Contributions of Genes and Environments to Stability and Change in Externalizing and Internalizing Problems During Elementary and Middle School
Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado 80309, USA. Behavior Genetics
(Impact Factor: 3.21).
08/2005; 35(4):381-96. DOI: 10.1007/s10519-004-1747-5
We examined longitudinally collected behavioral reports by teachers on a unique twin sample at the ages of 7, 8, 9, 10, 11, and 12 years. As twin and adoption studies implicate the role of genetic influence on behavioral problems found to be stable in epidemiological samples, the current study employs a developmental behavior genetic model to examine the extent to which genetic and environmental contributions to problem behaviors are stable and/or change during development. In this sample of 410 monozygotic (MZ) and 354 dizygotic (DZ) twins, MZ twins were rated as more similar than DZ twins on average. In general, boys were more frequently rated as displaying externalizing behaviors than were girls across each of the six observations, while girls' internalizing problems were found not to be significantly different from boys'. For both sexes, stability in externalizing problem behaviors was due to a single common genetic factor whose effects acted pleiotropically at each age in the presence of unique environmental influences that were transmitted from age-to-age. Change was largely due to uncorrelated age-specific non-shared environmental and additive genetic effects. Contributions to stability for internalizing problems were due to age-to-age transmission of earlier expressed genetic effects. Change for girls and boys internalizing problems were largely due to environmental experiences unique to siblings along with uncorrelated age-specific genetic effects. These results further inform the notion that individual environments are important factors in the etiology of problem behaviors, but suggest that heritable contributions to phenotypic stability are largely the same across middle childhood and early adolescence. Clinical implications of these findings are discussed.
Available from: Monika Waszczuk
- "The non-shared environmental influences on homotypic continuity of each symptom were largely time-specific, as expected (Scourfield et al. 2003; Van Der Valk et al. 2003; Bartels et al. 2004; Haberstick et al. 2005; Lau & Eley, 2006; Zavos et al. 2012; Garcia et al. 2013; Lewis & Plomin, 2015). Furthermore, we found new genetic influences emerged over time (genetic innovation; Kendler et al. 2008a) and previous genetic influences gradually declined over time (genetic attenuation), in agreement with other findings (Scourfield et al. 2003; Van Der Valk et al. 2003; Bartels et al. 2004; Haberstick et al. 2005; Lau & Eley, 2006; Kendler et al. 2008a, b; Zavos et al. 2012; Nivard et al. 2015; Lewis & Plomin, 2015). These newly emerging, developmentally dynamic environmental and genetic effects can contribute to change in the course of depression and anxiety symptoms. "
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ABSTRACT: Depression and anxiety persist within and across diagnostic boundaries. The manner in which common v. disorder-specific genetic and environmental influences operate across development to maintain internalizing disorders and their co-morbidity is unclear. This paper investigates the stability and change of etiological influences on depression, panic, generalized, separation and social anxiety symptoms, and their co-occurrence, across adolescence and young adulthood.
A total of 2619 twins/siblings prospectively reported symptoms of depression and anxiety at mean ages 15, 17 and 20 years.
Each symptom scale showed a similar pattern of moderate continuity across development, largely underpinned by genetic stability. New genetic influences contributing to change in the developmental course of the symptoms emerged at each time point. All symptom scales correlated moderately with one another over time. Genetic influences, both stable and time-specific, overlapped considerably between the scales. Non-shared environmental influences were largely time- and symptom-specific, but some contributed moderately to the stability of depression and anxiety symptom scales. These stable, longitudinal environmental influences were highly correlated between the symptoms.
The results highlight both stable and dynamic etiology of depression and anxiety symptom scales. They provide preliminary evidence that stable as well as newly emerging genes contribute to the co-morbidity between depression and anxiety across adolescence and young adulthood. Conversely, environmental influences are largely time-specific and contribute to change in symptoms over time. The results inform molecular genetics research and transdiagnostic treatment and prevention approaches.
Available from: Joseph A. Schwartz
- "For example, the results of a number of studies indicate that genetic factors explain between 32 and 83 percent of the variance in cholesterol levels, with environmental factors explaining the remaining variance (de Miranda Chagas et al., 2011; Pérusse et al., 1997). Research has also revealed a significant genetic influence on various outcomes related to other internalizing and externalizing problems including aggression (Ferguson, 2010; Miles and Carey, 1997; Rhee and Waldman, 2002), impulsivity (Beaver et al., 2008; Hur and Bouchard, 1997), depression (Johnson et al., 2002; Sullivan et al., 2000), and additional internalizing problems (Haberstick et al., 2005). One study, moreover, has revealed that measured genetic polymorphisms linked to regulation of serotonergic systems (such as the serotonin transporter gene 5-HTTLPR) significantly moderate the association between cholesterol levels and various deleterious "
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Low cholesterol levels have been found to be associated with a wide range of behavioral problems, including violent and criminal behavior, and a wide range of psychological problems including impulsivity, depression, and other internalizing problems. The casual mechanisms underlying these associations remain largely unknown, but genetic factors may play a role in the etiology of such associations as previous research has found significant genetic influence on cholesterol levels and various deleterious behavioral and psychological outcomes. The current study addressed this existing gap in the literature by performing a genetically sensitive test of the association between cholesterol levels and various outcomes including levels of self-control, depressive symptoms, anger expression, and neuroticism.
DeFries–Fulker (DF) analysis was used to analyze data from 388 twin pairs nested within the Survey of Midlife Development in the United States (MIDUS).
The results of the genetically informed models revealed that high-density lipoprotein (HDL) cholesterol levels were negatively and significantly associated with depressive symptoms, had a marginally significant effect on neuroticism, and a nonsignificant effect on both anger expression and self-control.
The findings may not extrapolate to the larger population of American adults since the subsample of twins with cholesterol information may not be nationally representative.
Genetic influences play a significant role in the association between cholesterol levels and various deleterious outcomes and failing to control for these influences may result in model misspecification and may increase the probability of detecting a significant association when one does not actually exist.
Available from: Stephanie H. Bader
- "More broadly, twin studies of child psychopathology also imply a genetic link for externalizing behaviors and internalizing symptoms (Haberstick, Schmitz, Young, & Hewitt, 2005; Towers et al., 2000). Longitudinal observations of same-sex twin pairs revealed correlations for externalizing behaviors and internalizing symptoms among pairs across six years (Haberstick et al., 2005). There were no significant differences between mono-and dizygotic pairs; however, monozygotic pairs had more similar externalizing behaviors and internalizing symptoms, further underscoring a possible genetic influence. "
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ABSTRACT: Existing literature regarding the adjustment of siblings of children with an autism spectrum disorder (ASD) remains inconclusive, with some studies showing positive adjustment, others showing negative adjustment, and others showing no difference when compared to siblings of typically-developing children. For the current study, 42 parents of a child with an ASD and a typically-developing sibling (ASD group) and 42 parents of two typically-developing siblings (control group) provided data via online questionnaires. Both diagnostic category and autism symptom severity were tested as possible moderators, but neither produced significant interactions with either externalizing behaviors or internalizing symptoms in the target child when predicting externalizing behaviors, internalizing symptoms, or social problems in the sibling. However, across the overall sample (ASD and control groups), maladjustment – particularly internalizing symptoms – in the target children significantly related to maladjustment in their siblings. Thus, these findings suggest that having a sibling with an ASD is neither a risk nor protective factor for maladjustment among typically-developing siblings above and beyond the relation between maladjustment among siblings in general. Given some of the mixed findings in the literature, other possible moderators that may put siblings of a child with an ASD at specific risk should be considered in future research.
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