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Kagan theorized biologically based temperament types that are present in infancy, stable across development, and essential for understanding individual differences. Despite evidence, temperament research remains focused on a few prominent dimensions of temperament, without adequately addressing covariance among dimensions and temperament types. Using longitudinal twin data, we took a person-centered statistical approach to identify temperament types and examined continuity and change across five developmental periods (Ninfancy = 602; Ntoddlerhood = 522; Nearly childhood = 390; Nlate childhood = 718; Nearly adolescence = 700). We then examined the genetic and environmental etiology of temperament types. Twins were boys and girls (51–53% female), primarily Hispanic/Latinx (23–30%) and non-Hispanic/Latinx White (56–63%), and from socioeconomically diverse families (28–38% near-or-below the poverty line). Using latent profile analysis, we identified three temperament types at each age characterized by negative reactivity and dysregulation, positive reactivity and strong self-regulation, and moderate reactivity and regulation. Latent transition analyses revealed considerable continuity in membership type for "negative dysregulated" beginning in infancy, log odds = 1.58 (SE =.65) to 3.16 (SE =.77), p <.01, of remaining relative to transitioning to "typical expressive", and "positive well-regulated" beginning in early childhood, log odds = 1.41 (SE =.56) to 2.25 (SE =.47), p <.05. Twin analyses revealed moderate heritability and a consistent role of the shared environment on positive well-regulated, with negative dysregulated and typical expressive also moderately heritable with the shared environment being important at some ages. Findings support the presence of theorized biologically based temperament types that develop rapidly in infancy and toddlerhood and provide a foundation for the study of individual differences and risk and resilience processes across the lifespan. Public Significance Statement: Children can be classified into three types based on their temperament: negative dysregulated, positive well-regulated, or typical expressive. These types develop rapidly across infancy and toddlerhood becoming more continuous by early childhood. Types are both heritable and influenced by the early environment, supporting a complex interplay between temperament and sociocultural context when predicting children and adolescent's adaptation. [ABSTRACT FROM AUTHOR]

ABSTRACT Background Method Results Conclusion Because premorbid BMI strongly predicts the amount of weight loss in anorexia nervosa (AN)/atypical AN, we hypothesize that weight loss triggers both disorders by inducing the endocrine adaptation to starvation.We propose research to capture the onset of AN/atypical AN following intentional, otherwise behaviorally motivated, or unintentional weight loss in relationship to premorbid weight.We propose retrospective and prospective studies to examine the temporal development of symptoms in AN/atypical AN. Given a greater frequency of weight loss behaviors in individuals with high BMIs, patients with intentionally driven weight loss should demonstrate a higher mean weight loss and greater premorbid weight and shape concerns. Practice guidelines necessitate weight gain for AN recovery, yet how weight gain induces improvements is unspecified and warrants systematic elucidation. Finally, we highlight implications for the current conceptualization of genetic and environmental contributors of AN/atypical AN in twin and molecular genetic studies.We propose separating the starvation‐induced mechanisms relevant for AN/atypical AN development from the reasons/mechanisms inherent to weight loss. [ABSTRACT FROM AUTHOR]

The frequency with which Internalizing and Externalizing symptoms co-occur suggests that, behind both domains, there may be a common susceptibility represented by a general psychopathology factor. However, it's still unclear whether this common susceptibility is affected by age-related variations. Internalizing (i.e., Fear and Distress) and Externalizing symptoms were evaluated in 803 twin pairs from the population-based Italian Twin Registry. Model-fitting analysis was performed separately in the 6–14 and 15–18 age groups to estimate genetic and environmental contributions to the covariance among symptoms. For the 6–14 group, a multivariate Cholesky model best fitted the data, while, for the 15–18 group, the best fit was provided by a Common Pathway model in which nearly 50% of total variance of each trait was mediated by common genetic factors. Our findings support a common susceptibility behind Internalizing and Externalizing symptoms, mainly genetic in origin, that becomes more evident at the beginning of puberty. [ABSTRACT FROM AUTHOR]

Objective: To systematically review the literature regarding the concordance of sleep bruxism (SB) between monozygotic (MZ) and dizygotic (DZ) twins. Methods: The registration for this systematic review was accomplished in the International Prospective Register of Systematic Reviews (PROSPERO, No. CRD42021251751). As of July 2022, four databases were searched, including PubMed, Scopus, Embase, and Web of Science, as well as the grey literature in Google Scholar and OpenGrey. Observational studies evaluating SB in MZ and DZ twins of any age and sex were included. For the evaluation of the risk of bias, the Joanna Briggs checklist was utilized. The certainty of evidence was assessed via the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system. Pooled and subgroup meta-analyses were performed to estimate concordance of SB ​​between twins (p < 0.05). Results: In total, 3,155 records were identified. In the qualitative analysis, eleven studies were included; of these, seven were included in the meta-analysis. The majority of the articles exhibited a low risk of bias (63.6%). Greater SB concordance was observed between MZ twins than between DZ twins in the analysis of general concordance (OR = 1.47; 95% CI = 1.07–2.02) and also positive concordance (OR = 1.53; 95% CI = 1.29–1.81). Within the subgroup analyses, the significance of the findings remained only for the reported/self-reported SB regarding general concordance (OR = 1.44; 95% CI = 1.07–1.95) and positive concordance (OR = 1.55; 95% CI = 1.28–1.88). Low certainty of the evidence was observed for the general concordance analysis, while moderate certainty was observed for the positive concordance. Conclusion: There was a higher concordance of SB in MZ twins compared to DZ twins, indicating a possible genetic influence on the condition's occurrence. [ABSTRACT FROM AUTHOR]

This article uses a behavioral genetics approach to study gender differences in expressed political interest, applying the enriched environment hypothesis to gendered political socialization. As girls are less stimulated to develop an interest in politics than boys, we theorize that these differences in the socialization environment reduce the expression of girls' genetic predispositions compared to boys', leading to a gender gap in the heritability of this trait. Analyses using data on German twins (11–25 years) demonstrate relevant differences by gender and age in heritability estimates. While differences in political interest between boys are largely explained by genes, this is less the case for girls, as they have considerably higher shared environment estimates. Our results imply that gender differences in expressed political interest are sustained by both genetic variation and environmental influences (such as socialization), as well as the interaction between the two. [ABSTRACT FROM AUTHOR]

Background: Research on genetic and environmental influences on speech and/or language difficulties (SaLD) is sparse, with inconsistent heritability estimates. We aimed to estimate the prevalence of parental reported SaLD and the relative contributions of genetic and environmental factors for the phenotype using a Swedish population‐based twin sample. We hypothesized that there would be a stronger genetic than environmental effect on SaLD. Methods: Data were collected from The Child and Adolescent Twin Study in Sweden. The study sample included 16,774 twin pairs (16,946 males, 16,602 females), of which 5141 were monozygotic, 5861 dizygotic (DZ), and 5772 opposite‐sex DZ pairs. The language items in the Autism–Tics, Attention‐Deficit Hyperactivity Disorder, and other Comorbidities inventory were used to categorize individuals as having parental‐reported SaLD. A classical twin design was used to estimate the relative contribution of genetic and environmental factors to the liability of SaLD. Results: The prevalence of SaLD was 7.85% (95% confidence interval (CI) [7.57%–8.15%]) and 7.27% (95% CI [6.99%–7.55%]) when excluding individuals with autism and intellectual disability (ID). We also found that SaLD were significantly more prevalent in males than females with a ratio of 2:1. The heritability was estimated to be 75% (95% CI [67%–83%]) for SaLD. Shared environment played a significant role with an estimated contribution of 22% (95% CI [14%–30%]). The heritability estimate was reduced to 70% but with overlapping CI when excluding individuals with autism and ID. Conclusions: We provide evidence that SaLD is common in the population and under strong genetic influence. Future studies should focus on mapping the genetic architecture of SaLD and related disorders. [ABSTRACT FROM AUTHOR]

