scholarly journals Prosocial peer affiliation suppresses genetic influences on non-aggressive antisocial behaviors during childhood

2013 ◽  
Vol 44 (4) ◽  
pp. 821-830 ◽  
Author(s):  
S. A. Burt ◽  
K. L. Klump
Keyword(s):  
Antisocial Behavior ◽  
Genetic Risk ◽  
Genetic Influences ◽  
Michigan State University ◽  
Environment Interaction ◽  
State University ◽  
Antisocial Behaviors ◽  
Deviant Peer Affiliation ◽  
Peer Affiliation ◽  
Gene Environment

BackgroundAvailable research has suggested that affiliation with prosocial peers reduces child and adolescent antisocial behavior. However, the etiologic mechanisms driving this association remain unclear. The current study sought to evaluate whether this association takes the form of a gene–environment interaction (G × E) in which prosocial peer affiliation acts to reduce the consequences of genetic risk for non-aggressive antisocial behavior during childhood.MethodOur sample consisted of 500 twin pairs aged 6–10 years from the Michigan State University Twin Registry (MSUTR).ResultsThe results robustly support moderation by prosocial peer affiliation. Genetic influences on non-aggressive antisocial behavior were observed to be several times larger in those with lower levels of prosocial peer affiliation than in those with higher levels of prosocial peer affiliation. This pattern of results persisted even after controlling for gene–environment correlations and deviant peer affiliation, and when restricting our analyses to those twins who shared all or nearly all of their friends.ConclusionsSuch findings not only suggest that prosocial peer affiliation moderates genetic influences on non-aggressive antisocial behaviors during childhood but also provide support for the theoretical notion that protective environmental experiences may exert their influence by promoting resilience to genetic risk.

scholarly journals The Etiological Moderation of Aggressive and Nonaggressive Antisocial Behavior by Age

2009 ◽  
Vol 12 (4) ◽  
pp. 343-350 ◽  
Author(s):  
S. Alexandra Burt ◽  
Kelly L. Klump
Keyword(s):  
Antisocial Behavior ◽  
Environmental Influences ◽  
Genetic Influences ◽  
Michigan State University ◽  
State University ◽  
Genetic Expression ◽  
Twin Registry ◽  
Age Related ◽  
Rule Breaking ◽  
Additional Support

AbstractA recent study has suggested that aggressive (AGG) and non-aggressive, rule-breaking (RB) antisocial behavior evidence differential and subtype-specific patterns of genetic expression during development. Namely, although genetic influences on RB increase dramatically during early- to mid-adolescence, genetic influences on AGG appear to remain stable. As no other study has examined age-related change in AGG versus RB, more research is clearly needed before any firm conclusions can be drawn. The current study thus examined whether and how age impacted genetic and environmental influences on AGG and RB in a sample of 252 10- to 15-year-old twin pairs assessed as part of the Michigan State University Twin Registry (MSUTR). Results constructively replicated and extended prior findings, indicating that while the magnitude of genetic and environmental influences on AGG remained stable across adolescence, genetic influences on RB increased dramatically with age. Such findings provide additional support for etiological distinctions within the broader construct of antisocial behavior based on the presence or absence of aggression, and offer insights into the expression of genetic influences during development.

scholarly journals Antisocial peer affiliation and externalizing disorders: Evidence for Gene × Environment × Development interaction

2016 ◽  
Vol 29 (1) ◽  
pp. 155-172 ◽  
Author(s):  
Diana R. Samek ◽  
Brian M. Hicks ◽  
Margaret A. Keyes ◽  
William G. Iacono ◽  
Matt McGue
Keyword(s):  
Substance Use ◽  
Antisocial Behavior ◽  
Substance Use Disorders ◽  
Critical Period ◽  
Externalizing Disorders ◽  
Childhood And Adolescence ◽  
Environment Interaction ◽  
Peer Affiliation ◽  
Gene Environment Interaction ◽  
Gene Environment

AbstractGene × Environment interaction contributes to externalizing disorders in childhood and adolescence, but little is known about whether such effects are long lasting or present in adulthood. We examined gene–environment interplay in the concurrent and prospective associations between antisocial peer affiliation and externalizing disorders (antisocial behavior and substance use disorders) at ages 17, 20, 24, and 29. The sample included 1,382 same-sex twin pairs participating in the Minnesota Twin Family Study. We detected a Gene × Environment interaction at age 17, such that additive genetic influences on antisocial behavior and substance use disorders were greater in the context of greater antisocial peer affiliation. This Gene × Environment interaction was not present for antisocial behavior symptoms after age 17, but it was for substance use disorder symptoms through age 29 (though effect sizes were largest at age 17). The results suggest adolescence is a critical period for the development of externalizing disorders wherein exposure to greater environmental adversity is associated with a greater expression of genetic risk. This form of Gene × Environment interaction may persist through young adulthood for substance use disorders, but it appears to be limited to adolescence for antisocial behavior.

