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Background: A critical issue in devising effective interventions for the treatment of children's behavioral and emotional problems identifying genuine family environmental factors that place children at risk. In most twin and family studies, environmental factors are confounded with both direct genetic risk from parents and the indirect effect of genes influencing parents' ability to provide an optimal rearing environment. The present study was undertaken to determine whether parental psychopathology, specifically parental antisocial behavior (ASP), is a genuine environmental risk factor for juvenile conduct disturbance, depression and hyperactivity, or whether the association between parental ASP and children's behavioral and emotional problems can be explained as a secondary consequence of the intergenerational transmission of genetic factors. Methods: An extended children of twins design comprised of data collected on 2,674 adult female and male twins, their spouses, and 2,454 of their children was used to test whether genetic and/or family environmental factors best accounted for the association between parental antisocial behavior and children's behavioral problems. An age-matched sample of 2,826 juvenile twin pairs from the Virginia Twin Study of Adolescent Behavioral Development was also included to examine developmental differences in gene expression by partitioning child-specific transmissible effects from those effects that persist into adulthood. The fit of alternative models was evaluated using the statistical program Mx. Results: We found distinct patterns of transmission between parental antisocial behavior and juvenile conduct, depression and hyperactivity. Genetic and family environmental factors accounted for the resemblance between parents' ASP and children's conduct disturbance. Family environmental factors alone explained the association between child depression and parental ASP, and the impact of parental ASP on hyperactivity was entirely genetic. Conclusions: These findings underscore differences in the contribution of genetic and environmental factors on the patterns of association between parental antisocial behavior and juvenile psychopathology, having important clinical implications for the prevention and amelioration of child behavioral and emotional problems.

Background: Despite the increased risk of depression and conduct problems in children of depressed parents, the mechanism by which parental depression affects their children's behavioral and emotional functioning is not well understood. The present study was undertaken to determine whether parental depression represents a genuine environmental risk factor in children's psychopathology, or whether children's depression/conduct can be explained as a secondary consequence of the genetic liability transmitted from parents to their offspring. Methods: Children of Twins (COT) data collected on 2,674 adult female and male twins, their spouses, and 2,940 of their children were used to address whether genetic and/or family environmental factors best account for the association between depression in parents and depression and conduct problems in their children. Data collected on juvenile twins from the Virginia Twin Study of Adolescent Behavioral Development (VTSABD) were also included to estimate child-specific genetic and environmental influences apart from those effects arising from the transmission of the parental depression itself. The fit of alternative Children of Twin models were evaluated using the statistical program "Mx." Results: The most compelling model for the association between parental and juvenile depression was a model of direct environmental risk. Both family environmental and genetic factors accounted for the association between parental depression and child conduct disturbance. Conclusions: These findings illustrate how a genetically mediated behavior such as parental depression can have both an environmental and genetic impact on children's behavior. We find developmentally specific genetic factors underlying risk to juvenile and adult depression. A shared genetic liability influences both parental depression and juvenile conduct disturbance, implicating child conduct disturbance (CD) as an early indicator of genetic risk for depression in adulthood. In summary, our analyses demonstrate differences in the impact of parental depression on different forms of child psychopathology, and at various stages of development.