Background: Autism and autistic traits onset in childhood but persist into adulthood. Little is known about how genetic and environmental factors influence autism and autistic traits into adulthood. We aimed to determine age effects on the heritability of clinically diagnosed autism and the etiological stability of autistic traits from childhood to adulthood using twin methods. Methods: From 23,849 twin pairs in the Swedish Twin Register born between 1959 and 2010, we identified 485 individuals (1.01%, 31.5% female) with a clinical autism diagnosis. We estimated and compared the relative contribution of genetic, shared, and nonshared environmental influences to autism in childhood and adulthood. We further used multivariate twin analysis with four measurement points among 1,348 twin pairs in the longitudinal Twin Study of Child and Adolescent Development to assess the phenotypic and etiological stability of autistic traits – measured with three scales from the Child Behavior Checklist – from childhood to adulthood. Results: Autism heritability was comparable from childhood, (96% [95% CI, 76–99%]) to adulthood (87% [67–96%]). Autistic traits were moderately stable (phenotypic correlation = 0.35–0.61) from childhood to adulthood, and their heritability varied between 52 and 71%. We observed stable as well as newly emerging genetic influences on autistic traits from ages 8–9 to 19–20, and unique nonshared environmental influences at each age. Conclusions: Genetic factors are important for autism and autistic traits in adulthood and separate genetic studies in adults are warranted. [ABSTRACT FROM AUTHOR]

Monozygotic twins share the same genotype; however, they can be phenotypically discordant on various traits. Studying discordant monozygotic twins allows the investigation of differences in associations between symptoms and psychopathological risk factors, controlled for shared genetic liability. The network approach to psychopathology suggests that depressive symptoms, along with risk and protective factors (e.g., cognition, daily activities), form a complex system of mutually interacting components. We compared monozygotic twins discordant for lifetime depression on their respective extended networks of depressive symptoms, cognitive functions and daily activities (intellectual, physical, social), and evaluated if these networks differ in their associations between variables and in the role of each variable within the network. Regularized partial correlations investigated the networks' composition in 147 monozygotic twin pairs discordant for depression from the Danish Twin Registry. Affected twins had stronger overall associations within their network of depressive symptoms, cognitive functions and daily activities than their unaffected co-twins, while the importance of the network components' associations did not differ between the co-twins. In affected twins, decreased frequency in experiencing happiness had the strongest association with remaining variables (i.e., the most influence in activating other network elements). Also, variables from different groups were significantly associated (e.g., loneliness with delayed memory, pessimism with low social activities, verbal learning with intellectual activities). In unaffected twins, both mood symptoms and cognitive functions were important, but between-groups associations were quasi-absent. These results suggest that external events affecting the ability to feel happiness likely trigger the psychopathological process (depression network activation), independently from the genetic predisposition to depression. [ABSTRACT FROM AUTHOR]

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Abstract The objective of this study was to assess the relative contributions of genetic and environmental factors to variation in palatal parameters in twins with completed maxillary growth. The subjects of this study comprised digital dental casts of 50 monozygotic and 35 dizygotic twin pairs. The subjects’ average age was 17.95 ± 2.83 years. Zygosity determination was carried out using 15 specific DNA markers and an amel fragment of the amelogenin gene. The interdental distances were measured between selected dental landmarks at the occlusal and gingival planes. The palatal height, surface area and volume were measured between the gingival plane and the midpalate suture. High heritability estimates were observed for all transverse intra-arch measurements. The palate height (a2 = 0.8), dental arch width in the molar area (a2 = 0.86), palatal surface area (a2 = 0.61) and palate volume (a2 = 0.69) were under strong additive genetic control. Moderate genetic dominance was observed for dental arch widths at the gingival line in the canine (d2 = 0.5) and premolar regions (d2 = 0.78–0.81). Sexual dimorphism was shown, with males exhibiting a greater arch width, palate surface area and volume than females (p

Abstract Objectives The aim of this study was to investigate associations between exposure to work-related violence/threats and harassment, and future sickness absence (SA) due to common mental disorders (CMDs), taking familial factors (shared genetics and early-life environment) and neuroticism into account. Methods The study sample included 8795 twin individuals from the Swedish Twin Project of Disability Pension and Sickness Absence (STODS), including survey data from the Study of Twin Adults: Genes and Environment (STAGE). Self-reported work-related violence and/or threats as well as work-related harassment (including bullying) and national register data on SA due to CMDs were analyzed using standard logistic regression, and conditional logistic regression among complete twin pairs discordant on exposures. Individuals were followed for a maximum of 13 years. Interactions between neuroticism and exposures were assessed using both multiplicative and additive interaction analyses. Results Exposure to work-related violence/threats was associated with higher odds of SA due to CMDs when adjusting for age, sex, marital status, children, education, type of living area, work characteristics, and symptoms of depression and burnout (OR 2.11, 95% CI 1.52–2.95). Higher odds of SA due to CMDs were also found for exposure to harassment (OR 1.52, 95% CI 1.10–2.11) and a combined indicator of exposure to violence/threats and/or harassment (OR 1.98, 95% CI 1.52–2.59), compared with the unexposed. Analyses of twins discordant on exposure, using the unexposed co-twin as reference, showed reduced ORs. These ORs were still elevated but no longer statistically significant, potentially due to a lack of statistical power. No multiplicative interaction was found between neuroticism and exposure to work-related violence/threats, or harassment. However, a statistically significant additive interaction was found between neuroticism and exposure to violence/threats, indicating higher odds of SA due to CMDs in the group scoring lower on neuroticism. Conclusions Exposure to work-related offensive behaviors was associated with SA due to CMDs. However, the results indicated that these associations may be partly confounded by familial factors. In addition, an interaction between exposure and neuroticism was suggested. Thus, when possible, future studies investigating associations and causality between offensive behaviors at work and mental health-related outcomes, should consider familial factors and neuroticism.

The objective of this study was to assess the relative contributions of genetic and environmental factors to variation in palatal parameters in twins with completed maxillary growth. The subjects of this study comprised digital dental casts of 50 monozygotic and 35 dizygotic twin pairs. The subjects' average age was 17.95 ± 2.83 years. Zygosity determination was carried out using 15 specific DNA markers and an amel fragment of the amelogenin gene. The interdental distances were measured between selected dental landmarks at the occlusal and gingival planes. The palatal height, surface area and volume were measured between the gingival plane and the midpalate suture. High heritability estimates were observed for all transverse intra-arch measurements. The palate height (a2 = 0.8), dental arch width in the molar area (a2 = 0.86), palatal surface area (a2 = 0.61) and palate volume (a2 = 0.69) were under strong additive genetic control. Moderate genetic dominance was observed for dental arch widths at the gingival line in the canine (d2 = 0.5) and premolar regions (d2 = 0.78–0.81). Sexual dimorphism was shown, with males exhibiting a greater arch width, palate surface area and volume than females (p < 0.01). The majority of palate parameters variation in twins was controlled by genetic effects, and most were highly heritable. [ABSTRACT FROM AUTHOR]