The Association Between Genetic Predisposition and Parental Socialization: An Examination of Gene–Environment Correlations Using an Adoption-Based Design

2019 ◽  
Vol 64 (2-3) ◽  
pp. 187-209
Author(s):  
Rachel A. Knoblach ◽  
Joseph A. Schwartz ◽  
Marianna McBride ◽  
Kevin M. Beaver
Keyword(s):  
Antisocial Behavior ◽  
Adoptive Parents ◽  
Genetic Influences ◽  
Parental Socialization ◽  
Adult Health ◽  
Antisocial Behaviors ◽  
Gene Environment ◽  
Biological Parents ◽  
Extensive Body ◽  
Do So

An extensive body of research has examined the role that genetic influences play in the development of antisocial behavior. Even so, there remains much that is unknown regarding the intersections among antisocial behavior, environments, and genetic influences. The current study is designed to shed some light on this issue by examining whether gene–environment correlations are present in the lives of adopted adolescents. More specifically, this article seeks to contribute to scholarship efforts aimed at understanding whether biological parents’ antisocial behavioral phenotypes—behaviors often attributed to an increased likelihood of receiving a genetic propensity for antisocial behaviors—predict variation in environments that are experienced by their adopted-away offspring. To do so, the biological parents of adoptees were assessed and used to identify ways in which children elicit certain responses from their adoptive parents based, in part, on their genotype. Correlational analyses were calculated on a sample of adoptees (the final analytic sample ranged between n = 229 and n = 293) drawn from the National Longitudinal Study of Adolescent to Adult Health (Add Health). The results of the study revealed very little evidence of gene–environment correlations. The implications of these findings are considered.

scholarly journals Delinquent peer affiliation as an etiological moderator of childhood delinquency

2012 ◽  
Vol 43 (6) ◽  
pp. 1269-1278 ◽  
Author(s):  
S. A. Burt ◽  
K. L. Klump
Keyword(s):  
Environmental Influences ◽  
Genetic Influences ◽  
Michigan State University ◽  
Childhood And Adolescence ◽  
State University ◽  
Prior Work ◽  
Peer Affiliation ◽  
Twin Registry ◽  
Delinquent Peer ◽  
Delinquent Peers

BackgroundPrior research has indicated that affiliation with delinquent peers activates genetic influences on delinquency during adolescence. However, because other studies have indicated that the socializing effects of delinquent peers vary dramatically across childhood and adolescence, it is unclear whether delinquent peer affiliation (DPA) also moderates genetic influences on delinquency during childhood.MethodThe current study sought to evaluate whether and how DPA moderated the etiology of delinquency in a sample of 726 child twins from the Michigan State University Twin Registry (MSUTR).ResultsThe results robustly supported etiological moderation of childhood delinquency by DPA. However, this effect was observed for shared environmental, rather than genetic, influences. Shared environmental influences on delinquency were found to be several-fold larger in those with higher levels of DPA as compared to those with lower levels. This pattern of results persisted even when controlling for the overlap between delinquency and DPA.ConclusionsOur findings bolster prior work in suggesting that, during childhood, the association between DPA and delinquency is largely (although not solely) attributable to the effects of socialization as compared to selection. They also suggest that the process of etiological moderation is not specific to genetic influences. Latent environmental influences are also amenable to moderation by measured environmental factors.

Gene–environment interplay in the etiology of psychosis

2018 ◽  
Vol 48 (12) ◽  
pp. 1925-1936 ◽  
Author(s):  
Alyson Zwicker ◽  
Eileen M. Denovan-Wright ◽  
Rudolf Uher
Keyword(s):  
Environmental Factors ◽  
Genetic Risk ◽  
Environmental Exposures ◽  
Response To Treatment ◽  
Human Potential ◽  
Specific Gene ◽  
Environment Interaction ◽  
Gene Environment ◽  
Increased Risk ◽  
The Impact

AbstractSchizophrenia and other types of psychosis incur suffering, high health care costs and loss of human potential, due to the combination of early onset and poor response to treatment. Our ability to prevent or cure psychosis depends on knowledge of causal mechanisms. Molecular genetic studies show that thousands of common and rare variants contribute to the genetic risk for psychosis. Epidemiological studies have identified many environmental factors associated with increased risk of psychosis. However, no single genetic or environmental factor is sufficient to cause psychosis on its own. The risk of developing psychosis increases with the accumulation of many genetic risk variants and exposures to multiple adverse environmental factors. Additionally, the impact of environmental exposures likely depends on genetic factors, through gene–environment interactions. Only a few specific gene–environment combinations that lead to increased risk of psychosis have been identified to date. An example of replicable gene–environment interaction is a common polymorphism in theAKT1gene that makes its carriers sensitive to developing psychosis with regular cannabis use. A synthesis of results from twin studies, molecular genetics, and epidemiological research outlines the many genetic and environmental factors contributing to psychosis. The interplay between these factors needs to be considered to draw a complete picture of etiology. To reach a more complete explanation of psychosis that can inform preventive strategies, future research should focus on longitudinal assessments of multiple environmental exposures within large, genotyped cohorts beginning early in life.

