Effects of Parenting and Community Violence on Aggression-Related Social Goals: a Monozygotic Twin Differences Study.

Community violence exposure and harsh parenting have been linked to maladaptive outcomes, possibly via their effects on social cognition. The Social Information Processing (SIP) model has been used to study distinct socio-cognitive processes, demonstrating links between community violence exposure, harsh parenting, and maladaptive SIP. Though much of this research assumes these associations are causal, genetic confounds have made this assumption difficult to rigorously test. Comparisons of discordant monozygotic (MZ) twins provide one empirical test of possible causality, as differences between MZ twins must be environmental in origin. The present study examined effects of parenting and community violence exposure on SIP - specifically aggressive and avoidant social goals - in a sample of 426 MZ twin dyads (N = 852 twins, 48% female). Phenotypically, we found that lower positive parenting and greater harsh parenting were associated with greater endorsement of dominance and revenge goals. We also found that indirect and direct community violence exposure was associated with greater endorsement of avoidance goals. Using an MZ difference design, we found that the relationships between lower levels of positive parenting and endorsement of dominance and revenge goals were due, in part, to environmental processes. Moreover, the relationships between the impact of indirect and direct community violence exposure and avoidance goals, as well as between the impact of indirect community violence exposure and revenge goals, appeared to be due to non-shared environmental processes. Our results establish social and contextual experiences as important environmental influences on children's social goals, which may increase risk for later psychopathology.

No sex differences in the origins of covariation between social and physical aggression.

BACKGROUND: Prior work has indicated both theoretical and empirical overlap between social and physical aggression. The extent to which their covariance can be explained by the same underlying genetic or environmental factors, however, remains unclear. It is also uncertain whether or how the origins of their covariance might vary across sex. The current study sought to fill these gaps in the literature. METHODS: We examined maternal and teacher reports of youth physical and social aggression in over 1000 6-10 years old (mean age = 8.02 years) twin pairs from the Michigan State University Twin Registry. We made use of the bivariate correlated factors model to clarify the origins of their association. We further tested both sex difference and no-sex difference versions of that model to determine whether there are sex differences in the association between social and physical aggression, as often assumed. RESULTS: The covariation between social and physical aggression was due to overlapping genetic factors and common environmental conditions. Specifically, 50-57% of the genetic factors, 74-100% of the shared environmental factors, and 28-40% of the unique environmental factors influencing physical aggression also influenced social aggression according to both mother and teacher reports. These shared etiological factors did not differ across sex. CONCLUSIONS: These findings argue against the common assumption that social aggression is the 'female version' of male physical aggression, and instead suggest that social aggression may be best conceptualized as a form of antisocial behavior that shares developmental pathways with other manifestations of externalizing pathology.

Special Editorial: Open science and the Journal of Child Psychology & Psychiatry - next steps?

The JCPP works at the cutting edge of clinical science to publish ground-breaking research across the full range of topics in the field of child psychology and psychiatry. As JCPP editors, who are also active researchers in our own right, we are conscious of the threat posed to our field by what has come to be known as the reproducibility crisis - the fact that many published findings, initially trumpeted as important developments in the field, cannot be replicated and are therefore likely to be spurious (Nature Human Behaviour, 1, 2017, 21). The JCPP is conscious of its responsibility to play its part in addressing this issue as best it can. The roots of the problem are complex and its causes multifaceted. As one part of its response, the JCPP embraces the principles of open science and encourage preregistration of study protocols. Furthermore, we are working towards implementing new systems to promote preregistration with the hope of increasing scientific transparency and accountability and reducing the risks of selective reporting and posthoc rationalisation of findings (Journal of Child Psychology & Psychiatry, 59, 2018, 1).

Associations between birth size and later height from infancy through adulthood: An individual based pooled analysis of 28 twin cohorts participating in the CODATwins project.