Objective: This study examined whether phenotypic correlations between psychopathological dimensions and personality traits of different hierarchical levels originate from common genetic and environmental sources of variance. Method: Participants were 386 monozygotic and 204 dizygotic twins. The Psychiatric Diagnostic Screening Questionnaire (PDSQ) was applied along with the Revised NEO Personality Inventory (NEO‐PI‐R). The results of the CFA confirmed the hypothesis of the internalizing and externalizing dimensions underlying PDSQ scales. Results: The results indicated a significantly greater role of genetic compared to environmental factors in the relationship between internalizing psychopathology and personality traits. Facets of neuroticism showed positive genetic links with internalizing disorders, while negative genetic links were shown for all facets of extraversion except excitement‐seeking, competence, self‐discipline, achievement striving, actions, and trust. Lower‐order personality traits were shown to be associated with internalizing disorders more intensively than the broader domains to which they belong, both at the phenotypic and genetic levels. Conclusions: High neuroticism, together with several facets from the domain of extraversion and conscientiousness seems to represent an increased genetic susceptibility to the disorders from the internalizing spectrum. Results also suggest that specific environmental factors which are not shared with personality traits contribute to the internalizing symptoms. [ABSTRACT FROM AUTHOR]

The purpose of this study was to explore if child-care intensity (hours/weeks) and age of onset could moderate genetic and environmental contributions to school readiness. A sample of 648 (85% Whites; 50% Females) pairs of twins was used to compute a GxE, CxE and ExE interaction analyses. The moderation model showed that shared environment explains 48% of individual differences in school readiness for children not attending formal child-care, and decreased gradually to a mere 3% for children attending formal child-care full time, e.g., 40 h per week. Age of onset exerted no moderation effect. The results support the hypothesis that child-care acts as a normalizing environment, possibly buffering negative effects from low-quality home environments on school readiness. [ABSTRACT FROM AUTHOR]

Researchers have proposed that culture significantly influences perceived stress (PS). To date, however, twin studies on PS have been conducted mostly in western, individualistic cultures, which demonstrate that PS due to controllable (personal) life events is more heritable than PS due to uncontrollable (network) life events. This study aimed to investigate genetic and environmental influences on PS in South Korean twins. South Korea practices a dominant collectivist culture. In total, 1372 twin individuals (mean age = 22.4 ± 2.5 years) completed an online survey on PS, which consisted of the scales, Friendship, Academic Stress, Future Career, Family Conflicts, and Family Financial Difficulties (FFD). Friendship, Academic Stress, and Future Career can be considered PS due to personal life events, and Family Conflict and FFD, PS due to network life events. The general sex-limitation model-fitting analysis revealed the absence of qualitative or quantitative sex differences in genetic and environmental influences. Specifically, additive genetic influences were predominant for Friendship (63%), Academic Stress (67%), and Future Career (57%) for both sexes, with the remaining variance attributable to nonshared environmental influences. In contrast, shared environmental influences were largest for Family Conflict (47% for both genders) and FFD (64% for males, 63% for females) with no significant genetic effects. Despite known cultural differences in the means and variances of PS, South Korean twins exhibited significant genetic effects in PS due to personal life events and large shared environmental effects in PS due to network life events, which is similar to western samples. [ABSTRACT FROM AUTHOR]

Twin studies have found gross cerebellar volume to be highly heritable. However, whether fine‐grained regional volumes within the cerebellum are similarly heritable is still being determined. Anatomical MRI scans from two independent datasets (QTIM: Queensland Twin IMaging, N = 798, mean age 22.1 years; QTAB: Queensland Twin Adolescent Brain, N = 396, mean age 11.3 years) were combined with an optimised and automated cerebellum parcellation algorithm to segment and measure 28 cerebellar regions. We show that the heritability of regional volumetric measures varies widely across the cerebellum (h2$$ {h}^2 $$ 47%–91%). Additionally, the good to excellent test–retest reliability for a subsample of QTIM participants suggests that non‐genetic variance in cerebellar volumes is due primarily to unique environmental influences rather than measurement error. We also show a consistent pattern of strong associations between the volumes of homologous left and right hemisphere regions. Associations were predominantly driven by genetic effects shared between lobules, with only sparse contributions from environmental effects. These findings are consistent with similar studies of the cerebrum and provide a first approximation of the upper bound of heritability detectable by genome‐wide association studies. [ABSTRACT FROM AUTHOR]

Abstract Background Research on genetic and environmental influences on speech and/or language difficulties (SaLD) is sparse, with inconsistent heritability estimates. We aimed to estimate the prevalence of parental reported SaLD and the relative contributions of genetic and environmental factors for the phenotype using a Swedish population‐based twin sample. We hypothesized that there would be a stronger genetic than environmental effect on SaLD. Methods Data were collected from The Child and Adolescent Twin Study in Sweden. The study sample included 16,774 twin pairs (16,946 males, 16,602 females), of which 5141 were monozygotic, 5861 dizygotic (DZ), and 5772 opposite‐sex DZ pairs. The language items in the Autism–Tics, Attention‐Deficit Hyperactivity Disorder, and other Comorbidities inventory were used to categorize individuals as having parental‐reported SaLD. A classical twin design was used to estimate the relative contribution of genetic and environmental factors to the liability of SaLD. Results The prevalence of SaLD was 7.85% (95% confidence interval (CI) [7.57%–8.15%]) and 7.27% (95% CI [6.99%–7.55%]) when excluding individuals with autism and intellectual disability (ID). We also found that SaLD were significantly more prevalent in males than females with a ratio of 2:1. The heritability was estimated to be 75% (95% CI [67%–83%]) for SaLD. Shared environment played a significant role with an estimated contribution of 22% (95% CI [14%–30%]). The heritability estimate was reduced to 70% but with overlapping CI when excluding individuals with autism and ID. Conclusions We provide evidence that SaLD is common in the population and under strong genetic influence. Future studies should focus on mapping the genetic architecture of SaLD and related disorders.

Dyslipidemia is one of the cardiometabolic risk factors that influences mortality globally. Unraveling the causality between blood lipids and metabolites and the complex networks connecting lipids, metabolites, and other cardiometabolic traits can help to more accurately reflect the body’s metabolic disorders and even cardiometabolic diseases. We conducted targeted metabolomics of 248 metabolites in 437 twins from the Chinese National Twin Registry. Inference about Causation through Examination of FAmiliaL CONfounding (ICE FALCON) analysis was used for causal inference between metabolites and lipid parameters. Bidirectional mediation analysis was performed to explore the linkages between blood lipids, metabolites, and other seven cardiometabolic traits. We identified 44, 1, and 31 metabolites associated with triglyceride (TG), total cholesterol (TC), and high-density lipoprotein-cholesterol (HDL-C), most of which were gut microbiota-derived metabolites. There were 9, 1, and 14 metabolites that showed novel associations with TG, TC, and HDL-C, respectively. ICE FALCON analysis found that TG and HDL-C may have a predicted causal effect on 23 and six metabolites, respectively, and one metabolite may have a predicted causal effect on TG. Mediation analysis discovered 14 linkages connecting blood lipids, metabolites, and other cardiometabolic traits. Our study highlights the significance of gut microbiota-derived metabolites in lipid metabolism. Most of the identified cross-sectional associations may be due to the lipids having a predicted causal effect on metabolites, but not vice versa, nor are they due to family confounding. These findings shed new light on lipid metabolism and personalized management of cardiometabolic diseases.

