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Brian M D'Onofrio,
Martin E Rickert,
Niklas Langström,
Kelly L Donahue,
Claire A Coyne,
Henrik Larsson,
Jarrod M Ellingson,
Carol A Van Hulle,
Anastasia N Iliadou,
Paul J Rathouz, Benjamin B Lahey,
Paul Lichtenstein
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ABSTRACT: CONTEXT Previous epidemiological, animal, and human cognitive neuroscience research suggests that maternal smoking during pregnancy (SDP) causes increased risk of substance use/problems in offspring. OBJECTIVE To determine the extent to which the association between SDP and offspring substance use/problems depends on confounded familial background factors by using a quasi-experimental design. DESIGN We used 2 separate samples from the United States and Sweden. The analyses prospectively predicted multiple indices of substance use and problems while controlling for statistical covariates and comparing differentially exposed siblings to minimize confounding. SETTING Offspring of a representative sample of women in the United States (sample 1) and the total Swedish population born during the period from January 1, 1983, to December 31, 1995 (sample 2). PATIENTS OR OTHER PARTICIPANTS Adolescent offspring of the women in the National Longitudinal Survey of Youth 1979 (n = 6904) and all offspring born in Sweden during the 13-year period (n = 1 187 360). MAIN OUTCOME MEASURES Self-reported adolescent alcohol, cigarette, and marijuana use and early onset (before 14 years of age) of each substance (sample 1) and substance-related convictions and hospitalizations for an alcohol- or other drug-related problem (sample 2). RESULTS The same pattern emerged for each index of substance use/problems across the 2 samples. At the population level, maternal SDP predicted every measure of offspring substance use/problems in both samples, ranging from adolescent alcohol use (hazard ratio [HR]moderate, 1.32 [95% CI, 1.22-1.43]; HRhigh, 1.33 [1.17-1.53]) to a narcotics-related conviction (HRmoderate, 2.23 [2.14-2.31]; HRhigh, 2.97 [2.86-3.09]). When comparing differentially exposed siblings to minimize genetic and environmental confounds, however, the association between SDP and each measure of substance use/problems was minimal and not statistically significant. CONCLUSIONS The association between maternal SDP and offspring substance use/problems is likely due to familial background factors, not a causal influence, because siblings have similar rates of substance use and problems regardless of their specific exposure to SDP.
Archives of general psychiatry 11/2012; 69(11):1140-50. · 12.26 Impact Factor
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ABSTRACT: It is likely that all complex behaviors and diseases result from interactions between genetic vulnerabilities and environmental factors. Accurately identifying such gene-environment interactions is of critical importance for genetic research on health and behavior. In a previous article we proposed a set of models for testing alternative relationships between a phenotype (P) and a putative moderator (M) in twin studies. These include the traditional bivariate Cholesky model, an extension of that model that allows for interactions between M and the underling influences on P, and a model in which M has a non-linear main effect on P. Here we use simulations to evaluate the type I error rates, power, and performance of the Bayesian Information Criterion under a variety of data generating mechanisms and samples sizes (n = 2,000 and n = 500 twin pairs). In testing the extension of the Cholesky model, false positive rates consistently fell short of the nominal Type I error rates ([Formula: see text]). With adequate sample size (n = 2,000 pairs), the correct model had the lowest BIC value in nearly all simulated datasets. With lower sample sizes, models specifying non-linear main effects were more difficult to distinguish from models containing interaction effects. In addition, we provide an illustration of our approach by examining possible interactions between birthweight and the genetic and environmental influences on child and adolescent anxiety using previously collected data. We found a significant interaction between birthweight and the genetic and environmental influences on anxiety. However, the interaction was accounted for by non-linear main effects of birthweight on anxiety, verifying that interaction effects need to be tested against alternative models.
