Father-child transmission of antisocial behavior: the moderating role of father's presence in the home.
ABSTRACT To demonstrate an environmental effect of being raised by an antisocial father and to test whether the transmission of antisocial behavior from father to child is moderated by the father's presence in the home.
A community sample of male and female 11- and 17-year-old twins and their biological parents participating in the Minnesota Twin Family Study was used. A series of hierarchical linear regression models was used to examine the relationship between father antisociality and his children's externalizing psychopathology and to determine whether the father's time spent in the home moderated this relationship. Models controlled for the child's sex.
A significant main effect of both father's antisociality and father's presence on the children's externalizing psychopathology was found: Children born to antisocial fathers evidenced higher rates of externalizing behavior, and children raised without their biological father in the home exhibited more externalizing behaviors. The interaction was also significant such that the association between father and child antisociality was stronger when the father was present for a longer period of the child's life. Furthermore, when fathers show high levels of antisociality, fathers' presence appears to have deleterious rather than beneficial effects on child behavior.
The present results suggest the transmission of antisociality from father to child is at least partially environmentally moderated.
SourceAvailable from: Arjan Blokland[Show abstract] [Hide abstract]
ABSTRACT: This study first examines the effects of parental divorce and paternal crime on offspring offending. Then, it tests whether parental divorce moderates the intergenerational transmission of crime. Diversity within the offending population is taken into account by examining whether effects are different for fathers who commit crimes at different points of the life-course and by distinguishing between violent and non-violent offending. A sample of 2374 individuals from three consecutive generations from 198 Dutch families was used. The results show that parental divorce increases offspring non-violent offending, but does not increase offspring violence after controlling for parental violence. Moreover, the intergenerational transmission of violence is moderated by parental divorce: empirical evidence for intergenerational transmission of violence is only found for children who did not experience parental divorce during their youth. This moderating effect of parental divorce is even stronger if the father committed violent crimes during the child’s youth. The moderating influence of parental divorce on the intergenerational transmission of non-violent crime is less clear, and the effects are overall stronger for violent crime than for non-violent crime. These results suggest that social learning mechanisms play an important role in the intergenerational transmission of violent crime, although genetic influences cannot be ruled out. (This article belongs to the Special Issue Parenting, Aggressive Behavior in Children, and Our Violent World)03/2015; 5(1):89-108. DOI:10.3390/soc5010089
[Show abstract] [Hide abstract]
ABSTRACT: This study developed a model linking maternal and offspring antisocial behavior, with particular emphasis on whether this link is especially strong in teenage mother–child dyads. Data were taken from a longitudinal government dataset; structural equation modeling and invariance testing was used to test the hypotheses. Good model fit indicated that maternal and offspring antisociality are linked, and antisocial behavior persists across childhood, but that these relationships are not dependent on the mother’s age at primiparity. These results suggest that although maternal behavior predicts offspring antisociality, being the child of a teenage mother is not an independent risk factor for the development of antisociality. Given that mothers in general tend to transmit their antisocial behavior patterns, intervention for antisocial behavior patterns in females before or during adolescence should contribute to a significant lessening of not only their own behavior problems, but also the incidence of antisocial behavior in their future offspring.Journal of Child and Family Studies 03/2014; 24(3). DOI:10.1007/s10826-013-9890-3 · 1.42 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: There is accumulating evidence of impairments in facial emotion recognition in adolescents with conduct disorder (CD). However, the majority of studies in this area have only been able to demonstrate an association, rather than a causal link, between emotion recognition deficits and CD. To move closer towards understanding the causal pathways linking emotion recognition problems with CD, we studied emotion recognition in the unaffected first-degree relatives of CD probands, as well as those with a diagnosis of CD. Method Using a family-based design, we investigated facial emotion recognition in probands with CD (n��=��43), their unaffected relatives (n��=��21), and healthy controls (n��=��38). We used the Emotion Hexagon task, an alternative forced-choice task using morphed facial expressions depicting the six primary emotions, to assess facial emotion recognition accuracy. Relative to controls, the CD group showed impaired recognition of anger, fear, happiness, sadness and surprise (all p��<��0.005). Similar to probands with CD, unaffected relatives showed deficits in anger and happiness recognition relative to controls (all p��<��0.008), with a trend toward a deficit in fear recognition. There were no significant differences in performance between the CD probands and the unaffected relatives following correction for multiple comparisons. These results suggest that facial emotion recognition deficits are present in adolescents who are at increased familial risk for developing antisocial behaviour, as well as those who have already developed CD. Consequently, impaired emotion recognition appears to be a viable familial risk marker or candidate endophenotype for CD.