Background and purpose: This article aims to identify epigenetic markers and detect early development of hematopoietic malignancies through an epigenome wide association study of DNA methylation data. Materials and methods: This register-based study includes 1,085 Danish twins with 31 hematopoietic malignancies and methylation levels from 450,154 5’-C-phospate-G-3’ (CpG) sites. Associations between methylation levels and incidence of hematopoietic malignancy is studied through time-to-event regression. The matched case-cotwin design, where one twin has a malignancy and the cotwin does not, is applied to enhance control for unmeasured shared confounding and false discoveries. Predictive performance is validated in the independent Older Finnish Twin Cohort. Results and interpretation: We identified 67 epigenetic markers for hematopoietic malignancies of which 12 are linked to genes associated with hematologic malignancies. For some markers, we discovered a 2–3-fold relative risk difference for high versus low methylation. The identification of these 67 sites enabled the formation of a predictor demonstrating a cross-validated time-varying area under the curve (AUC) of 92% 3 years after individual blood sampling and persistent performance above 70% up to 6 years after blood sampling. This predictive performance was to a large extent recovered in the validation sample showing an overall Harrell’s C of 73%. In conclusion, from a large population representative twin study on hematopoietic cancers, novel epigenetic markers were identified that may prove useful for early diagnosis.

Abstract Introduction Early motor development has been found to be a predictor of exercise behavior in children and adolescents, but whether this reflects a causal effect or confounding by genetic or shared environmental factors remains to be established. Methods For 20,911 complete twin pairs from the Netherlands Twin Register a motor development score was obtained from maternal reports on the timing of five motor milestones. During a 12-year follow-up, subsamples of the mothers reported on the twins’ ability to perform seven gross motor skills ability (N = 17,189 pairs), and weekly minutes of total metabolic equivalents of task (MET) spent on sports and exercise activities at age 7 (N = 3632 pairs), age 10 (N = 3735 pairs), age 12 (N = 7043 pairs), and age 14 (N = 3990 pairs). Multivariate phenotypic and genetic regression analyses were used to establish the predictive strength of the two motor development traits for future exercise behavior, the contribution of genetic and shared environmental factors to the variance in all traits, and the contribution of familial confounding to the phenotypic prediction. Results Significant heritability (h2) and shared environmental (c2) effects were found for early motor development in boys and girls (h2 = 43-65%; c2 = 16-48%). For exercise behavior, genetic influences increased with age (boys: h2 age7 = 22% to h2 age14 = 51%; girls: h2 age7 = 3% to h2 age14 = 18%) paired to a parallel decrease in the influence of the shared environment (boys: c2 age7 = 68% to c2 age14 = 19%; girls: c2 age7 = 80% to c2 age14 = 48%). Early motor development explained 4.3% (p

The aim of the study was to examine associations between life events and self-assessed loneliness in adolescence. We used data from a Norwegian population-based twin sample including seven birth cohorts (N = 2,879, 56% females). The participants completed self-report questionnaires three times throughout adolescence, with 2 years in between (i.e., 12–18 years old at Wave 1). By using a random intercept cross-lagged panel model (RI-CLPM), we were able to separate stable influences in the measured constructs from the within-person changes at each measurement occasion. In addition, using data from twins allowed us to examine to what degree the associations between life events and loneliness were genetic and/or environmental in nature. The results showed moderate stability of both loneliness and aggregation scores of life events throughout adolescence. The life events were assigned to clusters based on their independence (i.e., events considered dependent or independent on a person's behavior) and desirability (i.e., positive or negative). The time-stable between-person variance in all three measures, loneliness and person-dependent positive and negative life events, could almost exclusively be accounted for by genetic factors. However, as expected, also shared environmental factors influenced person-independent life events. The associations between time-stable between-person variance in loneliness and life events were small, and nearly exclusively due to shared genetic influences. Furthermore, life events do not seem to predict changes in loneliness or vice versa. In conclusion, the self-reported levels of loneliness throughout adolescence seems to be independent of life events. Public Significance Statement: This study suggests that life events do not influence levels of loneliness in adolescence. The weak associations between life events and loneliness were mainly due to shared genetic influences. Additionally, the results showed that levels of loneliness are moderately stable throughout this period of life, mainly due to genetic influences. Importantly, the study highlights the need of using genetically informative designs, also when studying the effects of assumed "environmental" measures. [ABSTRACT FROM AUTHOR]

Although research shows a strong positive association between perceived stress and loneliness, the genetic and environmental etiology underlying their association remains unknown. People with a genetic predisposition to perceived stress, for example, may be more prone to feeling lonely and vice versa. Conversely, unique factors in people's lives may explain differences in perceived stress levels that, in turn, affect feelings of loneliness. We tested whether genetic factors, environmental factors, or both account for the association between perceived stress and loneliness. Participants were 3,066 individual twins (nFemale = 2,154, 70.3%) from the Washington State Twin Registry who completed a survey during April–May, 2020. Structural equation modeling was used to analyze the item-level perceived stress and loneliness measures. The correlation between latent perceived stress and latent loneliness was.68. Genetic and nonshared environmental variance components underlying perceived stress accounted for 3.71% and 23.26% of the total variance in loneliness, respectively. The genetic correlation between loneliness and perceived stress was.45 and did not differ significantly between men and women. The nonshared environmental correlation was.54 and also did not differ between men and women. Findings suggest that holding constant the strong genetic association between perceived stress and loneliness, unique life experiences underlying people's perceived stress account for individual differences in loneliness. [ABSTRACT FROM AUTHOR]

Although previous studies have identified negative relationships between cognitive ability and emotional problems (EP), mechanism explaining these relationships remained unclear. This study evaluated two explanatory models using bivariate moderation model-fitting analysis in a twin design. The resilience model suggests that high cognitive ability decreases the risk of EP in adverse settings, and the scarring model suggests that EP symptoms lead to persistent cognitive deficits following onset. The Standard Progressive Matrices Plus (SPM) and EP scale were administered to a sample of 3,202 twins (mean age = 14.62 ± 1.74 years) attending public schools in Nigeria. The results of bivariate moderation model-fitting analyses only supported the resilience model. Moderation effects were not significant in the scarring model when genetic and environmental influences were incorporated. The best-fitting bivariate moderation model assuming the resilience model yielded a genetic correlation of − 0.57 (95% CI = − 0.40, − 0.84) with no significant environmental correlations. Moreover, the SPM moderated the environmental, not genetic, influences on EP, such that environmental influences were strong when protective factors were absent (low SPM) and weak when these were present (high SPM). These results indicate the need to develop targeted prevention and intervention strategies for EP in adolescents displaying low cognitive ability in deprived settings. [ABSTRACT FROM AUTHOR]

Early temperament precedes children's emerging Big Five personality, but shared models of temperament and personality are scarce. We wanted to estimate the genetic factor structure underlying both temperament and the Big Five in children, employing a genetically informed study. Within the Norwegian Mother and Child Cohort Study, we selected 26,354 twins, siblings, and cousins. Mothers rated their children's temperament three times between the ages of 1.5 and 5 years, and the children's Big Five personality at the age of 8. We analyzed the data using biometric modeling. The mean heritability of single-time temperamental traits and Big Five personality traits was.48 and.45, respectively. The mean genetic correlations of temperament across time were.80. The genetic correlations of temperament at 5 years and the Big Five at 8 years revealed two factors, the first comprising reversed Big Five Neuroticism, Agreeableness, Conscientiousness, and reversed EAS Emotionality, the second comprising Big Five Extraversion, Openness to Experience, EAS Activity, Sociability, and reversed Shyness. A confirmatory factor analysis estimated the two factors showing heritabilities of.96 and.72, respectively. The two factors mirrored the metatraits Stability and Plasticity by John M. Digman. Temperament and personality in childhood can be meaningfully bridged using just two metafactors. [ABSTRACT FROM AUTHOR]

