A twin study of genetic and environmental influences on psychological traits of eating disorders in a Japanese female sample.

The purpose of the present study was to clarify genetic and environmental origins of psychological traits of eating disorders using a Japanese female twin sample. Participants were 162 pairs of female twins consisting of 116 pairs of monozygotic (MZ) twins and 46 pairs of dizygotic (DZ) twins in their adolescence. Psychological traits of eating disorders were assessed with five subscales of the Eating Disorder Inventory (EDI). As a result of using univariate twin analyses, among five subscales of EDI (maturity fears, ineffectiveness, interpersonal distrust, interoceptive awareness, and perfectionism), perfectionism showed significant additive genetic contributions and individual specific environmental effects. On the other hand, maturity fears, ineffectiveness, interoceptive awareness, and interpersonal distrust indicated significant shared environment contributions and individual specific environment effects. The results suggest the importance of both genetic and shared environmental influences on psychological traits of eating disorders in the present study.     

Peer reports of adaptive behavior in twins and singletons: is twinship a risk or an advantage?

We compared twins to their gender-matched singleton classmates in peer-assessed behavioral adjustment. Our samples include 1874 11- to 12-year-old Finnish twins (687 monozygotic, MZ; 610 same-sex dizygotic, SSDZ; 577 opposite-sex dizygotic, OSDZ) and their 23,200 non-twin classmates. Data were collected using a 30-item Multidimensional Peer Nomination Inventory containing three factors and their subscales. We found twin-singleton differences: classmates rated twin girls and boys higher than gender-matched singletons in Adaptive Behaviors (constructive, compliant, and socially active behavior), and those effects were particularly evident among OSDZ twins for assessments of social interaction, popularity, and leadership. We found no evidence that individual twins differ from singletons in Externalizing (hyperactivity-impulsivity, inattention, aggression) or Internalizing Problem Behaviors (depressive symptoms, social anxiety). Nor did we find systematic differences between MZ and SSDZ twins. Among both twins and singletons, boys exceeded girls in Externalizing, and girls exceeded boys in Internalizing Problem Behaviors. Results suggest that a twinship forms a positive developmental environment for socioemotional behavior, particularly among OSDZ twins.     

Investigating the genetic and environmental structure of Cloninger's personality dimensions in adolescence.

In this study we examined the genetic and environmental structure of four dimensions from Cloninger's personality system: novelty-seeking (NS), harm-avoidance (HA), reward-dependence (RD), and persistence (PS). Although adult twin studies suggest that these personality dimensions are moderately heritable, this is the first twin study of Cloninger's personality dimensions in adolescence--a period marked by significant physiological and social changes. Study participants included 1851 adolescent twins between the ages of 11 and 18 years; 878 complete twin pairs and 95 singleton-responding twins. Subjects were participants in two community-based samples of twins residing in the state of Colorado. Results indicated that cross-sectional mean levels for NS, HA and RD tended to show modest increases across the adolescent years, while PS showed modest mean decreases. Consistent sex differences in means were found only for RD. Univariate biometrical twin models were used to decompose trait variance into genetic and environmental sources. Results indicated that for NS, HA and RD additive genetic influences and unique environmental effects were sufficient to explain the data. PS, however, could be explained by unique and common environmental effects only, with different patterns of common environmental effects for males and females. We found moderate heritability estimates for NS, HA and RD ranging from .28 to .36--with no evidence for sex-limitation in those influences.     

Individual differences in multiple dimensions of aggression: a univariate and multivariate genetic analysis.

Previous behaviour genetic studies of aggression have yielded inconsistent results: reported heritabilities for different types of aggressive behaviour ranging from 0 to 0.98. In the present study, 247 adult twin pairs (183 MZ pairs; 64 same-sex DZ pairs) were administered seven self-report questionnaires which yielded 18 measures of aggression. Univariate genetic analyses showed moderate to high heritabilities for 14 of these 18 measures and for a general aggression factor and three correlated aggression factors extracted from the measures. Multivariate genetic analyses showed sizeable genetic correlations between the different dimensions of aggression. Thus, individual differences in many types of aggressive behaviour are attributable to some extent to genetic factors and there is considerable overlap between the genes that operate on different types of aggressive behaviour.     