Background: A critical issue in devising effective interventions for the treatment of children's behavioral and emotional problems identifying genuine family environmental factors that place children at risk. In most twin and family studies, environmental factors are confounded with both direct genetic risk from parents and the indirect effect of genes influencing parents' ability to provide an optimal rearing environment. The present study was undertaken to determine whether parental psychopathology, specifically parental antisocial behavior (ASP), is a genuine environmental risk factor for juvenile conduct disturbance, depression and hyperactivity, or whether the association between parental ASP and children's behavioral and emotional problems can be explained as a secondary consequence of the intergenerational transmission of genetic factors. Methods: An extended children of twins design comprised of data collected on 2,674 adult female and male twins, their spouses, and 2,454 of their children was used to test whether genetic and/or family environmental factors best accounted for the association between parental antisocial behavior and children's behavioral problems. An age-matched sample of 2,826 juvenile twin pairs from the Virginia Twin Study of Adolescent Behavioral Development was also included to examine developmental differences in gene expression by partitioning child-specific transmissible effects from those effects that persist into adulthood. The fit of alternative models was evaluated using the statistical program Mx. Results: We found distinct patterns of transmission between parental antisocial behavior and juvenile conduct, depression and hyperactivity. Genetic and family environmental factors accounted for the resemblance between parents' ASP and children's conduct disturbance. Family environmental factors alone explained the association between child depression and parental ASP, and the impact of parental ASP on hyperactivity was entirely genetic. Conclusions: These findings underscore differences in the contribution of genetic and environmental factors on the patterns of association between parental antisocial behavior and juvenile psychopathology, having important clinical implications for the prevention and amelioration of child behavioral and emotional problems. [ABSTRACT FROM AUTHOR]

In this article, we explore the effect of public policy on the extent to which genes influence smoking desistance. Using a sample of adult twins (n(mz) = 363, n(dz) = 233) from a large population registry, we estimate Cox proportional hazards models that describe similarity in the timing of smoking desistance among adult twin pairs. We show that identical twin pairs are significantly more likely to quit smoking within a similar time frame compared with fraternal twin pairs. Importantly, we then show that genetic factors for smoking desistance increase in importance following restrictive legislation on smoking behaviors that occurred in the early and mid-1970s. These findings support the social push perspective and make important contributions to the social demography and genetic epidemiology of smoking as well as to the gene-environment interaction literatures. [ABSTRACT FROM AUTHOR]

The extended twin kinship design allows the simultaneous testing of additive and nonadditive genetic, shared and individual-specific environmental factors, as well as sex differences in the expression of genes and environment in the presence of assortative mating and combined genetic and cultural transmission (Eaves et al., 1999). It also handles the contribution of these sources of variance to the (co)variation of multiple phenotypes. Keller et al. (2008) extended this comprehensive model for family resemblance to allow or a flexible specification of assortment and vertical transmission. As such, it provides a general framework which can easily be reduced to fit subsets of data such as twin-parent data, children-of-twins data, etc. A flexible Mx specification of this model that allows handling of these various designs is presented in detail and applied to data from the Virginia 30,000. Data on height, body mass index, smoking status, church attendance, and political affiliation were obtained from twins and their families. Results indicate that biases in the estimation of variance components depend both on the types of relative available for analysis, and on the underlying genetic and environmental architecture of the phenotype of interest. [ABSTRACT FROM AUTHOR]

Considerable evidence from twin and adoption studies indicates that both genetic and shared environmental factors play a substantial role in the liability to antisocial behavior. Although twin and adoption designs can resolve genetic and environmental influences, they do not provide information about assortative mating, parent-offspring transmission, or the contribution of these factors to trait variation. We examined the role of genetic and environmental factors for conduct disorder (CD) using a twin-parent design. This design allows the simultaneous estimation of additive genetic, shared and individual-specific environmental effects, as well as sex differences in the expression of genes and environment in the presence of assortative mating and combined genetic and cultural transmission. A retrospective measure of CD was obtained from twins and their parents or guardians in the Virginia Twin Study of Adolescent Behavior Development and its Young Adult Follow up sample. Both genetic and environmental factors play a significant role in the liability to CD. Major influences on individual differences appeared to be additive genetic (38%-40%) and unique environmental (39%-42%) effects, with smaller contributions from the shared environment (18%-23%), assortative mating (-2%), cultural transmission (approximately 2%) and resulting genotype-environment covariance. This study showed significant heritability, which is slightly increased by assortative mating, and significant effects of primarily nonparental shared environment on CD. [ABSTRACT FROM AUTHOR]

