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.
Prior research has documented a strong and positive correlation between completed education and adults' mental health. Researchers often describe this relationship using causal language: higher ...levels of education are thought to enhance people's skills, afford important structural advantages, and empower better coping mechanisms, all of which lead to better mental health. An alternative explanation—the social selection hypothesis—suggests that schooling is a proxy for unobserved endowments and/or preexisting conditions that confound the relationship between the two variables. In this article, we seek to adjudicate between these hypotheses using a relatively large, US-based sample of identical adult twins. By relating within-twin-pair differences in education to within-twin-pair differences in mental health, we are able to control for the influence of genetic traits and shared family characteristics that may otherwise bias the estimates associated with educational attainment. Results from our analyses suggest that the observed association between education and mental health is attributable to confounding on unobserved variables. This finding holds across mental health conditions, is robust to several sensitivity checks, and survives a falsification test. Theoretical implications for the study of educational gradients in mental health are discussed.
Purpose
The course of conduct disorder (CD) is heterogeneous. Moffitt proposed the heuristic of life course persistent (LCP) and adolescence limited (AL) to differentiate etiologically distinct forms ...of antisocial behavior (AB), each with distinct predictors and consequences, although a few studies have assessed this demarcation within the context of CD. The objective of this study was to apply Moffitt’s taxonomy in a nationally representative US sample to investigate the prevalence, predictors, and outcomes of LCP and AL CD.
Methods
Data come from the Collaborative Psychiatric Epidemiology Studies, a set of population-based nationally representative cross-sectional surveys (
N
= 20,130). Predictors included harsh discipline, maternal and paternal closeness, poverty in childhood, history of learning disability, parental deviance, and nativity. Outcomes included substance use, employment status, education attainment, marital status, income level, and self-rated mental and physical health.
Results
The prevalence of LCP and AL CD was 0.5 and 4.6%, respectively, for females, and 1.9 and 5.1%, respectively, for males. Low childhood SES Odds Ratio (OR) = 3.49, lack of maternal closeness (OR = 2.50), and history of harsh discipline (OR = 2.17) increased odds of LCP group membership. The LCP group had higher odds of developing substance use disorders (OR = 2.00) relative to AL.
Conclusions
LCP CD is more strongly influenced by childhood environment and confers increased odds for substance use problems in adulthood relative to AL CD.
Depression is a highly heterogeneous condition, and identifying how symptoms present in various groups may greatly increase our understanding of its etiology. Importantly, Major Depressive Disorder ...is strongly linked with Substance Use Disorders, which may ameliorate or exacerbate specific depression symptoms. It is therefore quite plausible that depression may present with different symptom profiles depending on an individual's substance use status. Given these observations, it is important to examine the underlying construct of depression in groups of substance users compared to non-users. In this study we use a non-clinical sample to examine the measurement structure of the Beck Depression Inventory (BDI-II) in non-users and frequent-users of various substances. Specifically, measurement invariance was examined across those who do vs. do not use alcohol, nicotine, and cannabis. Results indicate strict factorial invariance across non-users and frequent-users of alcohol and cannabis, and metric invariance across non-users and frequent-users of nicotine. This implies that the factor structure of the BDI-II is similar across all substance use groups.
Background
Little is known about genetic and environmental influences on the components of disruptive mood dysregulation disorder (DMDD), tonic irritability (i.e., irritable mood) and phasic ...irritability (i.e., temper outbursts). This study examined prevalence, stability, and heritability of tonic irritability, phasic irritability, and a DMDD proxy (pDMDD) based on DSM‐5 criteria.
Methods
pDMDD was derived using data from clinical interviews of parents and their twins (N = 1,431 twin pairs), ages 8–17, participating in Waves 1 and 2 of the Virginia Twin Study of Adolescent Behavioral Development. Biometrical modeling was used to compare a common pathway model (CPM) and an independent pathway model (IPM), and heritability estimates were obtained for pDMDD using the symptoms of irritable mood (tonic irritability; DMDD Criterion D), intense temper outbursts (phasic irritability; DMDD Criterion A), and frequent temper outbursts (phasic irritability; DMDD Criterion C).
Results
Lifetime prevalence of pDMDD was 7.46%. The stability of DMDD symptoms and the pDMDD phenotype across approximately one year were moderate (.30–.69). A CPM was a better fit to the data than an IPM. Phasic irritability loaded strongly onto the pDMDD latent factor (.89–.96) whereas tonic irritability did not (.28). Genetic influences accounted for approximately 59% of the variance in the latent pDMDD phenotype, with the remaining 41% of the variance due to unique environmental effects. The heritability of tonic irritability (54%) was slightly lower than that of frequent and intense temper (components of phasic irritability; 61% and 63%, respectively).
Conclusions
Compared to tonic irritability, phasic irritability appears to be slightly more stable and heritable, as well as a stronger indicator of the latent factor. Furthermore, environmental experiences appear to play a substantial role in the development of irritability and DMDD, and researchers should seek to elucidate these mechanisms in future work.