Behavior Genetics 10/2012; · 2.52 Impact Factor
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ABSTRACT: This chapter reviews what is currently known about the developmental precursors to conduct disorder (CD). Specifically, it summarizes current findings on the potential developmental relations between attention-deficit/hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD) on the one hand, and CD on the other hand. Although ODD appears to be a developmental precursor to CD in both girls and boys, the existing evidence suggests that not all children who meet criteria for CD first exhibit a significant number of ODD behaviors. If childhood ODD is a developmental precursor to CD for some boys but not others, it should be possible eventually to identify the factors that govern the developmental progression from ODD to CD. If the findings reviewed in this chapter are correct in suggesting that ODD behaviors play the role of a developmental precursor to CD, how might this happen? We briefly advance one view in this chapter that is consistent with the existing data: ODD is characterized by frequently occurring behaviors that are defined in broad terms, that is, whereas CD behaviors refer to specific law-violating acts, ODD is defined in terms of broad tendencies to respond angrily. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
10/2012;
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ABSTRACT: Previous studies of the association between multiple parental relationship transitions (i.e., when a parent begins or terminates an intimate relationship involving cohabitation) and offspring antisocial behavior have varied in their efforts to rule out confounding influences, such as parental antisocial behavior and low income. They also have been limited in the representativeness of their samples. Thus, it remains unclear to what degree parents' multiple relationship transitions have independent effects on children's antisocial behavior. Analyses were conducted using data on 8,652 6-9-year-old, 6,911 10-13-year-old, and 6,495 14-17-year-old offspring of a nationally representative sample of U.S. women. Cousin-comparisons were used in combination with statistical covariates to evaluate the associations between maternal relationship transitions and offspring antisocial behavior in childhood and adolescence. Cousin-comparisons suggested that associations between maternal relationship transitions and antisocial behavior in childhood and early adolescence are largely explained by confounding factors. In contrast, the associations between maternal relationship transitions and offspring delinquency in late adolescence were robust to measured and unmeasured confounds. The present findings suggest that interventions aimed at reducing exposure to parental relationship transitions or addressing the psychosocial consequences of exposure to parental relationship transitions could reduce risk for offspring delinquency in late adolescence.
Journal of Abnormal Child Psychology 07/2012; · 3.09 Impact Factor
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ABSTRACT: A failure of neural changes initiated by the estrogen surge in late pregnancy to reverse the valence of infant stimuli from aversive to rewarding is associated with dysfunctional maternal behavior in nonhuman mammals. Estrogen receptor-α plays the crucial role in mediating these neural effects of estrogen priming. This preliminary study examines associations between estrogen receptor-α gene polymorphisms and human maternal behavior. Two polymorphisms were associated with human negative maternal parenting. Furthermore, hemodynamic responses in functional magnetic resonance imaging to child stimuli in neural regions associated with social cognition fully mediated the association between genetic variation and negative parenting. This suggests testable hypotheses regarding a biological pathway between genetic variants and dysfunctional human maternal parenting.
Neuroscience Letters 07/2012; 525(1):17-22. · 2.11 Impact Factor
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ABSTRACT: Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV) criteria for attention deficit/hyperactivity disorder (ADHD) specify two dimensions of inattention and hyperactivity-impulsivity symptoms that are used to define three nominal subtypes: predominantly hyperactive-impulsive type (ADHD-H), predominantly inattentive type (ADHD-I), and combined type (ADHD-C). To aid decision making for DSM-5 and other future diagnostic systems, a comprehensive literature review and meta-analysis of 546 studies was completed to evaluate the validity of the DSM-IV model of ADHD. Results indicated that DSM-IV criteria identify individuals with significant and persistent impairment in social, academic, occupational, and adaptive functioning when intelligence, demographic factors, and concurrent psychopathology are controlled. Available data overwhelmingly support the concurrent, predictive, and discriminant validity of the distinction between inattention and hyperactivity-impulsivity symptoms, and indicate that nearly all differences among the nominal subtypes are consistent with the relative levels of inattention and hyperactivity-impulsivity symptoms that define the subtypes. In contrast, the DSM-IV subtype model is compromised by weak evidence for the validity of ADHD-H after first grade, minimal support for the distinction between ADHD-I and ADHD-C in studies of etiological influences, academic and cognitive functioning, and treatment response, and the marked longitudinal instability of all three subtypes. Overall, we conclude that the DSM-IV ADHD subtypes provide a convenient clinical shorthand to describe the functional and behavioral correlates of current levels of inattention and hyperactivity-impulsivity symptoms, but do not identify discrete subgroups with sufficient long-term stability to justify the classification of distinct forms of the disorder. Empirical support is stronger for an alternative model that would replace the subtypes with dimensional modifiers that reflect the number of inattention and hyperactivity-impulsivity symptoms at the time of assessment. (PsycINFO Database Record (c) 2012 APA, all rights reserved).