Exploring the etiology of the association between birthweight and IQ in an adolescent twin sample.

The negative effects of very low birthweight on intellectual development have been well documented, and more recently this effect has been shown to generalize to birthweights within the normal range. In this study we investigate the etiology of this relationship by using a classical twin design to disentangle the contributions of genes and environment. A previous Dutch study (Boomsma et al., 2001) examining these effects indicated that genes were important in mediating the association of birthweight to full IQ measured at ages 7 and 10, but not at ages 5 and 12. Here the association between birthweight and IQ at age 16 is considered (N = 523 twin pairs). Using variance components modeling we found that the genetic variance in birthweight (4%) completely overlapped with that in verbal IQ but not performance or full IQ. Results further showed the importance of shared environmental effects on birthweight (~ 60%) but not on IQ (with genes explaining up to 72% of IQ variance). Models incorporating a direction of causation parameter between birthweight and IQ provided adequate fit to the data in either causal direction for performance and full IQ, but the model with verbal IQ causing birthweight was preferred to one in which birthweight influenced verbal IQ. As the measurement of birthweight precedes the measurement of twins' IQ at age 16, the influence of verbal IQ might be better considered as a proxy for parents' IQ or education, and it is possible that brighter mothers provide better prenatal environments for their children.     

Genetic and Environmental Contributions to BMI in Adolescent and Young Adult Women

The objective of this study was to determine the genetic and environmental contributions to variation in BMI over time in European‐American (EA) and African‐American (AA) adolescent and young adult women. Self‐reported BMI (kg/m²) data from 2,816 EA (1,306 twin pairs, 56.5% monozygotic (MZ)) and 404 AA (178 twin pairs, 42.7% MZ) women at baseline (T1; median age 15 years) and 3,225 EA (1,511 twin pairs, 55.3% MZ) and 539 AA (252 pairs, 43.3% MZ) women at follow‐up (T2; median age 22 years) from a Midwestern US, population‐based twin registry were used to construct biometrical genetic models. For EA women, the majority of the variance in BMI was attributable to additive genetic effects at both time points (82% for each), with the remaining variance attributable to nonshared environment. Genetic and nonshared environment correlations between adolescent and young adult BMI were 0.87 and 0.23, respectively. Among AA women, nonadditive genetic effects comprised 68% of the variance at T1 and 73% at T2, and were highly correlated (r_D = 0.94). The proportions of variance attributable to nonshared environment at T1 (29%) and T2 (25%) were more modestly correlated (r_E = 0.31). The remaining variance in AA women could be attributed to additive genetic effects. Additive vs. nonadditive genetic effects contribute differentially to BMI in AA vs. EA adolescent and young adult women. Additional research is needed to better characterize the environmental and genetic factors related to BMI in persons of different races to aid understanding of the complex determinants of body weight in individuals.     

Childhood obesity: genetic and environmental overlap with normal-range BMI

Objective: To understand the overlap between the etiology of obesity and normal variation in BMI in children. Methods and Procedures: Height and weight data were available from a large UK representative sample of twins: 2,342 same‐sex pairs at 7 years and 3,526 same‐sex pairs at 10 years. The twin method and model‐fitting techniques were used to estimate genetic and environmental contributions to BMI. DeFries‐Fulker (DF) extremes analysis was used to investigate genetic and environmental influences on the mean difference between obese and normal‐weight children. Obesity was classified using the International Obesity Task Force (IOTF) criteria. Results: At both ages, BMI and obesity were highly heritable (0.60–0.74) and only modestly influenced by shared environmental factors (0.12–0.22). Extremes analyses indicated that genetic and environmental influences on obesity are quantitatively and qualitatively similar to those operating across the range of BMI. Discussion: Obesity is the extreme of the same genetic and environmental factors responsible for variation throughout the distribution of BMI. This finding implies that genes that influence obesity will also be associated with BMI in the normal range, and similar environmental influences will affect BMI in the clinical and normal range. Knowing that obesity is influenced by the same genetic and environmental factors that affect weight at all levels has implications for investigating the mechanisms for weight gain and developing interventions for weight control.     

