effective personalized well-being interventions require the ability to predict who will thrive or not, and the understanding of underlying mechanisms. Here, using longitudinal data of a large population cohort (the Netherlands Twin Register, collected 1991-2022), we aim to build machine learning prediction models for adult well-being from the exposome and genome, and identify the most predictive factors ( N between 702 and 5874). The specific exposome was captured by parent and self-reports of psychosocial factors from childhood to adulthood, the genome was described by polygenic scores, and the general exposome was captured by linkage of participants' postal codes to objective, registry-based exposures. Not the genome ( R 2  = -0.007 [-0.026-0.010]), but the general exposome ( R 2  = 0.047 [0.015-0.076]) and especially the specific exposome ( R 2  = 0.702 [0.637-0.753]) were predictive of well-being in an independent test set. Adding the genome ( P  = 0.334) and general exposome ( P  = 0.695) independently or jointly ( P  = 0.029) beyond the specific exposome did not improve prediction. Risk/protective factors such as optimism, personality, social support and neighborhood housing characteristics were most predictive. Our findings highlight the importance of longitudinal monitoring and promises of different data modalities for well-being prediction., Competing Interests: Competing interestsThe authors declare no competing interests., (© The Author(s), under exclusive licence to Springer Nature America, Inc. 2024, corrected publication 2024.)

Background: The genetic component of Cannabis Use Disorder may overlap with influences acting more generally on early stages of cannabis use. This paper aims to determine the extent to which genetic influences on the development of cannabis abuse/dependence are correlated with those acting on the opportunity to use cannabis and frequency of use. Methods: A cross-sectional study of 3303 Australian twins, measuring age of onset of cannabis use opportunity, lifetime frequency of cannabis use, and lifetime DSM-IV cannabis abuse/dependence. A trivariate Cholesky decomposition estimated additive genetic (A), shared environment (C) and unique environment (E) contributions to the opportunity to use cannabis, the frequency of cannabis use, cannabis abuse/dependence, and the extent of overlap between genetic and environmental factors associated with each phenotype. Results: Variance components estimates were A = 0.64 [95% confidence interval (CI) 0.58–0.70] and E = 0.36 (95% CI 0.29–0.42) for age of opportunity to use cannabis, A = 0.74 (95% CI 0.66–0.80) and E = 0.26 (95% CI 0.20–0.34) for cannabis use frequency, and A = 0.78 (95% CI 0.65–0.88) and E = 0.22 (95% CI 0.12–0.35) for cannabis abuse/dependence. Opportunity shares 45% of genetic influences with the frequency of use, and only 17% of additive genetic influences are unique to abuse/dependence from those acting on opportunity and frequency. Conclusions: There are significant genetic contributions to lifetime cannabis abuse/dependence, but a large proportion of this overlaps with influences acting on opportunity and frequency of use. Individuals without drug use opportunity are uninformative, and studies of drug use disorders must incorporate individual exposure to accurately identify aetiology. [ABSTRACT FROM AUTHOR]

People vary in the degree to which they experience disgust toward--and, consequently, avoid--cues to pathogens. Prodigious work has measured this variation and observed that it relates to, among other things, personality, psychopathological tendencies, and moral and political sentiments. Less work has sought to generate hypotheses aimed at explaining why this variation exists in the first place, and even less work has evaluated how well data support these hypotheses. In this paper, we present and review the evidence supporting three such proposals. First, researchers have suggested that variability reflects a general tendency to experience anxiety or emotional distress. Second, researchers have suggested that variability arises from parental modelling, with offspring calibrating their pathogen avoidance based on their parents' reactions to pathogen cues. Third, researchers have suggested that individuals calibrate their disgust sensitivity to the parasite stress of the ecology in which they develop. We conclude that none of these hypotheses is supported by existing data, and we propose directions for future research aimed at better understanding this variation. This article is part of the Theo Murphy meeting issue 'Evolution of pathogen and parasite avoidance behaviours'. [ABSTRACT FROM AUTHOR]

From the genetic side, giftedness in cognitive development is the result of contribution of many common genetic variants of small effect size, so called polygenicity (Spain et al., 2016). From the environmental side, educationalists have argued for the importance of the environment for sustaining early potential in children, showing that bright poor children are held back in their subsequent development ( Feinstein, 2003a ). Such correlational data need to be complemented by mechanistic models showing how gifted development results from the respective genetic and environmental influences. A neurocomputational model of cognitive development is presented, using artificial neural networks to simulate the development of a population of children. Variability was produced by many small differences in neurocomputational parameters each influenced by multiple artificial genes, instantiating a polygenic model, and by variations in the level of stimulation from the environment. The simulations captured several key empirical phenomena, including the non-linearity of developmental trajectories, asymmetries in the characteristics of the upper and lower tails of the population distribution, and the potential of poor environments to hold back bright children. At a computational level, ‘gifted’ networks tended to have higher capacity, higher plasticity, less noisy neural processing, a lower impact of regressive events, and a richer environment. However, individual instances presented heterogeneous contributions of these neurocomputational factors, suggesting giftedness has diverse causes. [ABSTRACT FROM AUTHOR]

Sexual reproduction is inherently interactive, especially in animal species such as humans that exhibit extended pair bonding. Yet we have little knowledge of the role of male characteristics and their evolutionary impact on reproductive behavioural phenotypes, to the extent that biologists typically consider component traits (e.g. reproductive timing) as female-specific. Based on extensive genealogical data detailing the life histories of 6435 human mothers born across four centuries of modern history, we use an animal modelling approach to estimate the indirect genetic effect of men on the reproductive phenotype of their partners. These analyses showthat awoman's reproductive timing (age at first birth) is influenced by her partner's genotype. This indirect genetic effect is positively correlated with the direct genetic effect expressed in women, such that total heritable variance in this trait is doubled when heritable partner effects are considered. Our study thus suggests that much of the heritable variation in women's reproductive timing ismediated via partner effects, and that the evolutionary potential of this trait is far greater than previously appreciated. [ABSTRACT FROM AUTHOR]