Journal of Abnormal Psychology 05/2012; · 4.86 Impact Factor
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ABSTRACT: A better understanding of the nature and etiology of conduct disorder (CD) can inform nosology and vice versa. We posit that any prevalent form of psychopathology, including CD, can be best understood if it is studied in the context of other correlated forms of child and adolescent psychopathology using formal models to guide inquiry.
Review of both cross-sectional and longitudinal studies of the place of CD in the phenotypic and causal structure of prevalent psychopathology, with an emphasis on similarities and differences between CD and oppositional defiant disorder (ODD). Papers were located using Web of Science by topic searches with no restriction on year of publication.
Although some important nosologic questions remain unanswered, the dimensional phenotype of CD is well defined. CD differs from other disorders in its correlates, associated impairment, and course. Nonetheless, it is robustly correlated with many other prevalent dimensions of psychopathology both concurrently and predictively, including both other 'externalizing' disorders and some 'internalizing' disorders. Based on emerging evidence, we hypothesize that these concurrent and predictive correlations result primarily from widespread genetic pleiotropy, with some genetic factors nonspecifically influencing risk for multiple correlated dimensions of psychopathology. In contrast, environmental influences mostly act to differentiate dimensions of psychopathology from one another both concurrently and over time. CD and ODD share half of their genetic influences, but their genetic etiologies are distinct in other ways. Unlike most other dimensions of psychopathology, half of the genetic influences on CD appear to be unique to CD. In contrast, ODD broadly shares nearly all of its genetic influences with other disorders and has little unique genetic variance.
Conduct disorder is a relatively distinct syndrome at both phenotypic and etiologic levels, but much is revealed by studying CD in the context of its causal and phenotypic associations with other disorders over time. Advancing and refining formal causal models that specify the common and unique causes and biological mechanisms underlying each correlated dimension of psychopathology should facilitate research on the fundamental nature and nosology of CD.
Journal of Child Psychology and Psychiatry 12/2011; 53(5):536-57. · 4.28 Impact Factor
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Benjamin B Lahey
Journal of the American Academy of Child and Adolescent Psychiatry 10/2011; 50(10):975-7. · 4.98 Impact Factor
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ABSTRACT: A quasi-experimental comparison of cousins differentially exposed to levels of neighborhood disadvantage (ND) was used with extensive measured covariates to test the hypothesis that neighborhood risk has independent effects on youth conduct problems (CPs). Multilevel analyses were based on mother-rated ND and both mother-reported CPs across 4-13 years (n = 7,077) and youth-reported CPs across 10-13 years (n = 4,524) from the Children of the National Longitudinal Survey of Youth. ND was robustly related to CPs reported by both informants when controlling for both measured risk factors that are correlated with ND and unmeasured confounds. These findings are consistent with the hypothesis that ND has influence on conduct problems.
Journal of Abnormal Psychology 09/2011; 121(1):95-108. · 4.86 Impact Factor
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ABSTRACT: To investigate whether genetic contributions to major depressive disorder and conduct disorder comorbidity are shared with genetic influences on negative emotionality.
Primary caregivers of 2,022 same- and opposite-sex twin pairs 6 to 18 years of age comprised a population-based sample. Participants were randomly selected across five regions in Tennessee, with stratification by age and geographic location. Face-to-face structured interviews were conducted with the primary caregiver of a representative sample of twins.
After accounting for genetic influences on negative emotionality, genetic influences on major depressive disorder/conduct disorder comorbidity were nonsignficant, but only in male twins. Specifically, 19% of the variance in the two disorders was accounted for by genetic factors shared with negative emotionality in male twins. Although the full hypothesis could not be tested in female twins, 10% to 11% of the variance in the two disorders was also accounted for by genetic factors shared with negative emotionality. Common shared environmental and nonshared environmental influences were found for major depressive disorder/conduct disorder comorbidity in male and female twins.