scholarly journals Genetic Risk for Schizophrenia, Obstetric Complications, and Adolescent School Outcome: Evidence for Gene-Environment Interaction

2012 ◽  
Vol 39 (5) ◽  
pp. 1067-1076 ◽  
Author(s):  
Jennifer K. Forsyth ◽  
Lauren M. Ellman ◽  
Antti Tanskanen ◽  
Ulla Mustonen ◽  
Matti O. Huttunen ◽  
...  
Keyword(s):  
Genetic Risk ◽  
Obstetric Complications ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
School Outcome

scholarly journals It really does take a village: The role of neighbors in the etiology of nonaggressive rule-breaking behavior

2018 ◽  
Vol 31 (02) ◽  
pp. 713-725 ◽  
Author(s):  
S. Alexandra Burt ◽  
Amber L. Pearson ◽  
Amanda Rzotkiewicz ◽  
Kelly L. Klump ◽  
Jenae M. Neiderhiser
Keyword(s):  
Dynamic Networks ◽  
Sensitivity Analyses ◽  
Genetic Influences ◽  
Michigan State University ◽  
State University ◽  
Geographic Proximity ◽  
Self Reports ◽  
Contagion Model ◽  
Rule Breaking

AbstractAlthough there is growing recognition that disadvantaged contexts attenuate genetic influences on youth misbehavior, it is not yet clear how this dampening occurs. The current study made use of a “geographic contagion” model to isolate specific contexts contributing to this effect, with a focus on nonaggressive rule-breaking behaviors (RB) in the families’ neighbors. Our sample included 847 families residing in or near modestly-to-severely disadvantaged neighborhoods who participated in the Michigan State University Twin Registry. Neighborhood sampling techniques were used to recruit neighbors residing within 5km of a given family (the mean number of neighbors assessed per family was 13.09; range, 1–47). Analyses revealed clear evidence of genotype–environment interactions by neighbor RB, such that sibling-level shared environmental influences on child RB increased with increasing neighbor self-reports of their own RB, whereas genetic influences decreased. Moreover, this moderation appeared to be driven by geographic proximity to neighbors. Sensitivity analyses further indicated that this effect was specifically accounted for by higher levels of neighbor joblessness, rather than elements of neighbor RB that would contribute to neighborhood blight or crime. Such findings provocatively suggest that future genotype–environment interactions studies should integrate the dynamic networks of social contagion theory.

scholarly journals The effects of polygenic risk for psychiatric disorders and smoking behaviour on psychotic experiences in UK Biobank

2019 ◽  
Author(s):  
Judit García-González ◽  
Julia Ramírez ◽  
David M. Howard ◽  
Caroline H Brennan ◽  
Patricia B. Munroe ◽  
...  
Keyword(s):  
Psychiatric Disorders ◽  
Genetic Risk ◽  
Maternal Smoking ◽  
Smoking Status ◽  
Smoking Behaviour ◽  
Environment Interaction ◽  
Uk Biobank ◽  
Psychotic Experiences ◽  
Gene Environment Interaction ◽  
Gene Environment

ABSTRACTWhile psychotic experiences are core symptoms of mental health disorders like schizophrenia, they are also reported by 5-10% of the population. Both smoking behaviour and genetic risk for psychiatric disorders have been associated with psychotic experiences, but the interplay between these factors remains poorly understood. We tested whether smoking status, maternal smoking around birth, and number of packs smoked/year were associated with lifetime occurrence of three psychotic experiences phenotypes: delusions (n=2067), hallucinations (n=6689), and any psychotic experience (delusions or hallucinations; n=7803) in 144818 UK Biobank participants. We next calculated polygenic risk scores for schizophrenia (PRSSCZ), major depression (PRSDEP) and attention deficit hyperactivity disorder (PRSADHD) in the UK Biobank participants to assess whether association between smoking and psychotic experiences was attenuated after adjustment of diagnosis of psychiatric disorders and the PRSs. Finally, we investigated whether smoking exacerbates the effects of genetic predisposition on the psychotic phenotypes in gene-environment interaction models. Smoking status, maternal smoking, and number of packs smoked/year were significantly associated with psychotic experiences (p<1.77×10−5). Except for packs smoked/year, effects were attenuated but remained significant after adjustment for diagnosis of psychiatric disorders and PRSs (p<1.99×10−3). Gene-environment interaction models showed the effects of PRSDEP and PRSADHD(but not PRSSCZ) on delusions (but not hallucinations) were significantly greater in current smokers compared to never smokers (p<0.0028). There were no significant gene-environment interactions for maternal smoking nor for number of packs smoked/year. Our results suggest that both genetic risk of psychiatric disorders and smoking status may have independent and synergistic effects on specific types of psychotic experiences.

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