Extant research has highlighted meaningful distinctions in the correlates, developmental trajectories, and etiologies of physically aggressive (AGG) as compared to non-aggressive rule-breaking (RB) ...antisocial behavior. AGG is a highly heritable behavioral dimension that emerges in early childhood and exhibits specific ties to negative emotionality and executive dysfunction. Although the frequency of aggressive behaviors decreases after early childhood, those who are most aggressive early in life typically continue to aggress at relatively high rates across the lifespan. By contrast, RB demonstrates specific associations with impulsivity, is most frequent during adolescence, and evidences more moderate levels of stability and stronger environmental influences as compared to AGG. These etiological and developmental differences link up quite well to Moffitt's (1993) developmental taxonomy of antisocial behavior, providing a clear theoretical basis for examining differences between AGG and RB. Perhaps more importantly, however, the link between AGG/RB and Moffitt's taxonomy allows us to conceptualize her categorical taxonomy in dimensional terms, an important development given the recent emphasis on dimensional conceptualizations of psychopathology. Available evidence further indicates that neither AGG nor RB is redundant with callous–unemotional traits. The current review thus underscores the clear advantages of differentiating between AGG and RB when studying antisocial behavior.
► Aggression (AGG) is highly heritable and quite stable over time. ► Rule-breaking (RB) evidences moderate levels of stability and genetic influence. ► AGG emerges in early childhood, whereas RB typically onsets during adolescence. ► Age-of-onset types can be reframed via AGG and RB behavioral dimensions.
Behavioral genetic research has concluded that the more important environmental influences result in differences between siblings (referred to as
nonshared
;
e
2
), whereas environmental influences ...that create similarities between siblings (referred to as
shared
;
c
2
) are indistinguishable from zero. However, there is mounting evidence that during childhood and adolescence,
c
2
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
c
2
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,
c
2
generally ranged from 10%-30% of the variance. Importantly,
c
2
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.
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CEKLJ, FFLJ, NUK, ODKLJ, PEFLJ
Decades of research have indicated the foundational importance of parenting to offspring outcomes during childhood and beyond. Unearthing the specific origins of parenting is therefore a critically ...important research objective. Extant research on this topic has suggested that parenting behaviors are multidetermined (Belsky, 1984) and are associated with a wide range of contextual and familial characteristics (e.g., ethnicity, community, family financial stress), as well as characteristics of the parents (e.g., personality) and their children (e.g., temperament). Behavioral genetic studies have further indicated that parenting behaviors are in fact heritable-that is, individual differences in parenting are at least partially a function of genetic differences between persons. Critically, however, the estimates of these genetic influences have varied dramatically across studies. It is also unclear how factors such as parent gender, child age, and methodological considerations may impact genetic influences on parenting behavior. In the current set of meta-analyses, we sought to quantitatively synthesize twin and adoption studies (n = 56) examining the etiology of parenting behavior, with the goal of more definitively cataloguing genetic and environmental effects on parenting. Results reveal significant effects of parental genetic makeup on parental behavior, but also highlight the genetic makeup of the child as a particularly prominent source of genetic transmission (via evocative gene-environment correlation). Environmental contributions to parenting also emerged as important, including both shared and nonshared environmental effects. Theoretical implications of these findings are discussed.
Full text
Available for:
CEKLJ, FFLJ, NUK, ODKLJ, PEFLJ
Callous-unemotional (CU) traits increase risk for children to develop severe childhood aggression and conduct disorder. CU traits are typically described as highly heritable, and debate continues ...about whether the parenting environment matters in their etiology. Strong genetically informed designs are needed to test for the presence of environmental links between parenting practices and CU traits. Our objective was to determine whether parental harshness and parental warmth were related to children's aggression or CU traits when accounting for genetically mediated effects.