Negative emotionality represents an important dispositional trait that may explain genetic influences on major depressive disorder/conduct disorder comorbidity, at least for boys. Models of major depressive disorder/conduct disorder comorbidity must simultaneously measure common and specific genetic and environmental factors for a full understanding of this phenomenon. Gender differences require specific research attention in dispositional factors and developmental progression.
Journal of the American Academy of Child and Adolescent Psychiatry 08/2011; 50(8):818-27. · 4.98 Impact Factor
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ABSTRACT: In a representative sample of twin children and adolescents, we tested the hypothesis that a substantial proportion of the genetic and environmental influences underlying conduct disorder (CD) are shared with three socioemotional dispositions: Prosociality, Negative Emotionality, and Daring. Caretaker ratings of each dispositional dimension were uniquely associated with a latent CD dimension that included both caretaker- and youth-reports of CD as indicators. Behavior genetic analyses indicated that moderate-to-high additive genetic and moderate nonshared environmental influences underlie all three dispositions and CD, with modest shared environmental influences on Prosociality. Forty percent of the additive genetic influences and all of the nonshared environmental influences on the latent CD dimension were shared in common with the three socioemotional dispositions. The finding that CD shares a substantial proportion of its genetic influences with three distinct socioemotional dispositions suggests new perspectives on the heterogeneous etiology of CD and new approaches to exploring its specific etiological mechanisms.
Journal of Abnormal Psychology 02/2011; 120(1):57-70. · 4.86 Impact Factor
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ABSTRACT: It is necessary to understand the etiologic structure of child and adolescent psychopathology to advance theory and guide future research.
To test alternative models of the higher-order structure of etiologic effects on 11 dimensions of child and adolescent psychopathology using confirmatory factor analyses of genetic and environmental covariances.
Representative sample of twins.
Home interviews.
A total of 1571 pairs of 9- to 17-year-old twins.
Structured assessments of psychopathology using adult caregivers and youth as informants.
The best-fitting genetic model revealed that most genetic factors nonspecifically influence risk for either all 11 symptom dimensions or for dimensions of psychopathology within 1 of 2 broad domains. With some notable exceptions, dimension-specific genetic influences accounted for modest amounts of variance.
To inform theory and guide molecular genetic studies, an etiologic model is offered in which 3 patterns of pleiotropy are hypothesized to be the principal modes of genetic risk transmission for common forms of child and adolescent psychopathology. Some common environmental influences were found, but consistent with a "generalist genes, specialist environments" model, there was little sharing of environmental influences. This implies that prevalent dimensions of child and adolescent psychopathology mostly share their genetic liabilities but are differentiated by nonshared experiences.
Archives of general psychiatry 02/2011; 68(2):181-9. · 12.26 Impact Factor
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ABSTRACT: Mounting evidence suggests that genetic risks for mental disorders often interact with the social environment, but most studies still ignore environmental moderation of genetic influences. The authors tested interactions between maternal parenting and the variable number tandem repeat (VNTR) polymorphism in the 3' untranslated region of the dopamine transporter gene in the child to increase understanding of gene-environment interactions involving early parenting. Participants were part of a 9-year longitudinal study of 4- to 6-year-old children who met criteria for attention-deficit/hyperactivity disorder (ADHD) and demographically matched controls. Maternal parenting was observed during standard mother-child interactions in Wave 1. The child's conduct disorder (CD) symptoms 5-8 years later were measured using separate structured diagnostic interviews of the mother and youth. Controlling for ADHD symptoms and child disruptive behavior during the mother-child interaction, there was a significant inverse relation between levels of both positive and negative parenting at 4-6 years and the number of later CD symptoms, but primarily among children with 2 copies of the 9-repeat allele of the VNTR. The significant interaction with negative parenting was replicated in parent and youth reports of CD symptoms separately.