There has been recent interest in the possibility of dividing bulimia nervosa into two sub- types based on the method of weight prevention utilized by the individual. In an attempt to see if such division is justified, this study, compared 54 purging bulimics with G9 nonpurging bulimics ascertained from a population-based register of Virginia female twins. A bulimic was defined as a ‘purger’ if she engaged in vomiting or laxativee abuse. These two groups were examined on a variety of demographic, weight, and personality measures after controlling for the presence of obesity. No significant differences were found between the two groups on any of the variables examined. [ABSTRACT FROM AUTHOR]

The diversity and dominant bacterial taxa in the vagina are reported to be influenced by multiple intrinsic and extrinsic factors, including but not limited to pregnancy, contraceptive use, pathogenic states, socioeconomic status, and ancestry. However, the extent to which host genetic factors influence variation in the vaginal microbiota is unclear. We used a biometrical genetic approach to determine whether host genetic factors contribute to inter-individual differences in taxa from a sample of 332 twins who self-identified as being of African (44 pairs) or European ancestry (122 pairs). Lactobacillus crispatus, a major determinant of vaginal health, was identified as heritable among European American women (narrow-sense heritability = 34.7%, P-value = 0.018). Heritability of L. crispatus is consistent with the reduced prevalence of adverse reproductive disorders, including bacterial vaginosis and preterm birth, among women of European ancestry., (© 2021. The Author(s).)

Background: Childhood sexual abuse (CSA) is a traumatic life event associated with an increased lifetime risk for psychopathology/morbidity. The long-term biological consequences of CSA-elicited stress on chromosomal stability in adults are unknown. The primary aim of this study was to determine if the rate of acquired chromosomal changes, measured using the cytokinesis-block micronucleus assay on stimulated peripheral blood lymphocytes, differs in adult female monozygotic twins discordant for CSA., Methods: Monozygotic twin pairs discordant for CSA were identified from a larger population-based sample of female adult twins for whom the experience of CSA was assessed by self-report (51 individuals including a reference sample). Micronuclei (MN) contain chromatin from structurally normal or abnormal chromosomes that are excluded from the daughter nuclei during cell division and serve as a biomarker to assess acquired chromosomal instability., Results: Female twins exposed to CSA exhibited a 1.63-fold average increase in their frequency of MN compared to their nonexposed genetically identical cotwins (Paired t-test, t₁₆ = 2.65, P = 0.017). No additional effects of familial factors were detected after controlling for the effect of CSA exposure. A significant interaction between CSA history and age was observed, suggesting that the biological effects of CSA on MN formation may be cumulative., Conclusions: These data support a direct link between CSA exposure and MN formation measured in adults that is not attributable to genetic or environmental factors shared by siblings. Further research is warranted to understand the biological basis for the observed increase in acquired chromosomal findings in people exposed to CSA and to determine if acquired somatic chromosomal abnormalities/somatic clonal mosaicism might mediate the adult pathology associated with CSA.

The causes of correlation between parental treatment and offspring behavior are ambiguous since genetic and social factors are correlated in typical family studies. The problem is complicated by the need to characterize the effects of genes and environment on both juvenile and adult behavioral outcomes. A model is developed for the resemblance between juvenile and adult twins and their parents that allows some of these effects to be resolved. Data on childhood adversity, parental anti-social behavior, and longitudinal adult and juvenile anti-social behavior were obtained from 1,412 families of adolescent and young adult twins. A structural model is fitted that allows for the effects of genetic and social transmission of information from parents to children. Environmental effects of parents may be mediated through measured features of the home environment. Parameters were estimated by diagonal weighted least squares applied to the 33 distinct polychoric correlations between relatives and between variables within and between ages. Sub-hypotheses were tested. Results confirmed that effects of genes and environment were both highly significant. Genetic effects were large in juveniles and largely age and sex-specific. Approximately 30% of the variation due to the shared environment was due to the effect of childhood adversity. The remaining shared environmental effects are unexplained. Adversity is affected significantly by maternal anti-social behavior. The correlation between paternal ASP and adversity may be explained by antisocial fathers selecting (or creating) antisocial mothers. All significant environmental effects of parental ASP are mediated through the measure of adversity. Though transmission of ASP is both genetic and social, passive genotype-environment correlation is very small. Assortative mating for ASP has barely detectable consequence for the genetic correlation between siblings. The longitudinal study of twins and their parents makes it possible to demonstrate there is a direct causal effect of childhood adversity on child conduct disorder over and above any indirect genetic correlation.