Investigating the genetic and environmental architecture of interpack aggression in North American grey wolves

Aggression confers several fitness benefits including increased breeding opportunities and resource acquisition. Determining the relative contributions of genetic and environmental components to shaping aggression is essential for advancing our understanding of how selection affects the distribution of aggressive phenotypes in a population. In a From the Cover article in this issue of Molecular Ecology, vonHoldt et al. (2020) used RAD‐seq methods to obtain genome‐wide single nucleotide polymorphism (SNP) data to estimate heritability of interpack aggression of 141 North American grey wolves (Canis lupus) surveyed from 1995–2018. The authors inferred heritability using both a SNP‐based genetic relationship matrix (GRM) and a consensus pedigree informed by: (a) previously obtained microsatellite data; (b) past observations of parentage; and (c) statistical reconstruction of parent‐offspring pairs. SNP‐based (i.e., GRM) and pedigree‐based (i.e., consensus pedigree) heritability estimates were 37% and 14%, respectively, with an additional 14%–16% explained by natal pack effects. The study confirmed the previously discovered strong effects of relative pack size and breeding status on interpack aggression, illustrating how social dynamics and density‐dependent factors induce variance in aggressive behaviours. Finally, the authors found associations between average individual aggression scores (IAS) and specific candidate genes (MY09A and TRAK1). In sum, vonHoldt et al. (2020) provides an unprecedented and nuanced synthesis that not only suggests gene‐aggression associations, but also emphasizes how additive genetic variance and density‐dependent factors interact to maintain phenotypic variance in aggression over time.     

On the application of queuing theory for analysis of twin data.

A mathematical model based on queuing theory is used to study the dynamics of environmental influence on twin pairs. The model takes into consideration genetic factors and effects of nonshared environment. Histograms are exploited as base analysed characteristics, with the method of minimum chi-square yielding estimated characteristics. The proposed technique was applied to analysis of longitudinal data for MZ and DZ twins. It was shown that the same environment impact may yield different contributions to final variances of the IQ parameters under investigation. Magnitudes of these contributions depend on the genetic factor represented by distributions of an analysed parameter at the point of birth.     

Aetiology of teenage childbearing: reasons for familial effects.

The aims of the present study were to evaluate the contribution of the genetic and environmental factors to the risk of teenage childbearing, and to study whether life style, socio-economic conditions, and personality traits could explain possible familial effects. We linked two population-based registers: the Swedish Twin Register and the Swedish Medical Birth Register. The study covers female twin pairs born between 1953 and 1958, having their first infant before the age of 30 years (n = 1885). In order to separate familial effects from other environmental influences, and genetic effects from shared environmental effects, only complete twin pairs with known zygosity were included, in all 260 monozygotic and 370 dizygotic twin pairs. We used quantitative genetic analyses to evaluate the importance of genetic and environmental effects for liability to teenage childbearing. Logistic regression analyses were used to estimate the effects of life style, socio-economic situation, and personality on the probability of teenage childbearing, and to study whether psychosocial factors could explain possible familial effects. Fifty-nine percent (0-76%) of the variance in being a teenage mother was attributable to heritable factors; 0% (0-49%) was due to shared environmental factors; and 41% (23-67%) was explained by non-shared environmental factors. Thus, the data were consistent with the hypothesis that the familial aggregation of teenage childbearing is completely explained by genetic factors, although the alternative hypothesis that familial aggregation is entirely explained by shared environmental factors cannot be ruled out. Significant effects of smoking habits, housing conditions, and educational level were found in relation to liability to teenage childbearing. However, the familial effects on risk of teenage childbearing were not mediated through similarities in life style and socio-economic factors. When studying risk factors for teenage childbearing, it is recommended to include life style and socio-economic variables as well as information about family history of teenage childbearing. Twin Research (2000) 3, 23-27.     