BACKGROUND: There is evidence that birth size is positively associated with height in later life, but it remains unclear whether this is explained by genetic factors or the intrauterine environment. AIM: To analyze the associations of birth weight, length and ponderal index with height from infancy through adulthood within mono- and dizygotic twin pairs, which provides insights into the role of genetic and environmental individual-specific factors. METHODS: This study is based on the data from 28 twin cohorts in 17 countries. The pooled data included 41,852 complete twin pairs (55% monozygotic and 45% same-sex dizygotic) with information on birth weight and a total of 112,409 paired height measurements at ages ranging from 1 to 69 years. Birth length was available for 19,881 complete twin pairs, with a total of 72,692 paired height measurements. The association between birth size and later height was analyzed at both the individual and within-pair level by linear regression analyses. RESULTS: Within twin pairs, regression coefficients showed that a 1-kg increase in birth weight and a 1-cm increase in birth length were associated with 1.14-4.25 cm and 0.18-0.90 cm taller height, respectively. The magnitude of the associations was generally greater within dizygotic than within monozygotic twin pairs, and this difference between zygosities was more pronounced for birth length. CONCLUSION: Both genetic and individual-specific environmental factors play a role in the association between birth size and later height from infancy to adulthood, with a larger role for genetics in the association with birth length than with birth weight.

Maternal warmth and directiveness jointly moderate the etiology of childhood conduct problems.

BACKGROUND: Prior studies exploring gene-environment interactions (GxE) in the development of youth conduct problems (CP) have focused almost exclusively on single-risk experiences, despite research indicating that the presence of other risk factors and or the absence of protective factors can accentuate the influence of a given risk factor on CP. The goal of the current study was to fill this gap in the literature, evaluating whether risky and protective aspects of parenting might combine to jointly moderate the etiology of CP. METHODS: The sample consisted of 500 child twin pairs from the Michigan State University Twin Registry (MSUTR). Child CP was assessed using multiple informant reports. Maternal warmth and directiveness were assessed via videotaped dyadic interactions between mothers and each of their twins. RESULTS: Biometric GxE analyses revealed that directiveness and warmth did appear to jointly moderate the etiology of CP. In particular, shared environmental influences were accentuated by colder, less directive or 'less engaged' mothering, whereas genetic influences were strongest when the child was experiencing warmer, more directive or 'more authoritative' mothering. CONCLUSIONS: Such findings serve to highlight the synergistic effects of risky and protective experiences on child outcomes. They also provide additional empirical support for the bioecological form of GxE, which postulates that, in some cases, genetic influences may be most strongly expressed in the presence of low-risk environments.

Etiologic relationships between anxiety and dimensions of maladaptive perfectionism in young adult female twins.

BACKGROUND: Theory and research suggest that maladaptive perfectionism, specifically, concerns about mistakes (CM) and doubts about actions (DA), may be important etiologic and maintenance mechanisms for anxiety and its disorders. However, no studies speaking directly to the origins of the relationship, i.e. what etiologic factors underlie the phenotypic association between anxiety and maladaptive perfectionism, exist. The current study aimed to address this gap in the literature by exploring genetic and environmental relationships between anxiety symptoms and maladaptive perfectionism. METHODS: The sample consisted of 292 young adult same-sex female twins from the Michigan State University Twin Registry. Anxiety symptoms were assessed by the State Trait Anxiety Inventory-Trait version and an anxiety problems scale derived from the Young Adult Self Report. Maladaptive perfectionism was measured using the CM and DA subscales of the Frost Multidimensional Perfectionism Scale. RESULTS: Anxiety and maladaptive perfectionism were both moderately heritable, with estimates ranging from. 45 to .66. Moreover, multivariate analyses revealed that genetic factors were primarily responsible for associations between anxiety and maladaptive perfectionism (r(g) =.59-.88). CONCLUSION: This is the first study to demonstrate the role of genetic factors in the relationship between anxiety and maladaptive perfectionism. Future studies are needed to uncover the specific biologic and genetic factors that contribute to this relationship and to evaluate whether maladaptive perfectionism represents an intermediate trait or risk factor for anxiety.

Puberty moderates genetic influences on disordered eating.

BACKGROUND: Previous research suggests that genetic influences on disordered eating may be greater in pubertal than pre-pubertal girls. Although these findings are consistent with pubertal activation of genetic influences on disordered eating, earlier studies were unable to directly test this hypothesis. The purpose of the present study therefore was to directly examine this possibility by investigating whether pubertal development moderates genetic influences on disordered eating. METHOD: Participants were 510 female adolescent twins from the Minnesota Twin Family Study. Disordered eating was measured with the Total Score of the Minnesota Eating Behavior Survey, while pubertal status was assessed with the Pubertal Development Scale. RESULTS: Consistent with our hypothesis, model-fitting indicated significant increases in genetic influence on disordered eating with advancing pubertal development. CONCLUSIONS: These findings suggest that puberty influences the expression of genes for disordered eating.