Judy L. Silberg

Depression scale scores in 8–17‐year‐olds: effects of age and gender

BACKGROUND The excess of unipolar depression in females emerges in adolescence. However, studies of age effects on depression scale scores have produced divergent estimates of changes from childhood to adolescence. METHOD We explored possible reasons for this discrepancy in two large, longitudinal samples of twins and singletons aged 8-17. RESULTS There were no differences between twins and singletons in their scores on the Short Mood and Feelings Questionnaire (SMFQ), a 13-item self-report depression scale. SMFQ scores for boys fell over this age-range, while those for girls fell from age 9 to age 11 and then increased from age 12 to age 17. The mean scores of girls under 12 and those 12 and over differed by only around one-fifth of a standard deviation. However, given the non-normal distribution of the scores, a cut point that selected the upper 6% of scores created the expected female:male ratio of 2:1. CONCLUSIONS Implications for future research on adolescent depression are discussed.

Genetics and Child Psychiatry: II Empirical Research Findings

Key substantive findings from quantitative and molecular genetic research are reviewed in relation to affective disorder, schizophrenia, autism, hyperkinetic/attention deficit disorder, oppositional and conduct disorders, drug/alcohol problems, and Tourettes syndrome/chronic tics.

Genetic effects on the variation and covariation of attention deficit-hyperactivity disorder (ADHD) and oppositional-defiant disorder/conduct disorder (Odd/CD) symptomatologies across informant and occasion of measurement.

BACKGROUND Previous studies have shown that the presence of conduct disorder may contribute to the persistence of attention deficit-hyperactivity disorder (ADHD) symptomatology into adolescence; however, the aetiological relationship between the two phenotypes remains undetermined. Furthermore, studies utilizing multiple informants have indicated that teacher ratings of these phenotypes are more valid than maternal reports. METHODS The genetic structure underlying the persistence of ADHD and oppositional-defiant disorder/conduct disorder (ODD/CD) symptomatologies as rated by mothers and teachers at two occasions of measurement was investigated on a sample of 494 male and 603 female same sex adolescent twin pairs participating in the Virginia Twin Study of Adolescent Behavioral Development (VTSABD). RESULTS Using structural modelling techniques, one common genetic factor was shown to govern the covariation between the phenotypes across informants and occasion of measurement with additional genetic factors specific to ODD/CD symptomatology and persistence of symptomatology at reassessment. Genetic structures underlying the phenotypes were, to some extent, informant dependent. CONCLUSIONS The findings indicate that it is unlikely that the co-morbidity between ADHD and ODD/CD is due to environmental influences that are independent of ADHD. Rather it is likely to be due to a shared genetic liability either operating directly, or indirectly through gene-environment correlations or interactions. The covariation between phenotypes across informants and time is governed by a common set of genes, but it seems that ODD/CD is also influenced by additional genetic factors. Developmentally, different forms of genetic liability control ADHD in males and inattention in females.

Genetics and Child Psychiatry: I Advances in Quantitative and Molecular Genetics

Advances in quantitative psychiatric genetics as a whole are reviewed with respect to conceptual and methodological issues in relation to statistical model fitting, new genetic designs, twin and adoptee studies, definition of the phenotype, pervasiveness of genetic influences, pervasiveness of environmental influences, shared and nonshared environmental effects, and nature-nurture interplay. Advances in molecular genetics are discussed in relation to the shifts in research strategies to investigate multifactorial disorders (affected relative linkage designs, association strategies, and quantitative trait loci studies); new techniques and identified genetic mechanisms (expansion of trinucleotide repeats, genomic imprinting, mitochondrial DNA, fluorescent in-situ hybridisation, behavioural phenotypes, and animal models); and the successful localisation of genes.

Genetic and Environmental Influences on the Transmission of Parental Depression to Children's Depression and Conduct Disturbance: An Extended Children of Twins Study.

BACKGROUND Despite the increased risk of depression and conduct problems in children of depressed parents, the mechanism by which parental depression affects their childrens 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 childrens psychopathology, or whether childrens 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 childrens 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.

Genetic and environmental influences on the temporal association between earlier anxiety and later depression in girls

BACKGROUND The purpose of the present study was to investigate the role of genetic and environmental factors in the association between depressive symptoms and symptoms of overanxious disorder, simple phobias, and separation anxiety in 8-13-year-old and 14-17-year-old girls. METHODS Multivariate genetic models were fitted to child-reported longitudinal symptom data gathered from clinical interview on 415 MZ [corrected] and 194 DZ [corrected] female twin pairs from the Virginia Twin Study of Adolescent Behavioral Development (VTSABD) [corrected]. RESULTS Model-fitting results suggest there are distinct etiological [corrected] patterns underlying the association between depression and the different anxiety syndromes during the course of development: 1) specific genetic influences on depression after age 14 reflect liability to symptoms of earlier overanxious disorder (OAD) and simple phobias; 2) aspects of the shared environment that influence symptoms of depression before age 14 contribute to symptoms of separation anxiety and simple phobias later in adolescence [corrected]; 3) the shared environmental influence on [corrected] depression in 14+ girls also affects liability to symptoms of concurrent OAD and persistent separation anxiety. CONCLUSIONS These results suggest that depression before and after age 14 may be etiologically distinct syndromes. Earlier symptoms of OAD and (to a lesser extent phobic symptoms) [corrected] reflect the same genetic risk, and separation anxiety symptoms both before and after age 14 reflect the same environmental risk that influence liability to depressive symptoms expressed in middle to late adolescence.