Genetic and environmental correlations among serum lipids and apolipoproteins in elderly twins reared together and apart.

Genetic and environmental correlations among five serum-lipid measures were examined in the Swedish Adoption/Twin Study of Aging. The sample included 302 twin pairs; 146 of these twin pairs were separated at an early age and were reared apart. The lipid measures examined include total cholesterol, HDL-cholesterol, triglycerides, and apolipoproteins A-I and B. Genetic and environmental correlations were evaluated for two different age groups, formed by dividing the sample at the median. The younger group included individuals 41.8-65.4 years of age at the midpoint of testing, although only 24 individuals were < 50 years of age. The older group included all those > 65.4 years of age, up to age 87 years of age. Substantial genetic correlations were found within each age group, although there is no evidence for a single genetic factor common to all five lipids. The comparison of twins reared together with twins reared apart allowed estimation of the effects of shared rearing environment; however, shared rearing environment only appears to be a significant mediator of the phenotypic correlation between apolipoprotein B and cholesterol in the older group. Examination of the genetic and environmental covariances suggests that the relative contributions of genetic factors are lower in the older group. Nonshared environmental factors are relatively more important mediators of phenotypic correlations among the serum lipids in individuals > 65.4 years of age than they are for the younger group. Sex differences in the mediation of these serum lipids were not as clear.     

A rapid generalized least squares model for a genome-wide quantitative trait association analysis in families

Genome-wide association studies (GWAS) using family data involve association analyses between hundreds of thousands of markers and a trait for a large number of related individuals. The correlations among relatives bring statistical and computational challenges when performing these large-scale association analyses. Recently, several rapid methods accounting for both within- and between-family variation have been proposed. However, these techniques mostly model the phenotypic similarities in terms of genetic relatedness. The familial resemblances in many family-based studies such as twin studies are not only due to the genetic relatedness, but also derive from shared environmental effects and assortative mating. In this paper, we propose 2 generalized least squares (GLS) models for rapid association analysis of family-based GWAS, which accommodate both genetic and environmental contributions to familial resemblance. In our first model, we estimated the joint genetic and environmental variations. In our second model, we estimated the genetic and environmental components separately. Through simulation studies, we demonstrated that our proposed approaches are more powerful and computationally efficient than a number of existing methods are. We show that estimating the residual variance-covariance matrix in the GLS models without SNP effects does not lead to an appreciable bias in the p values as long as the SNP effect is small (i.e. accounting for no more than 1% of trait variance).     

INTERACTING PHENOTYPES AND THE EVOLUTIONARY PROCESS: I. DIRECT AND INDIRECT GENETIC EFFECTS OF SOCIAL INTERACTIONS

Interacting phenotypes are traits whose expression is affected by interactions with conspecifics. Commonly-studied interacting phenotypes include aggression, courtship, and communication. More extreme examples of interacting phenotypes—traits that exist exclusively as a product of interactions—include social dominance, intraspecific competitive ability, and mating systems. We adopt a quantitative genetic approach to assess genetic influences on interacting phenotypes. We partition genetic and environmental effects so that traits in conspecifics that influence the expression of interacting phenotypes are a component of the environment. When the trait having the effect is heritable, the environmental influence arising from the interaction has a genetic basis and can be incorporated as an indirect genetic effect. However, because it has a genetic basis, this environmental component can evolve. Therefore, to consider the evolution of interacting phenotypes we simultaneously consider changes in the direct genetic contributions to a trait (as a standard quantitative genetic approach would evaluate) as well as changes in the environmental (indirect genetic) contribution to the phenotype. We then explore the ramifications of this model of inheritance on the evolution of interacting phenotypes. The relative rate of evolution in interacting phenotypes can be quite different from that predicted by a standard quantitative genetic analysis. Phenotypic evolution is greatly enhanced or inhibited depending on the nature of the direct and indirect genetic effects. Further, unlike most models of phenotypic evolution, a lack of variation in direct genetic effects does not preclude evolution if there is genetic variance in the indirect genetic contributions. The available empirical evidence regarding the evolution of behavior expressed in interactions, although limited, supports the predictions of our model.     

