Behavior Genetics最新文献

Amidst growing visibility of gender diversity, the aetiology of gender identity has become a subject of increasing public interest. Prompted by the growing public debate, we review here the extant twin literature regarding the origins of gender diversity. Literature was reviewed systematically, searching Medline, Embase and PubMed databases. Studies were deemed eligible if they: (i) conducted a twin study, (ii) investigated gender identity or gendered behaviour, and (iii) provided an estimate of the magnitude of genetic or environmental contribution. After screening 290 non-duplicate titles and abstracts, 16 articles were included in the final review. Most eligible studies provided evidence of both genetic and environmental contributions to gender identity and gendered behaviour. For gendered behaviour, genetic contributions ranged from 0.10 to 0.77, non-shared environmental contributions ranged from 0.15 to 0.75, and shared environmental contributions ranged from 0.00 to 0.49. For gender identity, genetic contributions ranged from 0.00 to 0.84, non-shared environmental contributions ranged from 0.15 to 0.96 and shared environmental contributions ranged from 0.00 to 0.70. Given the variability in results and methodology between studies, the true magnitude of these contributions remains unclear. No consistent differences in contributions were identified between assigned males and assigned females. While there is also recent evidence that prenatal hormone exposure may contribute to gender identity, the overall evidence from the literature is inconsistent. Twin studies indicate both genetic and environmental contributions to gender diversity. These results are important to inform ongoing public debate in this area and highlight the complex interplay of both genetics and environment.

The impact of the COVID-19 pandemic on the wellbeing of 26,555 Dutch children and adolescents (ages 8-18, 50% female, 89% with parents born in the Netherlands) was investigated using three cohorts: a general population twin sample (NTR), a general population sample (KLIK), and a clinical sample (DREAMS). Data were collected in seven waves between 2020 and 2023. Linear mixed models were employed to examine changes in wellbeing, twin models were used to estimate genetic and environmental contributions, and a psychometric model was employed to explore potential rater bias. A 6.5% drop in wellbeing was observed at the onset of the pandemic in the NTR sample, followed by partial recovery but not a return to pre-pandemic levels. Mean wellbeing scores were consistently lower in the clinical cohort (DREAMS), which also showed different effects of age, gender, and parental educational attainment compared to the two general population samples (NTR and KLIK). Increased disagreement between fathers' and mothers' ratings during lockdown was also identified. Genetic factors were found to account for 26-28% of the variance in wellbeing during the pandemic, and 34-35% before and after. Shared environmental factors were higher during the lockdown period (60-62%) compared to before and after the lockdown (45-49%), indicating the key role of family and home environment in that period. Multi-rater analyses suggested that part of this increase in shared environmental variance likely reflects rater bias rather than true environmental influences. These findings highlight that children in psychiatric care may face additional challenges compared to their peers and emphasize the importance of multi-rater assessments. Results suggest that both genetic predispositions and environmental disruptions should be considered when developing strategies to support child wellbeing during crises.

Previous studies robustly link childhood peer victimization experience to the timing of substance use initiation. However, no study has investigated the contributions of genetic and environmental factors to this link. The current study focused on a sample of 779 twin pairs followed from age 9-10 to 19-20, which is racially/ethnically and socioeconomically representative of the greater Los Angeles area. The aims were to investigate (1) the associations between childhood victimization, including physical (e.g., kicking, pushing), verbal (e.g., taunting), and relational victimization (e.g., spreading rumors), and timing of substance use initiation, and (2) the contributions of genetic/environmental factors to these associations. Multinomial logistic regressions revealed several small associations, but none of these survived corrections for multiple testing. Univariate genetic models suggested genetic (A) and nonshared environmental influences (E) on verbal victimization (V_A = .43, V_E = .57), shared environmental (C) and nonshared environmental factors on relational victimization (V_C = .22, V_E = .78), and ambiguous familial influences and E on physical victimization (V_A = .34, V_E = .66; V_C = .26, V_E = .74). Timing of cigarette initiation were explained by A, C, and E (V_A = .48, V_C = .31, V_E = .21). Quantitative sex differences in contributions of A, C, and E were detected for alcohol (V_AM = .90, V_EM = .10; V_CF = .86, V_EF = .14) and marijuana initiation (V_AM = .89, V_EM = .11; V_CF = .79, V_EF = .21); however, A could be dropped for females and C could be dropped for males across both variables. Multivariate twin analyses were not feasible, due to the low cross-trait correlations. These findings call into question the robustness of links between self-reported victimization in childhood and prospectively measured timing of substance initiation across adolescence.