Introduction: Early motor development has been found to be a predictor of exercise behavior in children and adolescents, but whether this reflects a causal effect or confounding by genetic or shared environmental factors remains to be established. Methods: For 20,911 complete twin pairs from the Netherlands Twin Register a motor development score was obtained from maternal reports on the timing of five motor milestones. During a 12-year follow-up, subsamples of the mothers reported on the twins' ability to perform seven gross motor skills ability (N = 17,189 pairs), and weekly minutes of total metabolic equivalents of task (MET) spent on sports and exercise activities at age 7 (N = 3632 pairs), age 10 (N = 3735 pairs), age 12 (N = 7043 pairs), and age 14 (N = 3990 pairs). Multivariate phenotypic and genetic regression analyses were used to establish the predictive strength of the two motor development traits for future exercise behavior, the contribution of genetic and shared environmental factors to the variance in all traits, and the contribution of familial confounding to the phenotypic prediction. Results: Significant heritability (h2) and shared environmental (c2) effects were found for early motor development in boys and girls (h2 = 43-65%; c2 = 16-48%). For exercise behavior, genetic influences increased with age (boys: h2age7 = 22% to h2age14 = 51%; girls: h2age7 = 3% to h2age14 = 18%) paired to a parallel decrease in the influence of the shared environment (boys: c2age7 = 68% to c2age14 = 19%; girls: c2age7 = 80% to c2age14 = 48%). Early motor development explained 4.3% (p < 0.001) of the variance in future exercise behavior in boys but only 1.9% (p < 0.001) in girls. If the effect in boys was due to a causal effect of motor development on exercise behavior, all of the factors influencing motor development would, through the causal chain, also influence future exercise behavior. Instead, only the genetic parts of the regression of exercise behavior on motor development were significant. Shared and unique environmental parts of the regression were largely non-significant, which is at odds with the causal hypothesis. Conclusion: No support was found for a direct causal effect in the association between rapid early motor development on future exercise behavior. In boys, early motor development appears to be an expression of the same genetic factors that underlie the heritability of childhood and early adolescent exercise behavior. [ABSTRACT FROM AUTHOR]

Using a large sample of 1,120 twins and the multivariate ACE-Cholesky model, we estimated the heritability of trust using four distinct measures of trust – domain-specific political trust, general self-reported trust, and incentivized behavioral trust and trustworthiness. Across the different measures of trust we consider, our estimates for heritability range from 1 % to 37 %. Furthermore, the environmental correlates of trust also vary across the different measures with political trust having the largest set of environmental covariates. To reconcile the variation in the estimated heritability of trust in the literature, we provide a meta-analysis of the heritability of behavioral and stated trust. [ABSTRACT FROM AUTHOR]

Although earlier research has shown that individual differences on the spectrum of attention deficit hyperactivity disorder (ADHD) are highly heritable, emerging evidence suggests that symptoms are associated with complex interactions between genes and environmental influences. This study investigated whether a genetic predisposition [Note that the term 'genetic predisposition' was used in this manuscript to refer to an estimate based on twin modeling (an individual's score on the latent trait that resembles additive genetic influences) in the particular population being examined.] for the symptom dimensions hyperactivity and inattention determines the extent to which unique-environmental influences explain variability in these symptoms. To this purpose, we analysed a sample drawn from the Twins Early Development Study (TEDS) that consisted of item-level scores of 2168 16-year-old twin pairs who completed both the Strengths and Difficulties Questionnaire (SDQ; Goodman, in J Child Psychol Psychiatry 38:581–586, 1997) and the Strength and Weaknesses of ADHD Symptoms and Normal Behavior (SWAN; Swanson, in Paper presented at the meeting of the American Psychological Association, Los Angeles, 1981) questionnaire. To maximize the psychometric information to measure ADHD symptoms, psychometric analyses were performed to investigate whether the items from the two questionnaires could be combined to form two longer subscales. In the estimation of genotype-environment interaction, we corrected for error variance heterogeneity in the measurement of ADHD symptoms through the application of item response theory (IRT) measurement models. A positive interaction was found for both hyperactivity (e.g., β 1 = 2.20 with 95% highest posterior density interval equal to [1.79;2.65] and effect size equal to 3.00) and inattention (e.g., β 1 = 2.16 with 95% highest posterior density interval equal to [1.56;2.79] and effect size equal to 3.07). These results indicate that unique-environmental influences were more important in creating individual differences in both hyperactivity and inattention for twins with a genetic predisposition for these symptoms than for twins without such a predisposition. [ABSTRACT FROM AUTHOR]

We estimate whether risk preferences are affected by traumatic events by using a unique survey of Sri Lankan twins which contains information on individual’s exposure to the 2004 Indian Ocean Tsunami, validated measures of mental health and risk preferences, and a rich set of control variables. Our estimation strategy utilizes variation in experiences within twin pairs and allows us to explore wealth shocks and/or changes in mental health as mechanisms. We find that exposure to the tsunami lead to less risk aversion, a result that is not explained by mental health. [ABSTRACT FROM AUTHOR]

Aim: To identify the psychological distress (PD)–associated 5′‐cytosine‐phosphate‐guanine‐3′ sites (CpGs), and investigate the temporal relationship between dynamic changes in DNA methylation (DNAm) and PD. Methods: This study included 1084 twins from the Chinese National Twin Register (CNTR). The CNTR conducted epidemiological investigations and blood withdrawal twice in 2013 and 2018. These included twins were used to perform epigenome‐wide association studies (EWASs) and to validate the previously reported PD‐associated CpGs selected from previous EWASs in PubMed, Embase, and the EWAS catalog. Next, a cross‐lagged study was performed to examine the temporality between changes in DNAm and PD in 308 twins who completed both 2013 and 2018 surveys. Results: The EWAS analysis of our study identified 25 CpGs. In the validation analysis, 741 CpGs from 29 previous EWASs on PD were selected for validation, and 101 CpGs were validated to be significant at a false discovery rate <0.05. The cross‐lagged analysis found a unidirectional path from PD to DNAm at 14 CpGs, while no sites showed significance from DNAm to PD. Conclusions: This study identified and validated PD‐related CpGs in a Chinese twin population, and suggested that PD may be the cause of changes in DNAm over time. The findings provide new insights into the molecular mechanisms underlying PD pathophysiology. [ABSTRACT FROM AUTHOR]

Background: The Italian National Institute of Health (Istituto Superiore di Sanità) funded a 30-month project (July 2021–January 2024) to conduct a twin study of the relationships between Positive Mental Health (PMH) and cellular longevity. Only a few previous studies have focused on the biomarkers of aging in relation to psychological well-being, and none of them exploited the potential of the twin design. Method: In this project, following the standard procedures of the Italian Twin Registry (ITR), we aim to recruit 200 adult twin pairs enrolled in the ITR. They are requested to complete a self-report questionnaire battery on PMH and to undergo a blood withdrawal for the assessment of aging biomarkers, i.e., telomere length and mitochondrial DNA functionality. The association between psychological and aging biomarker measures will be assessed, controlling for genetic and familial confounding effects using the twin study design. Results and conclusions: Biomarker assays are underway. Once data are available for the total study sample, statistical analyses will be performed. The project's results may shed light on new mechanisms underlying the mind–body connection and may prove helpful to promote psychological well-being in conjunction with biological functioning. [ABSTRACT FROM AUTHOR]