Contributions of Dopamine-Related Genes and Environmental Factors to Highly Sensitive Personality: A Multi-Step Neuronal System-Level Approach

Traditional behavioral genetic studies (e.g., twin, adoption studies) have shown that human personality has moderate to high heritability, but recent molecular behavioral genetic studies have failed to identify quantitative trait loci (QTL) with consistent effects. The current study adopted a multi-step approach (ANOVA followed by multiple regression and permutation) to assess the cumulative effects of multiple QTLs. Using a system-level (dopamine system) genetic approach, we investigated a personality trait deeply rooted in the nervous system (the Highly Sensitive Personality, HSP). 480 healthy Chinese college students were given the HSP scale and genotyped for 98 representative polymorphisms in all major dopamine neurotransmitter genes. In addition, two environment factors (stressful life events and parental warmth) that have been implicated for their contributions to personality development were included to investigate their relative contributions as compared to genetic factors. In Step 1, using ANOVA, we identified 10 polymorphisms that made statistically significant contributions to HSP. In Step 2, these polymorphism''s main effects and interactions were assessed using multiple regression. This model accounted for 15% of the variance of HSP (p<0.001). Recent stressful life events accounted for an additional 2% of the variance. Finally, permutation analyses ascertained the probability of obtaining these findings by chance to be very low, p ranging from 0.001 to 0.006. Dividing these loci by the subsystems of dopamine synthesis, degradation/transport, receptor and modulation, we found that the modulation and receptor subsystems made the most significant contribution to HSP. The results of this study demonstrate the utility of a multi-step neuronal system-level approach in assessing genetic contributions to individual differences in human behavior. It can potentially bridge the gap between the high heritability estimates based on traditional behavioral genetics and the lack of reproducible genetic effects observed currently from molecular genetic studies.     

People’s desire to be in nature and how they experience it are partially heritable

Nature experiences have been linked to mental and physical health. Despite the importance of understanding what determines individual variation in nature experience, the role of genes has been overlooked. Here, using a twin design (TwinsUK, number of individuals = 2,306), we investigate the genetic and environmental contributions to a person’s nature orientation, opportunity (living in less urbanized areas), and different dimensions of nature experience (frequency and duration of public nature space visits and frequency and duration of garden visits). We estimate moderate heritability of nature orientation (46%) and nature experiences (48% for frequency of public nature space visits, 34% for frequency of garden visits, and 38% for duration of garden visits) and show their genetic components partially overlap. We also find that the environmental influences on nature experiences are moderated by the level of urbanization of the home district. Our study demonstrates genetic contributions to individuals’ nature experiences, opening a new dimension for the study of human–nature interactions.

Nature experiences have been linked to mental and physical health. This twin study reveals genetic influences on an individual’s orientation towards nature and nature experiences, opening a new dimension to understanding human-nature interactions.     

Genetic and Environmental Contributions to Phenotypic Components of Metabolic Syndrome: A Population‐based Twin Study

The increasing prevalence of metabolic syndrome (MS) poses a serious public‐health problem worldwide. Effective prevention and intervention require improved understanding of the factors that contribute to MS. We analyzed data on a large twin cohort to estimate genetic and environmental contributions to MS and to major MS components and their intercorrelations: waist circumference (WC), systolic (SBP) and diastolic blood pressure (DBP), fasting plasma glucose (FPG), triglycerides (TGs), and high‐density lipoprotein–cholesterol (HDL‐C). We applied structural equation modeling to determine genetic and environmental structure of MS and its major components, using 1,617 adult female twin pairs recruited from rural China. The heritability estimate for MS was 0.42 (95% confidence interval (CI): 0.00–0.83) in this sample with low MS prevalence (4.4%). For MS components, heritability estimates were statistically significant and ranged from 0.13 to 0.64 highest for WC, followed by TG, SBP, DBP, HDL‐C, and FPG. HDL‐C was mainly influenced by common environmental factors (0.62, 95% CI: 0.58–0.62), whereas the other five MS components were largely influenced by unique environmental factors (0.32–0.44). Bivariate Cholesky decomposition analysis indicated that the clinical clustering of MS components may be explained by shared genetic and/or environmental factors. Our study underscores the importance of examining MS components as intercorrelated traits, and to carefully consider environmental and genetic factors in studying MS etiology.     

