Behavior Genetics最新文献

Meta-analyses report small to moderate effect sizes or inconsistent associations (usually around r = -0.10) between wellbeing (WB) and social media use (SMU) and between anxious-depressive symptoms (ADS) and SMU (also around r = 0.10). This study employs the classical twin design, utilizing data from 6492 individuals from the Netherlands Twin Register, including 3369 MZ twins (893 complete twin pairs, 1583 incomplete twin pairs) and 3123 DZ twins (445 complete, 2233 incomplete) to provide insights into the sources of overlap between WB/ADS and SMU. Both hedonic and eudaimonic WB scales were used. SMU was measured by (1) the time spent on different social media platforms (SMU_t), (2) the frequency of posting on social media (SMU_f), and (3) the number of social media accounts individuals have (SMU_n). Our results confirmed the low phenotypic correlations between WB and SMU (between r = -0.09 and 0.04) as well as between ADS and SMU (between r = 0.07 and 0.10). For SMU, heritability estimates between 32 and 72% were obtained. The small but significant phenotypic correlations between WB/ADS and the SMU phenotypes were mainly determined by genetic factors (in the range of 80-90%). For WB and SMU, genetic correlations were between -0.10 and -0.0, and for ADS and SMU genetic correlations were between 0.10 and 0.23. Genetic correlations implied limited but statistically significant sets of genes that affect WB/ADS and SMU levels. Overall, the results indicate that there is evidence that the small associations between WB/ADS and SMU are partly driven by overlapping genetic influences. We encourage researchers and experts to consider more personalized approaches when considering the association between WB and SMU, as well as understanding the reasons for individuals' observed SMU levels.

Interest in the role of genetics in influencing key life outcomes such as educational attainment has grown quickly. However, the question of whether genetic influences on educational attainment, on average as well as in conjunction with socioeconomic circumstances, are moderated by macro-level factors has not yet received sufficient attention. This study combines polygenic indices for educational attainment (EA PGI) with high-quality register data in a large sample of Swedish twins of European ancestry born 1920-1999. Employing both conventional between-family and within-family models, the analyses suggest that the influences of education-related genetic propensities on educational attainment have increased in Sweden during the twentieth century, a period featuring major expansions of the Swedish educational system, and decreasing economic inequality. The analyses also suggest that the degree to which socioeconomic background enhances genetic influences on education has decreased across cohorts. Genetic influences on education do not appear to have translated into increased genetic influences on income. Additionally, there is some evidence of floor and ceiling effects in the analyses of dichotomous educational outcomes.

The interpersonal circumplex describes two major axes of personality that guide much of social behavior. Agency, one half of the interpersonal circumplex, refers to relatively stable behavioral patterns that center on self-focused dominance and assertiveness assessed in terms of goals, values, or personality traits. However, the psychometric overlap between agency and the most closely linked big five dimension, extraversion, is not well-established, and little behavior genetic work has documented evidence concerning the role of genetic and environmental influences on trait agency. We used the Midlife Development in the United States study to examine agency, big five, and generativity with replication and robustness checks (N_non-twins = 5,194; N_twins = 1,914; N_Milwaukee = 592). Results indicated that agency was higher in men (d = - 0.24), moderately heritable (44.4%), strongly correlated with extraversion (r =.51), moderately correlated with generativity (r =.36), and approximately 41% of the variance in agency was shared with the big five. The current brief measure of agency across two samples reflected smaller gender differences than historical expectations but supported its distinction from the big five traits at the current levels of analysis.

The environment is an important influence in the development of human behaviours and health outcomes. However, one of the most consistent findings from behavioural genetic studies is that most environmental influences are not shared between members of the same family. A compelling way of investigating these non-shared environmental influences is by using a monozygotic (MZ) twin differences design. Quantitative MZ differences studies have uncovered systematic non-shared environmental factors, i.e., those acting according to a general pattern in a population, for many traits, but may be omitting idiosyncratic or distinctive factors and mechanisms. Qualitative MZ differences design provides an alternative. In this study design, identical twins discordant on an outcome are interviewed in depth about the origins and context of their discordance, providing an insight into distinctive lived experiences. We conducted a systematic review examining the results and methodological features of studies using qualitative data collection and analyses to investigate differences in identical twins' experiences and outcomes. We applied a narrative synthesis. We identified seven studies, covering a range of phenotypes (e.g., anxiety or smoking) and participants (from children to older adults), which found a wide range of themes related to twins' discordance. A major theme arising from the narrative synthesis was the role of personality and individual traits, e.g., confidence or sexual orientation, in explaining MZ twins' discordant experiences and outcomes. Non-shared environmental factors are at least partly idiosyncratic and are therefore suitable for exploration with a qualitative research design, ideally in parallel with quantitative twin research in mixed-method research projects or programmes.

This study examined whether adolescent depressive and anxiety symptoms were differentially associated with alcohol use behaviors, and how these associations were explained by genetic, shared, and nonshared environmental influences. Participants were from the Nonshared Environment and Adolescent Development project of same-sex twin/sibling pairs from 720 families. Twin/sibling depressive and anxiety symptoms were measured by self-report at Time 1 (M_age = 13.71 years, range = 9-18 years). Alcohol initiation and alcohol use severity were measured by self-report three years after Time 1 (age range = 12-21 years). Phenotypic Cholesky models were used to estimate the variance of depressive symptoms and the unique variance of anxiety symptoms (independent of depressive symptoms), and how these variances were associated with alcohol initiation and alcohol use severity. Biometric Cholesky models then estimated contributions of genetic, shared and nonshared environmental influences to these variances and covariances. Antisocial behaviors were included in all analyses to account for their associations with depressive symptoms, anxiety symptoms and alcohol use behaviors. Analyses were conducted using the full, the younger half, and the older half of the sample to explore age differences in all associations. Depressive or anxiety symptoms were not associated with alcohol use behaviors after controlling for variance shared with antisocial behaviors, although age-specific analyses suggested some potential effects to explore in future studies for late adolescence. To conclude, longitudinal associations between depressive or anxiety symptoms and alcohol use behaviors during adolescence were mainly driven by the general psychopathology factor shared between internalizing and externalizing problems.

