A meta-analysis of 51 twin and adoption studies was conducted to estimate the magnitude of genetic and environmental influences on antisocial behavior. The best fitting model included moderate proportions of variance due to additive genetic influences (.32), nonadditive genetic influences (.09), shared environmental influences (.16), and nonshared environmental influences (.43). The magnitude of familial influences (i.e., both genetic and shared environmental influences) was lower in parent-offspring adoption studies than in both twin studies and sibling adoption studies. Operationalization, assessment method, zygosity determination method, and age were significant moderators of the magnitude of genetic and environmental influences on antisocial behavior, but there were no significant differences in the magnitude of genetic and environmental influences for males and females.
The authors investigated the development of a disposition toward empathy and its genetic and environmental origins. Young twins' (N = 409 pairs) cognitive (hypothesis testing) and affective (empathic concern) empathy and prosocial behavior in response to simulated pain by mothers and examiners were observed at multiple time points. Children's mean level of empathy and prosociality increased from 14 to 36 months. Positive concurrent and longitudinal correlations indicated that empathy was a relatively stable disposition, generalizing across ages, across its affective and cognitive components, and across mother and examiner. Multivariate genetic analyses showed that genetic effects increased, and that shared environmental effects decreased, with age. Genetic effects contributed to both change and continuity in children's empathy, whereas shared environmental effects contributed to stability and nonshared environmental effects contributed to change. Empathy was associated with prosocial behavior, and this relationship was mainly due to environmental effects.
Background:We conducted a sibling/twin/adoption study of substance initiation, use, and problem use, estimating the relative contribution of genetic and environmental influences on these phenotypes in adolescents. Methods:The participants were 345 monozygotic twin pairs, 337 dizygotic twin pairs, 306 biological sibling pairs, and 74 adoptive sibling pairs assessed by the Colorado Center for the Genetics and Treatment of Antisocial Drug Dependence, Denver and Boulder. The initiation, use, and problem use of tobacco, alcohol, marijuana, and other illicit drugs were assessed. Tetrachoric correlations were computed for each group, and univariate model-fitting analyses were conducted.Results: There were moderate to substantial genetic influences, with the exception of alcohol use and any drug use, and modest to moderate shared environmental influences on substance initiation, use, and problem use. For alcohol and any drug, heritability was higher and the magnitude of shared environmental influences was lower for
Several studies suggest that a two-factor model positing internalizing and externalizing factors explains the interrelationships among psychiatric disorders. However, it is unclear whether the covariation between internalizing and externalizing disorders is due to common genetic or environmental influences. We examined whether a model positing two latent factors, internalizing and externalizing, explained the interrelationships among six psychiatric disorders (major depressive disorder, generalized anxiety disorder, separation anxiety disorder, attention-deficit/ hyperactivity disorder, oppositional defiant disorder, and conduct disorder) in adolescents, and whether there are common genetic and environmental influences on internalizing and externalizing latent factors. Multivariate behavior genetic analyses of data from 1162 twin pairs and 426 siblings ascertained from the general population via the Colorado Center for Antisocial Drug Dependence (CADD) were conducted. We found support for a model positing two latent factors (internalizing and externalizing). These factors were moderately heritable and influenced by significant common genetic and nonshared environmental influences. These findings suggest that co-occurrence of internalizing and externalizing psychopathology in adolescents results from both genetic and environmental influences. Keywordsadolescence; psychopathology; comorbidity; genetics; environment Psychiatric comorbidity, or co-occurrence of disorders, is commonly observed in general population samples, and alternative theoretical models explaining the causes of comorbidity have been proposed (Angold, Costello, & Erkanli, 1999). Many behavioral genetic studies have examined the etiology of psychiatric comorbidity in adolescents and adults, as increased knowledge regarding the etiology of comorbidity informs the understanding of the etiology, course, and treatment of psychiatric disorders. An Internalizing-Externalizing Model for Co-Occurring DisordersAn internalizing-externalizing model has received considerable attention as a potential theoretical framework for understanding co-occurring psychiatric disorders (Krueger, 1999). Internalization is the propensity to express distress inwards; common internalizing disorders include mood disorders (e.g., major depressive disorder, dysthymia) and anxiety disorders (e.g., generalized anxiety disorder, separation anxiety disorder, phobias, obsessivecompulsive disorder). In contrast, externalization describes the propensity to express distress outwards; commonly recognized externalizing disorders include attention-deficit/ hyperactivity disorder, oppositional defiant disorder, conduct disorder, antisocial personality disorder, and substance use disorders. NIH Public AccessAuthor Manuscript J Abnorm Child Psychol. Author manuscript; available in PMC 2011 February 10. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptFactor analytic studies of psychiatric disorders have found support for two factors, internalizing and external...
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