S. Alexandra Burt

Rethinking Environmental Contributions to Child and Adolescent Psychopathology: A Meta-Analysis of Shared Environmental Influences

Behavioral genetic research has concluded that the more important environmental influences result in differences between siblings (referred to as nonshared; e2), whereas environmental influences that create similarities between siblings (referred to as shared; c2) are indistinguishable from zero. However, there is mounting evidence that during childhood and adolescence, c2 may make important contributions to most forms of psychopathology. The aim of the meta-analysis was to empirically confirm this hypothesis. The author examined twin and adoption studies (n=490) of internalizing and externalizing psychopathology prior to adulthood. Analyses revealed that c2 accounted for 10%-19% of the variance within conduct disorder, oppositional defiant disorder, anxiety, depression, and broad internalizing and externalizing disorders, regardless of their operationalization. When age, informant, and sex effects were considered, c2 generally ranged from 10%-30% of the variance. Importantly, c2 estimates did not vary across twin and adoption studies, suggesting that these estimates reflect actual environmental influences common to siblings. The only exception was attention-deficit/hyperactivity disorder, which appeared to be largely genetic (and particularly nonadditive genetic) in origin. Conceptual, methodological, and clinical implications of these findings are discussed.

Genetic and environmental influences on ADHD symptom dimensions of inattention and hyperactivity: a meta-analysis.

Behavioral genetic investigations have consistently demonstrated large genetic influences for the core symptom dimensions of attention-deficit/hyperactivity disorder (ADHD), namely inattention (INATT) and hyperactivity (HYP). Yet little is known regarding potential similarities and differences in the type of genetic influence (i.e., additive vs. nonadditive) on INATT and HYP. As these symptom dimensions form the basis of the current Diagnostic and Statistical Manual of Mental Disorders subtype classification system, evidence of differential genetic influences would have important implications for research investigating causal mechanisms for ADHD. The current meta-analysis aimed to investigate the nature of etiological influences for INATT and HYP by comparing the type and magnitude of genetic and environmental influences each. A comprehensive literature search yielded 79 twin and adoption studies of INATT and/or HYP. Of these, 13 samples of INATT and 9 samples of HYP were retained for analysis. Results indicated that both dimensions were highly heritable (genetic factors accounted for 71% and 73% of the variance in INATT and HYP, respectively). However, the 2 dimensions were distinct as to the type of genetic influence. Dominant genetic effects were significantly larger for INATT than for HYP, whereas additive genetic effects were larger for HYP than for INATT. Estimates of unique environmental effects were small to moderate and shared environmental effects were negligible for both symptom dimensions. The pattern of results generally persisted across several moderating factors, including gender, age, informant, and measurement method. These findings highlight the need for future studies to disambiguate INATT and HYP when investigating the causal mechanisms, and particularly genetic influences, behind ADHD.

Are there meaningful etiological differences within antisocial behavior? Results of a meta-analysis

There is mounting evidence of etiologically driven distinctions between aggressive (AGG) and non-aggressive rule-breaking (RB) forms of antisocial behavior. To date, however, these differences remain somewhat speculative. The current meta-analysis of twin and adoption studies sought to clarify these distinctions by comparing meta-analytic estimates of genetic, shared environmental, and non-shared environmental influences across AGG and RB to more clearly ascertain whether they evidence differential patterns of genetic and environmental influence. A comprehensive literature search resulted in the collection of 103 twin and adoption studies, of which 15 RB samples and 19 AGG samples were ultimately included in the analyses. Results reveal clear evidence of etiological distinctions between AGG and RB. Namely, AGG appears to be a highly heritable condition (genetic factors account for 65% of the variance), with little role for the shared or common environment, particularly after childhood. By contrast, while genetic influences also contribute to RB (48% of the variance), there is an important role for shared environmental effects as well (18% of the variance). Such findings are indicative of meaningful etiologic distinctions between aggressive and rule-breaking forms of antisocial behavior, and underscore the advantage of differentiating between these behavioral subtypes when studying the causal processes that underlie antisocial behavior.

