Dataset Information

Sex Differences in the Genetic and Environmental Influences on Self-Reported Non-aggressive and Aggressive Conduct Disorder Symptoms in Early and Middle Adolescence.

ABSTRACT: Decades of research into the etiology of conduct disorder (CD) has yet to yield a consensus on the existence of sex differences in underlying genetic and environmental influences. This may be partly due to the failure of many previous studies to make a distinction between non-aggressive and aggressive CD symptoms or test for potential developmental changes in sex differences in the etiology of conduct problems. To address these gaps, we fit a series of univariate and bivariate biometric sex-difference models to self-reported non-aggressive and aggressive CD symptoms in a community-based sample of twins (N?=?1548, ages 9-17 year), grouped into ages 9-13 and 14-17 years. Relative model fit was evaluated using the Bayesian Information Criterion (BIC), which favors parsimony, and by Chi square difference tests. The univariate sex-scalar model provided the best fit to the data for both non-aggressive and aggressive CD symptoms at ages 9-13 and 14-17 years. Thus, the same genetic and environmental factors influenced CD symptoms in both sexes, but the total variability was lower in females than males. At both ages, the heritability of non-aggressive CD symptoms was lower than heritability of aggressive CD symptoms, and shared environmental effects were only observed for non-aggressive CD symptoms. However, estimates for genetic and environmental factors could be not be constrained to be equal across age groups for either CD subtype, suggesting substantive developmental changes in the relative influence of genetic and environmental factors on individual differences in CD symptoms. For both subtypes, the heritability was larger, and shared environmental effect smaller, in the older age group than the younger age group. A bivariate quantitative sex differences model provided the best fit to the data at ages 9-13 years. Covariation between non-aggressive and aggressive CD symptoms was due to overlapping shared and non-shared environmental factors in males and females but the overall covariation was greater in males than females. In contrast, at ages 14-17 years, the sex-scalar bivariate model provided the best fit to the data, and covariation between non-aggressive and aggressive CD symptoms was due to overlapping genetic and non-shared environmental factors. Thus, the etiology of self-reported conduct disorder varied substantially by symptom type and age. However, quantitative sex differences were only apparent when the covariation between the two subtypes was considered.

SUBMITTER: Van Hulle CA

PROVIDER: S-EPMC6051422 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature

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Sex Differences in the Genetic and Environmental Influences on Self-Reported Non-aggressive and Aggressive Conduct Disorder Symptoms in Early and Middle Adolescence.

Van Hulle Carol A CA Waldman Irwin I Lahey Benjamin B BB

Behavior genetics 20180611 4

Decades of research into the etiology of conduct disorder (CD) has yet to yield a consensus on the existence of sex differences in underlying genetic and environmental influences. This may be partly due to the failure of many previous studies to make a distinction between non-aggressive and aggressive CD symptoms or test for potential developmental changes in sex differences in the etiology of conduct problems. To address these gaps, we fit a series of univariate and bivariate biometric sex-diff ...[more]

PMID: 29948512

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Project description:BackgroundPsychotic experiences (PEs) such as paranoia and hallucinations, and negative symptoms (NS) such as anhedonia and flat affect are common in adolescence. Psychotic experiences and negative symptoms (PENS) increase risk for later psychiatric outcomes, particularly when they persist. The extent to which genetic and environmental influences contribute to the stability of PENS in mid-to-late adolescence is unknown.MethodsUsing the Specific Psychotic Experiences Questionnaire (SPEQ) twice across ~9 months in adolescence, N = 1,448 twin pairs [M = 16.32 (0.68)] reported experiences of paranoia, hallucinations, cognitive disorganization, grandiosity and anhedonia, and their parents reported on a range of NS. Individuals were split into low-scoring, decreasing, increasing and persistent groups for each subscale. Frequencies and mean differences in distress, depression traits and emotional problems were investigated across groups. Longitudinal structural equation modelling was used to estimate the aetiological components underlying the stability of PENS.ResultsPhenotypic stability was moderate for all PENS (r = .59-.69). Persistent PENS across 9 months were associated with greater levels of distress (V = 0.15-0.46, for PEs only), depression traits (d = 0.47-1.67, except grandiosity) and emotional problems (d = 0.47-1.47, except grandiosity and anhedonia) at baseline compared to groups with transitory or low levels of PENS. At both ages PENS were heritable and influenced by shared and nonshared environment. Genetic influences contributed 38%-62% and shared environment contributed 13%-33% to the stability of PENS. Nonshared environment contributed 34%-41% (12% for parent-rated NS). There was strong overlap of genetic and shared environmental influences across time, and lower overlap for nonshared environment. Imperfect stability of PENS was at least partly due to nonshared environmental influences.ConclusionsWhen adolescent PENS persist over time, they are often characterized by more distress, and higher levels of other psychopathology. Both genetic and environmental effects influence stability of PENS.

Project description:IMPORTANCE:Attention-deficit/hyperactivity disorder (ADHD) is conceptualized as a neurodevelopmental disorder that is strongly heritable. However, to our knowledge, no study to date has examined the genetic and environmental influences explaining interindividual differences in the developmental course of ADHD symptoms from childhood to adolescence (ie, systematic decreases or increases with age). The reason ADHD symptoms persist in some children but decline in others is an important concern, with implications for prognosis and interventions. OBJECTIVE:To assess the proportional impact of genes and the environment on interindividual differences in the developmental course of ADHD symptom domains of hyperactivity/impulsivity and inattention between ages 8 and 16 years. DESIGN, SETTING, AND PARTICIPANTS:A prospective sample of 8395 twin pairs from the Twins Early Development Study, recruited from population records of births in England and Wales between January 1, 1994, and December 31, 1996. Data collection at age 8 years took place between November 2002 and November 2004; data collection at age 16 years took place between February 2011 and January 2013. MAIN OUTCOMES AND MEASURES:Both DSM-IV ADHD symptom subscales were rated 4 times by participants' mothers. RESULTS:Estimates from latent growth curve models indicated that the developmental course of hyperactivity/impulsivity symptoms followed a sharp linear decrease (mean score of 6.0 at age 8 years to 2.9 at age 16 years). Interindividual differences in the linear change in hyperactivity/impulsivity were under strong additive genetic influences (81%; 95% CI, 73%-88%). More than half of the genetic variation was specific to the developmental course and not shared with the baseline level of hyperactivity/impulsivity. The linear decrease in inattention symptoms was less pronounced (mean score of 5.8 at age 8 years to 4.9 at age 16 years). Nonadditive genetic influences accounted for a substantial amount of variation in the developmental course of inattention symptoms (54%; 95% CI, 8%-76%), with more than half being specific to the developmental course. CONCLUSIONS AND RELEVANCE:The large genetic influences on the developmental course of ADHD symptoms are mostly specific and independent of those that account for variation in the baseline level of symptoms. Different sets of genes may be associated with the developmental course vs the baseline level of ADHD symptoms and explain why some children remit from ADHD, whereas others persist. Recent longitudinal imaging data indicate that the maintenance or increase in symptoms is underpinned by atypical trajectories of cortical development. This may reflect a specific genetic liability, distinct from that which contributes to baseline ADHD symptoms, and warrants closer follow-up.

Dataset Information

Sex Differences in the Genetic and Environmental Influences on Self-Reported Non-aggressive and Aggressive Conduct Disorder Symptoms in Early and Middle Adolescence.

Publications

Sex Differences in the Genetic and Environmental Influences on Self-Reported Non-aggressive and Aggressive Conduct Disorder Symptoms in Early and Middle Adolescence.

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