Background: If the adaptive significance of specific fears changes with age, the genetic contribution to individual differences may be lowest at the age of greatest salience. The roles of genes and environment in the developmental-genetic trajectory of five common childhood fears are explored in 1094 like-sex pairs of male and female monozygotic and dizygotic twins assessed on up to three occasions during adolescence (ages 8-18 years)., Methods: Dichotomous self-ratings of a cluster of five correlated fears from Ollendick's schedule of fears (FSSC-R) were extracted for subjects at each occasion of assessment. The effects of genes and environment on overall level of fears and rates of adolescent decline were explored by fitting an item-response theory ('IRT') model that allowed for individual genetic and environmental differences in initial fear level ('intercept') and rates of adolescent change ('slope') across the repeated waves of measurement. Different forms of the model were explored using Markov Chain Monte Carlo (MCMC) methods to derive the posterior distribution of subject and item parameters from the raw responses., Results: Additive genetic differences affect the common factor underlying the five fear-items. The same genes also affect rates of change with age, especially in boys. Male adolescents with higher overall genetic predisposition to childhood fears tended to show slower recovery with age than subjects with relatively low initial values. Thus, the genetic variance apparently increases with age., Conclusions: This finding is consistent with a prediction that the regulation of genetic differences will be strongest, and thus the additive genetic variance will be smallest, at the age when the particular stimulus is most salient. Items differed in the extent to which they were sensitive to underlying random differences in the rate of developmental change. Individual differences in rates of change with age were more marked in boys than girls.

Background: Considerable evidence from twin and adoption studies indicates that genetic and shared environmental factors play a significant role in the initiation of smoking behavior. Although twin and adoption designs are powerful to detect genetic and environmental influences, they do not provide information on the processes of assortative mating and parent-offspring transmission and their contribution to the variability explained by genetic and/or environmental factors., Methods: We examined the role of genetic and environmental factors for smoking initiation using an extended kinship design. This design allows the simultaneous testing of additive and non-additive genetic, shared and individual-specific environmental factors, as well as sex differences in the expression of genes and environment in the presence of assortative mating and combined genetic and cultural transmission. A dichotomous lifetime smoking measure was obtained from twins and relatives in the Virginia 30,000 sample., Results: Results demonstrate that both genetic and environmental factors play a significant role in the liability to smoking initiation. Major influences on individual differences appeared to be additive genetic and unique environmental effects, with smaller contributions from assortative mating, shared sibling environment, twin environment, cultural transmission and resulting genotype-environment covariance. The finding of negative cultural transmission without dominance led us to investigate more closely two possible mechanisms for the lower parent-offspring correlations compared to the sibling and DZ twin correlations in subsets of the data: (i) age x gene interaction, and (ii) social homogamy. Neither mechanism provided a significantly better explanation of the data, although age regression was significant., Conclusions: This study showed significant heritability, partly due to assortment, and significant effects of primarily non-parental shared environment on smoking initiation.