We aimed to understand the long-term impact of negative life events on epigenetic aging in 1783 adults from the Netherlands Twin Register, analyzing five epigenetic biomarkers (Hannum, Horvath, PhenoAge, GrimAge, DunedinPACE) and a series of negative life events, including victimization and economic hardship. In population-level analyses, associations between a higher number of negative life events (particularly financial adversities, sexual crimes, and job loss) were seen for the GrimAge biomarker. The association between the number of negative life events and financial problems and epigenetic age acceleration measured by the GrimAge biomarker persisted after adjusting for BMI, smoking, and white blood cell counts. In monozygotic twin pairs discordant for negative life events (263 pairs) the associations were diminished, indicating that the population associations may be confounded by shared familial (genetic and environmental) factors. These findings underscore the intricate link between environmental stressors and biological aging, stressing the need for comprehensive studies considering both genetic and environmental influences.

Diverse tests of cognitive abilities correlate about 0.30 phenotypically and about 0.60 genetically. Their phenotypic overlap defines general cognitive ability (g), driven largely by genetic overlap. Consequently, much of our understanding of the genetic landscape of specific cognitive tests likely reflects g rather than the tests themselves. Removing this g-associated genetic variance will sharpen research on cognitive tests. Here, we use Genomic Structural Equation Modelling (Genomic SEM) to remove shared genetic variance among 12 diverse cognitive tests that capture verbal and nonverbal cognitive domains. We applied Genomic SEM to summary statistics from the largest genome-wide association studies of verbal tests (GenLang Consortium, five tests) and largely nonverbal tests (UK Biobank, seven tests) to chart the genetic landscape of the 12 tests independent of g as compared to uncorrected cognitive tests. We found that SNP heritabilities were nearly as high for the tests corrected for g as uncorrected: the average SNP heritability was 0.16 (SE = 0.02) for the uncorrected tests and 0.13 (SE = 0.02) for the tests corrected for g. Despite this, the genetic landscape of the cognitive tests transformed after controlling for genomic g. The matrix of positive genetic correlations for the cognitive tests (average 0.45) disappeared after g-correction, and some strong negative correlations emerged; for instance, Memory and Word (-0.72), Fluid and Symbol (-0.72), and Tower and Spelling (-0.79). The summary statistics for these g-corrected cognitive tests can be used by researchers to create polygenic scores that focus on the specificity of the tests.

Previous research has supported the use of latent variables as the gold-standard in measuring executive function. However, for logistical reasons genome-wide association studies (GWAS) of executive function have largely eschewed latent variables in favour of singular task measures. As low correlations have traditionally been found between individual executive function (EF) tests, it is unclear whether these GWAS have truly been measuring the same construct. In this study, we addressed this question by performing a factor analysis on summary statistics from eleven GWAS of EF taken from five studies, using GenomicSEM. Models demonstrated a bifactor structure consistent with previous research, with factors capturing common EF and working memory- specific variance. Furthermore, the GWAS performed on this model identified 20 new genomic risk loci for common EF and 4 for working memory reaching genome-wide significance beyond what was found in the constituent GWAS, together resulting in 29 newly mapped EF genes. These results help to clarify the underlying genetic structure of EF and support the idea that EF GWAS are capable of measuring genetic variance related to latent EF constructs even when not using factor scores. Furthermore, they demonstrate that GenomicSEM can combine GWAS with divergent and non-ideal measures of the same phenotype to improve statistical power.

Breastfeeding is hypothesised to benefit child health and cognitive functioning by providing long-chain polyunsaturated fatty acids, which are essential for brain development. In 2007, Caspi et al. found evidence in two cohorts for an interaction between genetic variation in the FADS2 gene (a gene involved in fatty acid metabolism) and breastfeeding on IQ. However, subsequent studies have provided mixed evidence for the existence of an interaction. We investigated the relationship between genetic variation in the FADS2 region, breastfeeding, and their interaction in up to 335,650 individuals from the UK Biobank. We tested for the interaction over a range of cognitive functioning tests, as well as educational attainment and other traits thought to be influenced by breastfeeding, including cardiometabolic traits, number of offspring, and atopic allergy. FADS2 alleles associated with an increase in docosahexaenoic acid in blood serum (the C allele of rs174575) were associated with decreased verbal-numerical reasoning ( $p=2.28\times {10}^{-5}$ ) and triglycerides ( $p=1.40\times {10}^{-41}$ ), increased number of offspring ( $p=3.40\times {10}^{-5}$ ), total cholesterol ( $p=5.28\times {10}^{-36}$ ), HDL ( $p=1.42\times {10}^{-51}$ ), and LDL cholesterol ( $p=1.46\times {10}^{-21}$ ). We observed no evidence of an interaction in any of the traits, regardless of the modelling strategy on any cognitive or non-cognitive traits. We postulate that the previous positive findings are likely to be spurious, perhaps due to lack of appropriate control for latent population structure.