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 Little is known about paternal psychosocial factors and childhood asthma. Objective We sought to examine the link between maternal and paternal psychosocial stress and asthma outcomes in ...young children. Methods Parents of 339 pairs of Puerto Rican twins were interviewed individually about their own psychosocial stress and about asthma in their children at age 1 year and again about their child's asthma at age 3 years. Fathers were asked about symptoms of posttraumatic stress disorder (PTSD), depression, and antisocial behavior. Mothers were asked about depressive symptoms. Outcomes assessed in children included recent asthma symptoms, oral steroid use and hospitalizations for asthma in the prior year, and asthma diagnosis. Generalized estimated equation models were used for the multivariate analysis of parental psychosocial stress and asthma morbidity in childhood. Results After multivariable adjustment, paternal PTSD symptoms, depression, and antisocial behavior were each associated with increased asthma symptoms at age 1 year (eg, odds ratio, 1.08 for each 1-point increase in PTSD score; 95% CI, 1.03-1.14). Maternal depressive symptoms were associated with an increased risk of asthma hospitalizations at age 1 year. At age 3 years, maternal depressive symptoms were associated with asthma diagnosis and hospitalizations for asthma (odds ratio for each 1-point increase in symptoms, 1.16; 95% CI, 1.00-1.36). In an analysis combining 1- and 3-year outcomes, paternal depression was associated with oral steroid use, maternal depressive symptoms were associated with asthma hospitalizations and asthma diagnosis, and parental depression was associated with hospitalizations for asthma. Conclusions Both paternal and maternal psychosocial factors can influence asthma morbidity in young Puerto Rican children.
The Mid-Atlantic Twin Registry (MATR) is a population-based registry of more than 56,000 twins primarily born or living in Virginia, North Carolina, and South Carolina. The MATR employs several ...methods of ascertaining twins, and devotes considerable resources to tracking and maintaining communication with MATR participants. Researchers may utilize the MATR for administration of research services including study recruitment, collection of DNA, archival data set creation, as well as data collection through mailed, phone, or online surveys. In addition, the MATR houses the MATR Repository, with over 1,200 blood samples available for researchers interested in DNA genotyping. For over 35 years MATR twins have participated in research studies with investigators from diverse scientific disciplines and various institutions. These studies, which have resulted in numerous publications, have covered a range of topics, including the human microbiome, developmental psychopathology, depression, anxiety, substance use, epigenetics of aging, children of twins, pre-term birth, social attitudes, seizures, eating disorders, as well as sleep homeostasis. Researchers interested in utilizing twins are encouraged to contact the MATR to discuss potential research opportunities.
Insomnia is a highly prevalent sleep disorder yet little is known about the role of genetic factors in its pathophysiology. The aim of this study was to examine the relative contributions of genetic ...and environmental factors in explaining variability in insomnia symptoms.
Traditional twin design.
Academic medical center.
1412 twin pairs aged 8-16 years (48.8% MZ, 47.2% DZ, 4.0% indeterminate).
None.
Ratings of insomnia symptoms, depression, and overanxious disorder were made by trained interviewers based on DSM-III-R criteria. ACE models were conducted using Mx statistical software. Insomnia symptoms were prevalent in this sample based both on parental (6.6%) and youth (19.5%) reports. The overall heritability of insomnia symptoms was modest (30.7%), with the remaining variance attributed to unique environmental effects. There was no evidence of sex differences in the prevalence of insomnia symptoms or in the contribution of genetic and environmental effects. In multivariate models, there was support for insomnia-specific unique environmental effects over and above overlapping effects with depression and overanxious disorder, but no evidence for insomnia-specific genetic effects.
Genetic factors play a modest role in the etiology of insomnia symptoms in 8-16 year-olds. These effects overlap with the genetics of depression and overanxious disorder. Further work is needed to determine which genes confer risk for all three disorders.
Illicit substance use is dangerous in both acute and chronic forms, frequently resulting in lethal poisoning, addiction, and other negative consequences. Similar to research in other psychiatric ...conditions, whose ultimate goal is to enable effective prevention and treatment, studies in substance use are focused on factors elevating the risk for the disorder. The rapid growth of the substance use problem despite the effort invested in fighting it, however, suggests the need in changing the research approach. Instead of attempting to identify risk factors, whose neutralization is often infeasible if not impossible, it may be more promising to systematically reverse the perspective to the factors enhancing the aspect of liability to disorder that shares the same dimension but is opposite to risk, that is, resistance to substance use. Resistance factors, which enable the majority of the population to remain unaffected despite the ubiquity of psychoactive substances, may be more amenable to translation. While the resistance aspect of liability is symmetric to risk, the resistance approach requires substantial changes in sampling (high-resistance rather than high-risk) and using quantitative indices of liability. This article provides an overview and a practical approach to research in resistance to substance use/addiction, currently implemented in a NIH-funded project. The project benefits from unique opportunities afforded by the data originating from two longitudinal twin studies, the Virginia Twin Study of Adolescent and Behavioral Development and the Minnesota Twin Family Study. The methodology described is also applicable to other psychiatric disorders.
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