Genetic and environmental influences on a measure of infant attachment security.

A twin study of infant attachment security at age 24 months was conducted on archival data for a sample of 99 MZ pairs and 108 DZ pairs from the Louisville Twin Study. MZ concordance for attachment was 62.6%, which was significantly greater than the DZ concordance of 44.4%. Concordances were transformed into polychoric correlations, and LISREL was used to conduct a quantitative genetic analysis of the data. Results indicated that 25% of the variability in attachment was attributable to genetic factors, and the remaining 75% was attributable to non-shared environmental effects. No evidence was found for a contribution from shared environmental influences to attachment security. Possible concerns about the validity of twin methodology are addressed and various interpretations of the results are presented.     

A twin study of genetic influences on epilepsy outcome.

The identification of genetic factors that confer susceptibility to the epilepsies has to date been the focus of genetic efforts in this field. Few studies have assessed the genetic contribution to disease course in epilepsy, yet an understanding of the genetic influences on epilepsy outcome is key to developing new therapeutic strategies. The aim of this study was to assess the genetic contributions to epilepsy outcome in twin pairs concordant for epilepsy. We studied 37 epilepsy concordant twin pairs (27 monozygotic, 10 dizygotic) in whom there were no recognized environmental contributions (e.g., acquired brain injury) to epilepsy, and in whom the most likely cause for epilepsy was a shared genetic susceptibility. Clinical outcome was determined using the binary measure of Seizure Status (seizure remission or recurrence) and on a six-category ordinal Outcome Scale. Epilepsy outcome was independent of age of seizure onset, age at assessment and major epilepsy syndrome diagnosis. The proportion of twin pairs concordant for Seizure Status was 0.81 (22/27) for monozygous and 1.0 (10/10) for dizygous pairs, p = 0.3. Within-pair correlation in outcome (Outcome Scale) was 0.60 (95% CI: 0.32, 0.78) in monozygous and 0.78 (0.48, 0.92) in dizygous pairs. These data provide no evidence for genetic influences on epilepsy outcome independent of those that contribute to disease susceptibility. The observed high correlations for outcome suggest that, for epilepsy, susceptibility genes also have a major influence on outcome.     

Heritability of eleven metabolic phenotypes in Danish and Chinese twins: A cross‐population comparison

Objectives : A twin‐based comparative study on the genetic influences in metabolic endophenotypes in two populations of substantial ethnic, environmental, and cultural differences was performed. Design and Methods : Data on 11 metabolic phenotypes including anthropometric measures, blood glucose, and lipids levels as well as blood pressure were available from 756 pairs of Danish twins (309 monozygotic and 447 dizygotic twin pairs) with a mean age of 38 years (range: 18‐67) and from 325 pairs of Chinese twins (183 monozygotic and 142 dizygotic twin pairs) with a mean age of 40.5 years (range: 18‐69). Twin modeling was performed on full and nested models with the best fitting models selected. Results : Heritability estimates were compared between Danish and Chinese samples to identify differential genetic influences on each of the phenotypes. Except for hip circumference, all other body measures exhibited similar heritability patterns in the two samples with body weight showing only a slight difference. Higher genetic influences were estimated for fasting blood glucose level in Chinese twins, whereas the Danish twins showed more genetic regulation over most lipids phenotypes. Systolic blood pressure was more genetically controlled in Danish than in Chinese twins. Conclusions : Metabolic endophenotypes show disparity in their genetic determinants in populations under distinct environmental conditions.