Journal of Abnormal Psychology 02/2011; 120(1):33-45. · 4.86 Impact Factor
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ABSTRACT: Three subtypes of attention-deficit/hyperactivity disorder (ADHD) based on numbers of symptoms of inattention (I) and hyperactivity-impulsivity (HI) were defined in the Diagnostic and Statistical Manual of Mental Disorders (4th ed.) to reduce heterogeneity of the disorder, but the subtypes proved to be highly unstable over time. A continuous alternative to nominal subtyping is evaluated in a longitudinal study of 129 four- to six-year-old children with ADHD and 130 comparison children. Children who met criteria for all subtypes in Year 1 continued to exhibit greater functional impairment than comparison children during Years 2 to 9. Among children with ADHD in Year 1, I and HI symptoms differentially predicted teacher-rated need for treatment and reading and mathematics achievement scores over the next 8 years in controlled analyses. Consistent with other studies, these findings suggest that the use of diagnostic modifiers specifying the numbers of I and HI symptoms could reduce heterogeneity and facilitate clinical intervention, prognosis, and research.
Journal of Clinical Child & Adolescent Psychology 11/2010; 39(6):761-75. · 1.92 Impact Factor
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ABSTRACT: Data are presented from 3 studies of children and adolescents to evaluate the predictive validity of childhood oppositional defiant disorder (ODD) and conduct disorder (CD) as defined in the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV; American Psychiatric Association, 1994) and the International Classification of Diseases, Version 10 (ICD-10; World Health Organization, 1992). The present analyses strongly support the predictive validity of these diagnoses by showing that they predict both future psychopathology and enduring functional impairment. Furthermore, the present findings generally support the hierarchical developmental hypothesis in DSM-IV that some children with ODD progress to childhood-onset CD, and some youth with CD progress to antisocial personality disorder (APD). Nonetheless, they reveal that CD does not always co-occur with ODD, particularly during adolescence. Importantly, the present findings suggest that ICD-10 diagnostic criteria for ODD, which treat CD symptoms as ODD symptoms when diagnostic criteria for CD are not met, identify more functionally impaired children than the more restrictive DSM-IV definition of ODD. Filling this "hole" in the DSM-IV criteria for ODD should be a priority for the DSM-V. In addition, the present findings suggest that although the psychopathic trait of interpersonal callousness in childhood independently predicts future APD, these findings do not confirm the hypothesis that callousness distinguishes a subset of children with CD with an elevated risk for APD.
Journal of Abnormal Psychology 11/2010; 119(4):739-51. · 4.86 Impact Factor
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ABSTRACT: Major depression and dysthymia in adolescence are associated with substantial disability, need for mental health services, and risk for recurrence. Concrete suicidal ideation and attempts during adolescence are particularly associated with significant distress, morbidity, and risk for completed suicide.
To test the hypothesis that young children with attention-deficit/hyperactivity disorder (ADHD) are at increased risk for depression and suicidal ideation and attempts during adolescence and to identify early predictors of which young children with ADHD are at greatest risk.
Prospective follow-up study.
Chicago, Illinois, and Pittsburgh, Pennsylvania. Patients A cohort of 125 children who met DSM-IV criteria for ADHD at 4 to 6 years of age and 123 demographically matched comparison children without ADHD were prospectively followed up in 7 structured diagnostic assessments of depression and suicidal behavior in assessment years 6 through 14, spanning 9 through 18 years of age.
DSM-IV criteria for depressive disorders and suicidal behavior.
Children with ADHD at 4 to 6 years of age were at greatly increased risk for meeting DSM-IV criteria for major depression or dysthymia (hazard ratio, 4.32) and for attempting suicide (hazard ratio, 3.60) through the age of 18 years relative to comparison children. There were marked variations in risk for these outcomes among children with ADHD, however. Within the ADHD group, children with each subtype of ADHD were at risk but for different adverse outcomes. Girls were at greater risk for depression and suicide attempts. Maternal depression and concurrent child emotional and behavior problems at 4 to 6 years of age predicted depression and suicidal behavior.