Sources of covariation among attention-deficit/hyperactivity disorder, oppositional defiant disorder, and conduct disorder: the importance of shared environment.

Research has documented high levels of covariation among childhood externalizing disorders, but the etiology of this covariation is unclear. To unravel the sources of covariation among attention-deficit/hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), and conduct disorder (CD), the authors studied 11-year-old twins (N = 1,506) from the Minnesota Twin Family Study. Symptom counts for each of these disorders were obtained from interviews administered to the twins and their mothers. A model was fit that allowed the parsing of genetic, shared environmental (factors that make family members similar to each other), and nonshared environmental (factors that make family members different from each other) contributions to covariation. The results revealed that although each disorder was influenced by genetic and environmental factors, a single shared environmental factor made the largest contribution to the covariation among ADHD, ODD, and CD.

Identifying shared environmental contributions to early substance use: The respective roles of peers and parents

Although behavior genetic studies have suggested that early substance use is primarily environmentally mediated, no study has sought to identify the specific sources of environmental variance. Using data obtained from multiple informants, this study assessed the contributions of peer deviance and parent-child relationship problems to substance use in 14-year-old male and female twins (N = 1,403) drawn from the Minnesota Twin Family Study (MTFS). All three phenotypes were influenced primarily by shared environmental variance (average c(2) =.51), as was the overlap among them. Moreover, peer deviance and parent-child relationship problems accounted for approximately 77% of the variance in early substance use. Findings also indicated that peer deviance, but not parent-child relationship problems, accounted uniquely for variance in early substance use.

Genetic and environmental influences on personality trait stability and growth during the transition to adulthood: A three wave longitudinal study

During the transition to adulthood individuals typically settle into adult roles in love and work. This transition also involves significant changes in personality traits that are generally in the direction of greater maturity and increased stability. Competing hypotheses have been offered to account for these personality changes: The intrinsic maturation hypothesis suggests that change trajectories are endogenous, whereas the life-course hypothesis suggests that these changes occur because of transactions with the social environment. This study investigated the patterns and origins of personality trait changes from ages 17 to 29 using 3 waves of Multidimensional Personality Questionnaire data provided by twins. Results suggest that (a) trait changes were more profound in the first relative to the second half of the transition to adulthood; (b) traits tend to become more stable during the second half of this transition, with all the traits yielding retest correlations between .74 and .78; (c) Negative Affectivity declined over time, and Constraint increased over time; minimal change was observed on agentic or communal aspects of Positive Emotionality; and (d) both genetic and nonshared environmental factors accounted for personality changes. Overall, these genetically informed results support a life-course perspective on personality development during the transition to adulthood.

Measured Gene-by-Environment Interaction in Relation to Attention-Deficit/ Hyperactivity Disorder

OBJECTIVE To summarize and evaluate the state of knowledge regarding the role of measured gene-by-environment interactions in relation to attention-deficit/hyperactivity disorder. METHOD A selective review of methodologic issues was followed by a systematic search for relevant articles on measured gene-by-environment interactions; the search yielded 16 studies, which are discussed in qualitative fashion. RESULTS Relatively consistent evidence points to the interaction of genotype with psychosocial factors in the development of attention-deficit/hyperactivity disorder. The next step is to identify the mechanisms on the environment side and the gene combinations on the genetic side accounting for this effect. In contrast, evidence for gene-by-environment interactions involving pre- and perinatal risk factors is generally negative or unreplicated. The aggregate effect size for psychosocial interaction with genotype is more than double that for the interaction of pre- and perinatal risks with genotype. Only a small fraction of candidate environments and gene markers has been studied, and multivariate methods to integrate multiple gene or environment markers have yet to be implemented. CONCLUSIONS Gene-by-environment interaction appears likely to prove fruitful in understanding the etiology of attention-deficit/hyperactivity disorder. Findings to date already suggest new avenues of investigation particularly involving psychosocial mechanisms and their interplay with genotype. Further pursuit of theoretically promising leads is recommended.

