Pair-bonding has been suggested to be a critical factor in the evolutionary development of the social brain. The brain neuropeptide arginine vasopressin (AVP) exerts an important influence on pair-bonding behavior in voles. There is a strong association between a polymorphic repeat sequence in the 5 flanking region of the gene (avpr1a) encoding one of the AVP receptor subtypes (V1aR), and proneness for monogamous behavior in males of this species. It is not yet known whether similar mechanisms are important also for human pair-bonding. Here, we report an association between one of the human AVPR1A repeat polymorphisms (RS3) and traits reflecting pair-bonding behavior in men, including partner bonding, perceived marital problems, and marital status, and show that the RS3 genotype of the males also affects marital quality as perceived by their spouses. These results suggest an association between a single gene and pair-bonding behavior in humans, and indicate that the well characterized influence of AVP on pair-bonding in voles may be of relevance also for humans.monogamy ͉ neuropeptide ͉ polymorphism ͉ social behavior P rimate social organization is often characterized by bonded relationships, and recent analyses suggest that it may have been the particular demands for pair-bonding behavior that triggered the evolutionary development of the primate social brain (1). The brain neuropeptide arginine vasopressin (AVP), acting through the receptor subtype V1aR, plays a key role in the regulation of pairbonding behavior in male rodents, as revealed by a series of elegant studies on closely related vole species, i.e., montane voles (Microtus montanus), meadow voles (Microtus pennsylvanicus), and prairie voles (Microtus ochrogaster) (2). In prairie voles, which in contrast to montane and meadow voles are socially monogamous and highly social, pair-bond formation and related behaviors are facilitated by AVP and prevented by a V1aR antagonist (3). Supporting the theory that the striking difference in pair-bonding between monogamous and nonmonogamous voles is related to the influence of AVP on this behavior, the neuroanatomical distribution of V1aR differs considerably between these vole species (4) and is associated with sexual and social fidelity among prairie voles (5). Moreover, partner preference is enhanced in the nonmonogamous meadow vole when the V1aR density is increased in relevant brain areas by using viral vector gene transfer (6). Although there are no major differences in the coding sequence of the gene encoding V1aR (avpr1a) between prairie, montane or meadow voles, the former species displays a 428-base pair sequence in the 5Ј flanking region that is not found in the latter two species. When the avpr1a of the prairie vole, including the sequence in the 5Ј region, is transgenically inserted into the nonmonogamous species mouse (7), more pronounced social behavior, similar to that displayed by prairie voles, is generated. Furthermore, variation in the 5Ј flanking region of prairie vole avpr1a affects brain ex...

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Objective. The transmission of anxiety within families is well-recognised, but the underlying processes are poorly understood. Twin studies of adolescent anxiety demonstrate both genetic and environmental influence, and multiple aspects of parenting are associated with offspring anxiety. To date, the Children-ofTwins design has not been used to evaluate the relative contributions of genetic versus direct transmission of anxiety from parents to their offspring. Method. Anxiety and neuroticism measures were completed by 385 monozygotic and 486 dizygotic same-sex twin families (37% male twin pair families) from the Twin and Offspring Study in Sweden (TOSS). Structural equation models tested for the presence of both genetic and environmental transmission from one generation to the next. Results. For both anxiety and neuroticism the models provide support for significant direct environmental transmission from parents to their adolescent offspring. In contrast there was no evidence of significant genetic transmission. Conclusions. The association between parental and offspring anxiety largely arises due to a direct association between parents and their children independent of genetic confounds. The lack of genetic transmission may reflect there being different genetic effects on these traits in adolescence and adulthood. Direct environmental transmission is in line with developmental theories of anxiety suggesting that children and adolescents learn anxious behaviours from their parents via a number of pathways such as modelling. Future analyses should combine children-of-twins data with child twin data in order to examine whether this direct effect solely represents parental influences on the offspring or whether it also includes child/adolescent anxiety evoking parental anxiety.

This study presents an extended children-of-twins model, allowing us to test the direction of the association between parenting and child adjustment. Three mechanisms can be examined: direct phenotypic influence of parenting on child behavior (controlling for both parental and child genotype), passive genotype-environment correlation and evocative genotype-environment correlation. This model has been tested using Monte-Carlo simulations. We generated datasets consisting of 1000 twin parent pairs together with their children, and 1000 twin children pairs together with their parents. These simulated datasets were then used to estimate the model and the procedure was repeated 1000 times. The simulation results showed that our model recovered the true values of parameters with high precision. The model was also applied to an observed dataset to analyze, as a first example, the association between maternal emotional overinvolvement and child internalizing problems. The results showed that this association was best explained by evocative genotype-environment correlation.

Objective Callous-unemotional behaviors in early childhood identify children at high risk for severe trajectories of antisocial behavior and callous-unemotional traits that culminate in later diagnoses of conduct disorder, antisocial personality disorder, and psychopathy. Studies have demonstrated high heritability of callous-unemotional traits, but little research has examined specific heritable pathways to earlier callous-unemotional behaviors. Additionally, studies indicate that positive parenting protects against the development of callous-unemotional traits, but genetically informed designs have not been used to confirm that these relationships are not the product of gene-environment correlations. Method Using an adoption cohort of 561 families, biological mothers reported their history of severe antisocial behavior. Observations of adoptive mother positive reinforcement at 18 months were examined as predictors of callous-unemotional behaviors when children were 27 months old. Results Biological mother antisocial behavior predicted early callous-unemotional behaviors despite having no or limited contact with offspring. Adoptive mother positive reinforcement protected against early callous-unemotional behaviors in children not genetically related to the parent. High levels of adoptive mother positive reinforcement buffered the effects of heritable risk for callous-unemotional behaviors posed by biological mother antisocial behavior. Conclusions The findings elucidate heritable and non-heritable pathways to early callous-unemotional behaviors. The results provide a specific heritable pathway to callous-unemotional behaviors and compelling evidence that parenting is an important non-heritable factor in the development of callous-unemotional behaviors. As positive reinforcement buffered heritable risk for callous-unemotional behaviors, these findings have important translational implications for the prevention of trajectories to serious antisocial behavior.