All subtypes of ADHD in young children robustly predict adolescent depression and/or suicide attempts 5 to 13 years later. Furthermore, female sex, maternal depression, and concurrent symptoms at 4 to 6 years of age predict which children with ADHD are at greatest risk for these adverse outcomes. Identifying high-risk young children with ADHD sets the stage for early prevention trials to reduce risk for later depression and suicidal behavior.
Archives of general psychiatry 10/2010; 67(10):1044-51. · 12.26 Impact Factor
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ABSTRACT: Psychologists in both basic and applied fields are keenly interested in the environmental influences that shape our lives. Therefore, researchers test causal hypotheses to construct models of environmental influences that can withstand attempts at refutation. Randomized experiments provide the strongest tests of causal hypotheses, but are not always feasible and their assumptions cannot always be met. In such cases, a number of quasi-experimental research designs can be used to substantially reduce confounding in tests of causal hypotheses. Sibling-comparison designs provide robust quasi-experimental tests of causal environmental hypotheses, but they are underused in psychology in spite of their power, feasibility, and convenience.
Current Directions in Psychological Science 10/2010; 19(5):319-323. · 3.93 Impact Factor
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ABSTRACT: Lahey and Waldman (2003, 2005) proposed a model in which three dispositions-sympathetic response to others; negative emotional response to threat, frustration, and loss; and positive response to novelty and risk-transact with the environment to influence risk for conduct disorder (CD). To test this model, the Child and Adolescent Dispositions Scale (CADS) was developed to measure these dispositions using parent ratings of the child. Here we report psychometric evaluations of a parallel youth self-report version (CADS-Y). Exploratory factor analysis of CADS-Y items among 832 9- to 17-year-olds yielded a 3-factor structure that was consistent with the model and invariant across sex and informants. In 1,582 pairs of 9- to 17-year-old twins, confirmatory factor analyses supported the CADS-Y 3-factor model. Each CADS-Y dimension was associated with CD and related personality dimensions as predicted.
Journal of Clinical Child & Adolescent Psychology 05/2010; 39(3):351-61. · 1.92 Impact Factor
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ABSTRACT: It is necessary to determine if causal influences on developing antisocial behavior change with age to guide both research and theory on its origins. The extent to which the same genetic factors influence antisocial behavior across 4-17 years of age was estimated using 2,482 sibling pairs of varying genetic relatedness. Assessments of antisocial behavior by mothers (4-9 years), mothers and youth (10-13 years), and youth (14-17 years) reflected the changing validity of informants across development. Genetic influences on antisocial behavior at 14-17 years were entirely shared with those on antisocial behavior at 10-13 years according to both informants. Genetic influences on antisocial behavior at 14-17 years were distinct from those at 4-9 years, however. These age differences in genetic influences cannot be fully distinguished from informant differences across age, but the present findings indicate that youth reported to be persistently antisocial during childhood and adolescence are influenced by one set of genetic factors influencing parent-report conduct problems in childhood and a second set of genetic influences on youth-reported delinquency that come into play around the time of the pubertal transition.
Journal of Abnormal Psychology 11/2009; 118(4):711-21. · 4.86 Impact Factor
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ABSTRACT: Although the study of relational aggression is gaining attention in the literature, little is known about the underlying causes of this behavior and the relative validity of various informants. These issues were addressed in a sample of 1,981 6- to 18-year-old twin pairs (36% female, 34% male, 30% opposite-sex). Relational aggression was assessed via maternal and self-report using a structured interview. Univariate models estimated genetic and environmental influences by informant and examined evidence for gender differences. A psychometric model combined data from both informants to estimate etiologic influences that were both common to the informants and informant specific. In both sexes, the latent variable reflecting the mother's and child's shared perception of the child's relational aggression was substantially influenced by both additive genetic (63%) and shared environmental (37%) influences, although this latent variable accounted for much greater variance in the maternal report (66%) than it did in the youth report (9%). In addition, informant-specific additive genetic and shared environmental influences were found only for the youth report, with all remaining variance in the mother's report attributed to nonshared environmental influences. Results are discussed in the context of measuring relational aggression and the importance of multiple informants.
Journal of Abnormal Psychology 11/2009; 118(4):722-33. · 4.86 Impact Factor