Introduction: Psychotic‐like experiences (PLE) have been associated with the subsequent emergence of psychotic disorders as well as several other domains of psychopathology. In this twin study, we estimated the genetic and environmental correlations between PLE and 10 personality disorders (PD). Methods: Diagnoses of 10 PDs according to the Diagnostic and Statistical Manual of Mental Disorders (DSM‐IV) and PLE from the Composite International Diagnostic Interview (CIDI) were retrieved for 2793 young adult twins from the Norwegian Twin Registry. Risk for having a PD and PLEs was modeled using item response theory. Biometric twin models were fitted to estimate the genetic and environmental correlations between PDs and PLEs. Co‐twin control analysis was performed to estimate additional within‐family risk for PLEs when having a PD. Results: Phenotypic overlap between PDs and PLEs ranged from 14% to 44% in males and from 11% to 39% in females, with the highest overlap for borderline PD in both sexes. In general, we found higher genetic correlations (r = 0.14–0.72) than environmental correlations (r = 0.06–0.28) between PDs and PLEs. The highest genetic correlations between PLE and PDs were found for borderline (r = 0.72), paranoid (r = 0.56), schizotypal (r = 0.56) and antisocial PD (r = 0.49). Conclusion: We found that the co‐occurrence between PDs and PLE is the best explained by shared genetic determinants, with minor contributions from environmental factors. Interestingly, borderline PD was highly genetically correlated with PLE, warranting molecular genetic studies of this association. [ABSTRACT FROM AUTHOR]

Age is a dominant risk factor for some of the most common neurological diseases. Biological ageing encompasses interindividual variation in the rate of ageing and can be calculated from clinical biomarkers or DNA methylation data amongst other approaches. Here, we tested the hypothesis that a biological age greater than one's chronological age affects the risk of future neurological diagnosis and the development of abnormal signs on clinical examination. We analysed data from the Swedish Adoption/Twin Study of Aging (SATSA): a cohort with 3175 assessments of 802 individuals followed-up over several decades. Six measures of biological ageing were generated: two physiological ages (created from bedside clinical measurements and standard blood tests) and four blood methylation age measures. Their effects on future stroke, dementia or Parkinson's disease diagnosis, or development of abnormal clinical signs, were determined using survival analysis, with and without stratification by twin pairs. Older physiological ages were associated with ischaemic stroke risk; for example one standard deviation advancement in baseline PhenoAgePhys or KDMAgePhys residual increased future ischaemic stroke risk by 29.2% [hazard ratio (HR): 1.29, 95% confidence interval (CI) 1.06–1.58, P = 0.012] and 42.9% (HR 1.43, CI 1.18–1.73, P = 3.1 × 10−4), respectively. In contrast, older methylation ages were more predictive of future dementia risk, which was increased by 29.7% (HR 1.30, CI 1.07–1.57, P = 0.007) per standard deviation advancement in HorvathAgeMeth. Older physiological ages were also positively associated with future development of abnormal patellar or pupillary reflexes, and the loss of normal gait. Measures of biological ageing can predict clinically relevant pathology of the nervous system independent of chronological age. This may help to explain variability in disease risk between individuals of the same age and strengthens the case for trials of geroprotective interventions for people with neurological disorders. [ABSTRACT FROM AUTHOR]

Objective: Evidence suggests that caffeine use disproportionately impacts sleep functioning among youth with attention-deficit/hyperactivity disorder (ADHD). The present study aimed to examine the association of caffeine use with disrupted sleep, and to test moderating effects of ADHD, by leveraging differences within twin pairs to explore potential quasi-causal (i.e., within-pair) effects. Method: N = 765 complete same-sex twin pairs (mean age at baseline = 10.14 [SD = .5]; 49% girls; 73% white) from the ABCD study reported caffeine use and frequency of disrupted sleep; parents reported youth ADHD symptoms. Cotwin control analyses predicted disrupted sleep from caffeine use, ADHD, and their interaction at ages 10 and 12. Results: Neither quasi-causal within-pair effects of caffeine use on disrupted sleep, nor a moderating role of ADHD were identified. Posthoc biometric models indicated that genetic and environmental influences on these phenotypes may change over time, such that genetic influences on disrupted sleep began to emerge more robustly around early adolescence. Additionally, caffeine use and disrupted sleep, but not ADHD, displayed overlapping genetic influences (12-13% of total phenotypic variance) at age 10. Conclusions: In a sample of preadolescent twin pairs from the ABCD Study, we did not observe evidence that caffeine use was quasi-causally associated with disrupted sleep at this early developmental stage. However, caffeine use and disrupted sleep emerged with shared etiologic influences. In sum, this study sets the stage for examining these dynamic patterns in future examinations of this critical and timely ABCD study sample, as genetic and environmental influences on behavior are known to change throughout development. [ABSTRACT FROM AUTHOR]

Abstract Background Emerging research suggests that attention-deficit/hyperactivity disorder (ADHD) increases the risk for cardiovascular (CVDs) and metabolic disorders (i.e., cardiometabolic disorders) in adulthood. Yet, available studies are scarce and have mainly been focused on individuals receiving clinical ADHD diagnoses. We aimed to investigate the prospective associations of ADHD symptoms in young and mid-adulthood with subsequent cardiometabolic disorders and the underlying mechanisms. Methods We studied 10,394 twins from the Swedish Twin Registry (STR), born between 1958 and 1985 without previous medical history of cardiometabolic disorders. They provided self-assessment of ADHD symptoms (score range 0–36) via a validated, DSM-IV-based scale in a web-based questionnaire/telephone interview within the Study of Twin Adults: Genes and Environment (STAGE), in 2005–2006 (aged 19–47 years), and were followed until the end of 2018 (33–59 years) to identify incident clinical diagnoses/medication prescriptions for cardiometabolic disorders acquired from Swedish national registers. We used Cox regression models to investigate the associations between ADHD symptoms score and cardiometabolic outcomes, with and without adjustment for relevant covariates, and a co-twin control design to study familial confounding. Results A one-unit increase in the level of ADHD symptoms was associated with a 2% increase in the rate of CVDs (hazard ratio [HR] = 1.02, 95% confidence interval 1.01–1.04) and a 3% increase in the rate of metabolic disorders (HR = 1.03, 1.02–1.05), after adjusting for birth year and sex. The associations were no longer significant after adjusting for educational attainment, lifestyle factors, and comorbid psychiatric disorders. The associations remained significant after adjusting for familial factors shared by dizygotic twin pairs but became nonsignificant after adjusting for factors shared by monozygotic twin pairs. However, the strength of the associations attenuated significantly in monozygotic twins compared to dizygotic twins for CVDs only, suggesting genetic confounding. Conclusions ADHD symptom score is associated with a higher risk for cardiometabolic disorders, which may be explained by lower educational attainment, adverse lifestyle factors, and psychiatric comorbidities. Moreover, the associations appear to be partly confounded by shared genetic factors, especially for CVDs. Further research is needed to investigate the identified associations at the level of individual cardiometabolic disorders and to follow-up participants until a more advanced older age.