Differential Parent–Child Relationships and Adolescent Externalizing Symptoms: Cross-Lagged Analyses Within a Monozygotic Twin Differences Design

Research has indicated that differential parental treatment is linked to differences in externalizing symptomology (EXT) across siblings, even those siblings who are genetically identical. However, the direction of causation and longitudinal significance of this relationship remains unclear. Thus, in the present study, the authors examined 486 monozygotic twin pairs, assessed at ages 11, 14, and 17 years, within a cross-lagged twin differences design. Results revealed that differential parent-child conflict at age 11 years uniquely contributed to differential sibling EXT 3 years later but only in the most discordant twin pairs. In the full, unselected sample, this relationship was not significant. These results suggest that markedly different parent-child conflict has an environmentally mediated impact on child behavior through mid-adolescence, findings that yield insights into environmental influences on behavior.

Prenatal hormone exposure and risk for eating disorders: a comparison of opposite-sex and same-sex twins.

CONTEXT Although the sex difference in eating disorder prevalence has typically been attributed to psychosocial factors, biological factors may also play a role. Prenatal testosterone exposure is a promising candidate, since it masculinizes behavior in animals and humans via its permanent effects on the central nervous system. OBJECTIVE To examine whether in utero testosterone exposure has masculinizing effects on disordered eating (DE) by comparing opposite-sex (OS) and same-sex (SS) twins. Twin type (SS vs OS) is considered a proxy measure of prenatal hormone exposure, since females from OS pairs are exposed to more testosterone in utero than females from SS pairs. A linear trend in mean levels of DE was predicted based on expected prenatal testosterone exposure, with SS female twins exhibiting the highest levels of DE followed by OS female twins, OS male twins, and SS male twins. DESIGN A twin study comparison of OS vs SS twins. SETTING Michigan State University Twin Registry. PARTICIPANTS Participants included 304 SS female twins, 59 OS female twins, 54 OS male twins, and 165 SS male twins. MAIN OUTCOME MEASURE Overall levels of DE were assessed with the Minnesota Eating Behavior Survey. RESULTS Confirming hypotheses, DE exhibited significant linear trends, with SS female twins exhibiting the highest levels of DE followed by OS female twins, OS male twins, and SS male twins. This linear trend could not be accounted for by levels of anxiety or socialization effects. Indeed, OS female twins exhibited lower levels of DE compared with an independent sample of undergraduate women (n = 69) who were raised with 1 or more brothers. CONCLUSIONS The masculinization of DE in OS female twins is unlikely to be due to socialization effects alone. Biological factors, such as the masculinization of the central nervous system by prenatal testosterone exposure, may also contribute to sex differences in DE prevalence.

Puberty and the genetic diathesis of disordered eating attitudes and behaviors.

Twin studies from the Minnesota Twin Family Study (MTFS) suggest negligible genetic effects on eating pathology before puberty but increased genetic effects during puberty. However, an independent study found no pubertal differences in genetic and environmental effects (R. Rowe, A. Pickles, E. Simonoff, C. M. Bulik, & J. L. Silberg, 2002). Discrepant results may be due to methodological differences. The MTFS studies divided twins at mid-puberty, whereas R. Rowe et al. (2002) divided twins based on menarche alone. In the present study, the authors aimed to reconcile discrepant findings by examining differences in etiologic effects for disordered eating attitudes and behaviors (i.e., levels of weight preoccupation, body dissatisfaction, binge eating, compensatory behaviors) using both classification methods in a new sample of 656 female twins. Using the MTFS method (i.e., K. L. Klump, M. McGue, & W. G. Iacono, 2003), the authors observed nominal genetic effects in prepubertal twins but significant genetic effects in pubertal and young adult twins. Conversely, genetic effects were moderate and equal in all groups using the R. Rowe et al. (2002) method. Findings highlight the potentially important role of puberty in the genetic diathesis of disordered eating attitudes and behaviors and the need to use early indicators of pubertal status in studies of developmental effects.