We examined 227 monozygotic twin pairs (454 children) drawn from population-based and at-risk samples of twin families, leading to oversampling of twins living in poverty. We computed multi-informant difference scores combining mother and father reports of their harshness and warmth toward each twin, and differences in mother reports of each twin's aggression and CU traits.
Twin differences in parental harshness were related to differences in both aggression and CU traits, such that the twin who received harsher parenting had higher aggression and more CU traits. Differences in parental warmth were uniquely related to differences in CU traits, such that the twin receiving warmer parenting evidenced lower CU traits. These effects were not moderated by child sex, age, or family income, with the exception that the relationship between differential parental harshness and differential child aggression was stronger among low-income families.
Parenting is related to child CU traits and aggression, over and above genetically mediated effects, with low parental warmth being a unique environmental correlate of CU traits.
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.
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. (Contains 4 tables.)
The aggressive and rule-breaking behaviors that constitute youth antisocial behavior (ASB) are shaped by intertwined genetic, developmental, familial, spatial, temporal, cultural, interpersonal, and ...contextual influences operating across multiple levels of analysis. Genetic influences on ASB, for example, manifest in different ways during different developmental periods, and do so in part as a function of exposure to harsh parenting, delinquent peers, and disadvantaged neighborhoods. There is also clear evidence documenting societal effects, time-period effects, sex-assigned-at-birth effects, and cohort effects, all of which point to prominent (and possibly interconnected) cultural influences on ASB. In short, ASB is shaped by individuals' current and prior environmental experiences, genetic risks, and the time and place in which they live. This review seeks to illuminate already documented instances of interplay among the multilevel etiologic forces impinging on youth ASB, with the goal of facilitating additional research.
Background
Behavioral genetic research has historically concluded that the more important environmental influences were nonshared or result in differences between siblings, whereas environmental ...influences that create similarities between siblings (referred to as shared environmental influences) were indistinguishable from zero. Recent theoretical and meta‐analytic work {Burt. Psychological Bulletin 135 (2009) 608} has challenged this conclusion as it relates to child and adolescent psychopathology, however, arguing that the shared environment is a moderate, persistent, and identifiable source of individual differences in such outcomes prior to adulthood.
Methods
The current review seeks to bolster research on the shared environment by highlighting both the logistic advantages inherent in studies of the shared environment, as well as the use of nontraditional but still genetically informed research designs to study shared environmental influences.
Results
Although often moderate in magnitude prior to adulthood and free of unsystematic measurement error, shared environmental influences are nevertheless likely to have been underestimated in prior research. Moreover, the shared environment is likely to include proximal effects of the family, as well as the effects of more distal environmental contexts such as neighborhood and school. These risk and protective factors could influence the child either as main effects or as moderators of genetic influence (i.e. gene‐environment interactions). Finally, because the absence of genetic relatedness in an otherwise nonindependent dataset also qualifies as ‘genetically informed’, studies of the shared environment are amenable to the use of novel and non‐traditional designs (with appropriate controls for selection).
Conclusions
The shared environment makes important contributions to most forms of child and adolescent psychopathology. Empirical examinations of the shared environment would thus be of real and critical value for understanding the development and persistence of common mental health issues prior to adulthood.
Twin and adoption studies compare the similarities of people with differing degrees of relatedness to estimate genetic and environmental contributions to trait population variance. The analytic ...workhorse of these kinds of variance-focused designs is the intraclass correlation, which estimates similarity between pairs of individuals. Group means, by contrast, play no overt role in estimating genetic and environmental influences. Although this focus on variance has made very important contributions to understanding psychological characteristics, we contend that the exclusion of mean effects from behavioral genetic designs may have obscured key environmental influences and impeded full appreciation of the ubiquity and nature of gene–environment interplay in human outcomes. We provide empirical examples already in the literature and a theoretical framework for thinking through the incorporation of mean effects using largely forgotten, non-Mendelian theory regarding how genes influence human outcomes. We conclude that the field needs to develop models capable of fully incorporating mean effects into twin and adoption studies.
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