BackgroundEpidemiological research on dementia is hampered by differences across studies in how dementia is classified, especially where clinical diagnoses of dementia may not be available.ObjectiveWe apply structural equation modeling to estimate dementia likelihood across heterogeneous samples within a multi-study consortium and use the twin design of the sample to validate the results.MethodsUsing 10 twin studies, we implement a latent variable approach that aligns different tests available in each study to assess cognitive, memory, and functional ability. The model separates general cognitive ability from components indicative of dementia. We examine the validity of this continuous latent dementia index (LDI). We then identify cut-off points along the LDI distributions in each study and align them across studies to distinguish individuals with and without probable dementia. Finally, we validate the LDI by determining its heritability and estimating genetic and environmental correlations between the LDI and clinically diagnosed dementia where available.ResultsResults indicate that coordinated estimation of LDI across 10 studies has validity against clinically diagnosed dementia. The LDI can be fit to heterogeneous sets of memory, other cognitive, and functional ability variables to extract a score reflective of likelihood of dementia that can be interpreted similarly across studies despite diverse study designs and sampling characteristics. Finally, the same genetic sources of variance strongly contribute to both the LDI and clinical diagnosis.ConclusionThis latent dementia indicator approach may serve as a model for other research consortia confronted with similar data integration challenges.

Abstract Background Cardiometabolic diseases (CMDs) including heart disease, stroke, and type 2 diabetes have been individually linked to depression. However, their combined impact on depression risk is unclear. We aimed to examine the association between cardiometabolic multimorbidity and depression and explore the role of genetic background in this association. Methods Within the Swedish Twin Registry, 40,080 depression-free individuals (mean age 60 years) were followed for 18 years. Cardiometabolic multimorbidity was defined as having ≥2 CMDs. CMDs and depression were ascertained based on the National Patient Register. Cox regression was used to estimate the CMD-depression association in a classical cohort study design and a matched co-twin design involving 176 twin pairs. By comparing the associations between monozygotic and dizygotic co-twins, the contribution of genetic background was estimated. Results At baseline, 4809 (12.0%) participants had one CMD and 969 (2.4%) had ≥2 CMDs. Over the follow-up period, 1361 participants developed depression. In the classical cohort design, the multi-adjusted hazard ratios (95% confidence interval [CIs]) of depression were 1.52 (1.31–1.76) for those with one CMD and 1.83 (1.29–2.58) for those with ≥2 CMDs. CMDs had a greater risk effect on depression if they developed in mid-life (

Background: Emerging research suggests that attention-deficit/hyperactivity disorder (ADHD) increases the risk for cardiovascular (CVDs) and metabolic disorders (i.e., cardiometabolic disorders) in adulthood. Yet, available studies are scarce and have mainly been focused on individuals receiving clinical ADHD diagnoses. We aimed to investigate the prospective associations of ADHD symptoms in young and mid-adulthood with subsequent cardiometabolic disorders and the underlying mechanisms. Methods: We studied 10,394 twins from the Swedish Twin Registry (STR), born between 1958 and 1985 without previous medical history of cardiometabolic disorders. They provided self-assessment of ADHD symptoms (score range 0–36) via a validated, DSM-IV-based scale in a web-based questionnaire/telephone interview within the Study of Twin Adults: Genes and Environment (STAGE), in 2005–2006 (aged 19–47 years), and were followed until the end of 2018 (33–59 years) to identify incident clinical diagnoses/medication prescriptions for cardiometabolic disorders acquired from Swedish national registers. We used Cox regression models to investigate the associations between ADHD symptoms score and cardiometabolic outcomes, with and without adjustment for relevant covariates, and a co-twin control design to study familial confounding. Results: A one-unit increase in the level of ADHD symptoms was associated with a 2% increase in the rate of CVDs (hazard ratio [HR] = 1.02, 95% confidence interval 1.01–1.04) and a 3% increase in the rate of metabolic disorders (HR = 1.03, 1.02–1.05), after adjusting for birth year and sex. The associations were no longer significant after adjusting for educational attainment, lifestyle factors, and comorbid psychiatric disorders. The associations remained significant after adjusting for familial factors shared by dizygotic twin pairs but became nonsignificant after adjusting for factors shared by monozygotic twin pairs. However, the strength of the associations attenuated significantly in monozygotic twins compared to dizygotic twins for CVDs only, suggesting genetic confounding. Conclusions: ADHD symptom score is associated with a higher risk for cardiometabolic disorders, which may be explained by lower educational attainment, adverse lifestyle factors, and psychiatric comorbidities. Moreover, the associations appear to be partly confounded by shared genetic factors, especially for CVDs. Further research is needed to investigate the identified associations at the level of individual cardiometabolic disorders and to follow-up participants until a more advanced older age. [ABSTRACT FROM AUTHOR]

Cognitive control has been strongly linked to midfrontal theta (4–8 Hz) brain activity. Such control processes are known to be impaired in individuals with psychiatric conditions and neurodevelopmental diagnoses, including attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). Temporal variability in theta, in particular, has been associated with ADHD, with shared genetic variance underlying the relationship. Here, we investigated the phenotypic and genetic relationships between theta phase variability, theta-related signals (the N2, error-related negativity, and error positivity), reaction time, and ADHD and ASD longitudinally in a large twin study of young adults to investigate the stability of the genetic relationships between these measures over time. Genetic multivariate liability threshold models were run on a longitudinal sample of 566 participants (283 twin pairs). Characteristics of ADHD and ASD were measured in childhood and young adulthood, while an electroencephalogram was recorded in young adulthood during an arrow flanker task. Cross-trial theta phase variability in adulthood showed large positive phenotypic and genetic relationships with reaction time variability and both childhood and adult ADHD characteristics. Error positivity amplitude was negatively related phenotypically and genetically to ADHD and ASD at both time points. We showed significant genetic associations between variability in theta signaling and ADHD. A novel finding from the current study is that these relationships were stable across time, indicating a core dysregulation of the temporal coordination of control processes in ADHD that persists in individuals with childhood symptoms. Error processing, indexed by the error positivity, was altered in both ADHD and ASD, with a strong genetic contribution. [ABSTRACT FROM AUTHOR]

Background: Little is currently known about epigenetic alterations associated with body composition in obesity. Thus, we aimed to explore epigenetic relationships between genome‐wide DNA methylation levels and three common traits of body composition as measured by body fat percentage (BF%), fat mass (FM) and lean body mass (LBM) among Chinese monozygotic twins. Methods: Generalized estimated equation model was used to regress the methylation level of CpG sites on body composition. Inference about Causation Through Examination Of Familial Confounding was used to explore the evidence of a causal relationship. Gene expression analysis was further performed to validate the results of differentially methylated genes. Results: We identified 32, 22 and 28 differentially methylated CpG sites (p < 10−5) as well as 20, 17 and eight differentially methylated regions (slk‐corrected p < 0.05) significantly associated with BF%, FM and LBM which were annotated to 65 genes, showing partially overlapping. Causal inference demonstrated bidirectional causality between DNA methylation and body composition (p < 0.05). Gene expression analysis revealed significant correlations between expression levels of five differentially methylated genes and body composition (p < 0.05). Conclusions: These DNA methylation signatures will contribute to increased knowledge about the epigenetic basis of body composition and provide new strategies for early prevention and treatment of obesity and its related diseases. [ABSTRACT FROM AUTHOR]