Objective: To assess the course and short-term outcomes associated with separation anxiety disorder (SAD) in a community setting., Method: The subjects were 161 of 2,061 8- to 17-year-old twins with SAD from a community-based twin study. Subjects were born between 1974 and 1983. Subjects and parents were personally interviewed about the subject's current psychiatric history between 1990 and 1993. A follow-up interview was conducted, on average, 18 months later. Logistic regression was used to identify predictors and outcomes of persistent SAD., Results: Of the 161 subjects with SAD at time 1, 80% had remitted and 59% were free of any disorder at follow-up. Children with persistent SAD had a significantly higher prevalence of oppositional defiant disorder, significantly more impairment associated with symptoms of attention-deficit/hyperactivity disorder, and mothers who were less satisfied with their marriage at time 1 than children with transient episodes. Children with persistent SAD had a significantly higher prevalence of overanxious disorder or a new minor or major depressive disorder at time 2 than children with transient SAD. After controlling for comorbidity, only an elevated risk of new depressive disorders at time 2 distinguished children with persistent SAD., Conclusions: Many children with SAD in a community setting are well at follow-up, on average, 18 months later. A minority of children with persistent SAD are at significantly increased risk of a new depressive disorder, especially those with a history of oppositional defiant disorder, impairment associated with symptoms of attention deficit hyperactivity disorder, or parental marital difficulties., (Copyright 2004 American Academy of Child and Adolescent Psychiatry)

Background: Very little is known about how different sets of risk factors interact to influence risk for psychiatric disorder., Objective: To replicate a recent report of a genotype-environment interaction that predicts risk for antisocial behavior in boys., Design: Characterizing risk for conduct disorder in boys in association with monoamine oxidase A genotype and exposure to familial adversity, defined by interparental violence, parental neglect, and inconsistent discipline., Setting: A community-based sample of twin boys., Participants: Five hundred fourteen male twins aged 8 to 17 years., Main Outcome Measure: Conduct disorder., Results: There was a main effect of adversity but not of monoamine oxidase A on risk for conduct disorder. Low monoamine oxidase A activity increased risk for conduct disorder only in the presence of an adverse childhood environment. Neither a passive nor an evocative genotype-environment correlation accounted for the interaction., Conclusion: This study replicates a recent report of a genotype-environment interaction that predicts individual variation in risk for antisocial behavior in boys.

Background: Determination of causal connections between parental measures and child outcomes using typical samples is limited by the inability to account for all confounds, both environmental and genetic. This paper discusses the strength of the Children of Twins (COT) design to highlight the role of specific environments., Methods: A new analytical model is presented which helps differentiate and quantify the environmental and genetic processes underlying associations between family-level risk factors and child adjustment. In order to illustrate the COT design, the relation between smoking during pregnancy and child birth weight (BW) is examined in a sample of female twins and their children from Norway and the United States., Results: The results illustrate that smoking during pregnancy is influenced by genetic factors. However, the Children of Twins model supports the claim that smoking during pregnancy has a direct environmental influence on BW and that genetic and shared environmental confounds cannot account for the association., Conclusions: An assessment of the strengths and limitations of the Children of Twins design and a comparison with other research strategies suggest that the design plays a unique role in the study of developmental psychology and psychopathology. Finally, the authors describe how methodological advances and future applications of the design will provide additional insight into the causal processes underlying children's adjustment to environmental stimuli.

Background: The aim was to compare the psychometric properties of absolute versus differential ratings of the within-family environments and to examine their associations with conduct problems in 8-16-year-old twins., Methods: The sample comprised 1117 pairs of like-sex male and female twins and their parents, recruited from the school population of Virginia. The within-family environment was assessed from the Twin Inventory of Relationships and Experiences (TIRE), which provided measures of differential parental criticism, parental preference for one twin, and twins' peers' conduct problems, as rated by mothers, fathers and each of the twins. Twins' conduct problems were assessed by a modified version of the Olweus questionnaire., Results: Although differential ratings and absolute ratings had similar psychometric properties, the use of absolute ratings to differentiate the twins resulted in a construct with weak inter-rater agreement and low stability over time. Differential ratings of the twins' environment showed significant associations with differences in conduct problems between the twins, whereas the difference in absolute ratings of each twin did not. The differential parental criticism effect was uninfluenced by the overall level of criticism in the family., Conclusions: A direct contrast between siblings or twins, as part of the rating procedure (as provided by differential ratings), may be a more efficient way to assess aspects of the within-family environment that are reliable and which are associated with psychopathology. Both differential parental criticism and peers' conduct disturbance were associated with conduct problems in the twins.