Genetic and Environmental Transmission of Political Attitudes Over a Life Time

Recently political scientists have looked anew at the source of political preferences and find support for the heuristic that political attitudes and behaviors are influenced by endogenous factors. The present research attempts to characterize how the transmission of political orientations develops over the life course. Using longitudinal data collected on twins throughout childhood and adolescence combined with cross-sectional data from adult twins, the present study finds that genetic influences on political attitudes are absent prior to young adulthood. During childhood and adolescence, individual differences in political attitudes are accounted for by a variety of environmental influences with the role of shared “family” environment, including parental socialization, accumulating markedly between the ages of 9 and 17. However, at the point of early adulthood (in the early 20s), for those who left their parental home, there is evidence of a sizeable genetic influence on political attitudes which remains stable throughout adult life. The pattern of genetic transmission shows some similarity to an “impressionable years” model of attitude crystallization showing both the important influence of family and other shared environmental influences in adolescence and then an increased role of genetic factors as familial environmental influences diminish.

Genetic effects on ADHD symptomatology in 7- to 13-year-old twins: results from a telephone survey.

The magnitude of genetic and environmental factors and the influence of contrast effects on attention-deficit hyperactivity disorder (ADHD) symptomatology were examined on a sample of 900 twin pairs, aged 7–13, participating in the Virginia Twin Study of Adolescent Behavioral Development (VTSABD). In addition, the genetic and environmental correlations between ADHD and oppositional-defiant disorder/conduct disorder (ODD/CD) symptomatology were estimated. A series of structural models was applied to maternal ratings from a telephone survey, designed to screen for the three dimensions of ADHD symptomatology (hyperactivity, impulsivity, and inattention) and ODD/CD symptomatology. Model-fitting results suggested that ADHD symptomatology is highly heritable and influenced mostly by additive genetic, specific environmental, and contrast effects. However, this analysis could not exclude with statistical significance additional effects from dominance. The results of the best-fitting bivariate model suggested that the genetic correlation between the two traits is 50% and replicated previous findings of a common genetic factor influencing the comorbidity of ADHD and ODD/CD symptomatologies.

Genetic and environmental causes of covariation in interview assessments of disruptive behavior in child and adolescent twins

Multirater, face-to-face, interview data relating to conduct disorder (CD), oppositional-defiant disorder (ODD), and inattentive, impulsive, and hyperactive components of attention-deficit hyperactivity disorder (ADHD) in a population-based sample of 1376 pairs of 8- to 16-year-old MZ and DZ twins are analyzed to examine (1) the genetic and environmental causes of correlation among ratings of ODD and CD symptoms and (2) the pattern of genetic and environmental correlation among the three components of ADHD. Parental ratings of ADHD showed marked sibling contrast effects, specific within raters but partly common across components. After these effects were removed, there was a modest genetic correlation between maternal and paternal ratings, but genetic effects were virtually uncorrelated across boys and girls. Genetic correlations among inattention, impulsivity, and hyperactivity were all large but fell well short of unity. There was little evidence that counts of symptoms of CD and ODD were genetically independent but the genetic correlations among ratings of twins, mothers, and fathers were all relatively modest. ODD and CD showed much higher genetic correlations across sexes than did the measures of ADHD. There was no evidence of rater contrast effects or of shared family environment influences in the twin resemblance for ODD and CD.

Analysing the contributions of genes and parent–child interaction to childhood behavioural and emotional problems: a model for the children of twins

BACKGROUND Despite the demonstrable influence of both genes and the family environment on childrens behavioural and emotional development, the mechanisms by which these factors are transmitted from parents to their children are not known. Numerous aspects of the family have long been associated with behavioural and emotional problems in children; it is not clear, however, whether these family variables represent genuine environmental risks or secondary consequences of the underlying genetic liability shared between parents and their children. METHOD In this study we present a model for analysing the non-genetic contributions of family background to risk for childhood and adolescent depression and conduct disturbance using simulated data on adult MZ and DZ twins, their spouses and children. RESULTS The twin offspring design provides substantial power to detect remarkably small non-genetic effects on parent-offspring resemblance against the background of genetic transmission. As presented, the model is able to resolve the direction of transmission from both parent to child (passive genotype environment correlation) and child to parent (evocative genotype environment correlation). CONCLUSIONS Unlike many other genetic studies, a study of twins and their children can sort out which putative family environmental risk factors do actually have a significant environmental impact on the child and which ones only appear to do so because they are associated with genetic mediation.