Background: Attention‐deficit/hyperactivity disorder (ADHD) is an increasingly commonly diagnosed neurodevelopmental condition. One possibility is that this reflects a genuine increase in the prevalence of ADHD due to secular environmental changes, yet this hypothesis remains untested. We therefore investigated whether the genetic and environmental variance underlying ADHD, and traits of ADHD, has changed over time. Methods: We identified twins born from 1982 to 2008 from the Swedish Twin Registry (STR). We linked the STR with the Swedish National Patient Register and Prescribed Drug Register to identify diagnoses of ADHD and prescriptions of ADHD medication for these twins. We also utilized data collected from participants in the Child and Adolescent Twin Study in Sweden (CATSS), born from 1992 to 2008. Their parents completed a structured ADHD screening tool, which was used to measure traits of ADHD and assign broad screening diagnoses of ADHD. We used the classical twin design to test whether the degree to which variation in these measures was influenced by genetic and environmental variation changed over time. Results: We included 22,678 twin pairs from the STR and 15,036 pairs from CATSS. The heritability of ADHD in the STR ranged from 66% to 86% over time, although these fluctuations were not statistically significant. We observed a modest increase in variance in ADHD traits, from 0.98 to 1.09. This was driven by small increases in the underlying genetic and environmental variance, with heritability estimated as 64%–65%. No statistically significant changes in variance in screening diagnoses were observed. Conclusions: The relative contribution of genetic and environmental factors to ADHD has remained stable over time, despite its increasing prevalence. Thus, changes in the underlying etiology of ADHD over time are unlikely to explain the increase in ADHD diagnoses. [ABSTRACT FROM AUTHOR]

Understanding the biological basis of cognitive differences between individuals is the goal in human intelligence research. The surface area of the cortex is considered to be a key determinant of human intelligence. Adolescence is a period of development characterized by physiological, emotional, behavioral, and psychosocial changes, which is related to the recombination and optimization of the cerebral cortex, and cognitive ability changes significantly in children and adolescents. This study examined the effects of common genetic and environmental factors between the surface area of the cerebral cortex and intelligence in typical developing adolescents (twins, n = 114, age 12–18 years old). Cortical surface area data were parsed into subregions (i.e., frontal, parietal, occipital, and temporal areas) and intelligence into verbal and nonverbal skills. We found a phenotypic correlation between regional surface areas and verbal intelligence. No correlation was observed between regional surface areas and nonverbal intelligence, except for the occipital lobe and the right hemisphere. In the bivariate twin analyses, the differences in phenotypic correlation between regional surface areas and verbal intelligence were not due to unshared environmental effects or measurement error, but to genetic effects. In summary, the current study has broadened the previous genetic investigations of cognitive ability and cortical surface area. [ABSTRACT FROM AUTHOR]

Background: Many studies aggregate prescription opioid misuse (POM) and heroin use into a single phenotype, but emerging evidence suggests that their genetic and environmental influences may be partially distinct. Methods: In total, 7164 individual twins (84.12% complete pairs; 59.81% female; mean age = 30.58 years) from the Australian Twin Registry reported their lifetime misuse of prescription opioids, stimulants, and sedatives, and lifetime use of heroin, cannabis, cocaine/crack, illicit stimulants, hallucinogens, inhalants, solvents, and dissociatives via telephone interview. Independent pathway models (IPMs) and common pathway models (CPMs) partitioned the variance of drug use phenotypes into general and drug-specific genetic (a), common environmental (c), and unique environmental factors (e). Results: An IPM with one general a and one general e factor and a one-factor CPM provided comparable fit to the data. General factors accounted for 55% (a = 14%, e = 41%) and 79% (a = 64%, e = 15%) of the respective variation in POM and heroin use in the IPM, and 25% (a = 12%, c = 8%, e = 5%) and 80% (a = 38%, c = 27%, e = 15%) of the respective variation in POM and heroin use in the CPM. Across both models, POM emerged with substantial drug-specific genetic influence (26–39% of total phenotypic variance; 69–74% of genetic variance); heroin use did not (0% of total phenotypic variance; 0% of genetic variance in both models). Prescription sedative misuse also demonstrated significant drug-specific genetic variance. Conclusions: Genetic variation in POM, but not heroin use, is predominantly drug-specific. Misuse of prescription medications that reduce experiences of subjective distress may be partially influenced by sources of genetic variation separate from illicit drug use. [ABSTRACT FROM AUTHOR]

Objective: Eating disorders are associated with subsequent alcohol problems, but it is not known whether this association also extends to broader eating disorder symptoms not captured by clinical diagnoses. We assessed the longitudinal association of broad eating disorder symptoms with alcohol problems in a nationwide twin sample (FinnTwin16). Methods: Finnish women (N = 1905) and men (N = 1449) self‐reported their eating disorder symptoms using the Eating Disorder Inventory‐2 Bulimia, Drive for Thinness, and Body Dissatisfaction subscales at the mean age of 24.4 years in 2000–2003. A subsample of participants also completed items on drive for muscularity, height dissatisfaction, and muscle‐enhancing supplement use. Alcohol problems were assessed 10 years later at the age of 34.1 in 2010–2012 with the Rutgers Alcohol Problem Index. Results: Eating disorder symptoms were associated with later alcohol problems (odds ratio per point increase 1.02–1.18). Bulimia showed stronger associations among men than women (p for interaction.012). Drive for muscularity and height dissatisfaction were also associated with later alcohol problems, but supplement use was not. When accounting for baseline alcohol problems, only Bulimia (among women and men) and Drive for Thinness (among men) were significantly associated with later alcohol problems. Bulimia was also significantly associated with later alcohol problems in within‐twin‐pair analyses among dizygotic twins, but not among monozygotic twins. Discussion: In a longitudinal setting, eating disorder symptoms were associated with later alcohol problems. Bulimic symptoms were a stronger risk factor for men than women. These associations may be attributable to baseline alcohol problems, childhood environment and genetic liability. Public significance: This study found that both young adult women and men with broad eating disorder symptoms are at a higher risk of alcohol‐related problems than those without such symptoms. Men with bulimic symptoms were at a particularly high risk. These findings emphasize the need for better prevention and treatment of disordered eating, body image concerns and alcohol problems for both young adult women and men. [ABSTRACT FROM AUTHOR]

Background: Rapid weight gain during infancy is a strong predictor of childhood obesity and is affected by genetic and environmental factors. Identifying ages with low heritability will allow for targeted interventions that might be able to prevent the adverse effects of childhood obesity. Objectives: The objective of the study is to estimate the heritability of weight gain from birth to defined ages during infancy, as well as during 6‐month periods from birth to 18 months of age. We address this by leveraging large‐scale computerised anthropometric data from the state‐run network of well‐baby clinics in Israel. Methods: We performed a population‐based twin study. We extracted weight measurements recorded between birth to 24 months from well‐baby clinics for 9388 twin pairs born in Israel between 2011 and 2015. The reported sexes of the twins were used as a proxy for their zygosity status. We estimated the heritability of the weight z‐score change from birth to specific ages and during particular periods in infancy. To assess the validity of the results, we repeated the analysis in a sub‐cohort of twin pairs with complete weight measurements. Results: During the first 2 years of life, heritability was lowest for birthweight (h2=0.40±0.11). Heritability for weight gain since birth was highest at 4 months (h2=0.87±0.13), and then gradually decreased until age 18 months (h2=0.62±0.13). Estimating the heritability in 6‐month intervals from birth to 18 months, heritability was highest during the 6–12‐month interval (h2=0.84±0.14), and was substantially lower during the subsequent 12–18‐month interval (h2=0.43±0.16). Conclusions: Heritability of weight gain decreases substantially in the second year of life, suggesting that this period could be an appropriate time for interventions for infants who are at an increased risk of childhood obesity. [ABSTRACT FROM AUTHOR]