Hand preference first appears in early development, yet twin studies and GWAS show that only a minority of variance is explained by heritable genetic factors. Using UK Biobank data and multivariable logistic regression to test associations between potential causes of handedness and offspring hand preference, we then investigated the potential causal effect of maternal smoking during pregnancy on offspring handedness using a proxy gene-by-environment (GxE) Mendelian randomization design. We used rs16969968 in the CHRNA5 gene and a polygenic risk score of genome-wide significant smoking-heaviness variants to proxy smoking behaviour. We stratified based on reported maternal smoking during pregnancy because, regardless of genotype, any causal effect of maternal smoking heaviness on offspring handedness should only manifest in individuals whose mothers smoked during pregnancy. Using traditional epidemiological methods, we found maternal smoking during pregnancy increased the probability of being right-handed after adjustment for covariates. Despite this, when using the GxE MR analyses we found no strong causal effect of maternal smoking during pregnancy on offspring hand-preference. Our findings using the UK Biobank cohort align with previous findings and emphasise the impact of factors such as birth year, birthweight, being part of a multiple birth and breastfeeding on hand preference. However, we found no strong evidence for a causal link between maternal smoking and offspring handedness. The main factors contributing to variation in hand preference remain unresolved.

Mitochondrial DNA (mtDNA) plays a crucial role in numerous cellular processes, yet its impact on human complex behavior remains underexplored. The current paper proposes a novel covariance structure model with seven parameters to specifically isolate and quantify mtDNA effects on human complex traits. This approach uses extended pedigrees to obtain estimates of mtDNA variance while controlling for other genetic and environmental influences. Our Monte-Carlo simulations indicate that a sample size of approximately 5,000 individuals is sufficient to detect medium mtDNA effects ([Formula: see text]), while a more substantial cohort of around 30,000 is required for small effects ([Formula: see text]). We show that deeper pedigrees increase power to detect the mtDNA effect while wider pedigrees decrease power, given the equal total sample size. We evaluated how missing kinship records and mtDNA mutations impact bias. Both lead to underestimation of mtDNA variance, and an overestimation of the interaction between nuclear DNA and mtDNA. In addition, the false positive rate of mtDNA effect estimation is low when fitting the model with data generated without mtDNA effects. Collectively, we demonstrate that using extended pedigrees to quantify the influence of mtDNA on human behavior is robust and powerful.

Substance use has been associated with differences in adult brain morphology; however, it is unclear whether these differences precede or are a result of substance use substance use. We investigated the impact of polygenic risk scores (PRSs) for cannabis use disorder (CUD) and general substance use and substance use disorder liability (SU/SUD) on brain morphology in drug-naïve adolescents. Baseline data were used from 1874 European-descent participants (ages 9-11) comprising 222, 328 and 387 pairs of MZ twins, DZ twins, and Non-Twin Siblings, respectively, in the Adolescent Brain Cognitive Development Study. We fitted multivariate twin models to estimate the putative effects of CUD, SU/SUD, and brain region-specific PRSs. These models assessed their influence on six subcortical and two cortical phenotypes. PRS for CUD and SU/SUD were created based on GWAS conducted by Johnson et al. (Lancet Psychiatry 7:1032, 2020) and Hatoum et al. (Nat Ment Health 1:210-223, 2023), respectively. When decomposing variance in each brain region of interest (ROI), we used the corresponding ROI-specific PRS. Brain morphometry in drug-naive subjects was unrelated to CUD PRS. The variance explained in each ROI by its corresponding PRS ranged from 0.8 to 4.4%. The SU/SUD PRS showed marginally significant effects (0.2-0.4%) on cortical surface area and nucleus accumbens volume, but overall effect sizes were small. This study failed to reject the null hypothesis of no association between genetic risk for substance use and brain morphometry among baseline drug-naive adolescents. Genetic risk for CUD was not associated with brain morphometry among drug-naive adolescents, but a weak association with general addiction and substance use risk (SU/SUD) particularly in nucleus accumbens volume and total cortical surface area, was observed.

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.