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Heterogeneity in the development of proactive and reactive aggression in childhood: Common and specific genetic - environmental factors.

ABSTRACT: Few studies are grounded in a developmental framework to study proactive and reactive aggression. Furthermore, although distinctive correlates, predictors and outcomes have been highlighted, proactive and reactive aggression are substantially correlated. To our knowledge, no empirical study has examined the communality of genetic and environmental underpinning of the development of both subtypes of aggression. The current study investigated the communality and specificity of genetic-environmental factors related to heterogeneity in proactive and reactive aggression's development throughout childhood.Participants were 223 monozygotic and 332 dizygotic pairs. Teacher reports of aggression were obtained at 6, 7, 9, 10 and 12 years of age. Joint development of both phenotypes were analyzed through a multivariate latent growth curve model. Set point, differentiation, and genetic maturation/environmental modulation hypotheses were tested using a biometric decomposition of intercepts and slopes.Common genetic factors accounted for 64% of the total variation of proactive and reactive aggression's intercepts. Two other sets of uncorrelated genetic factors accounted for reactive aggression's intercept (17%) on the one hand, and for proactive (43%) and reactive (13%) aggression's slopes on the other. Common shared environmental factors were associated with proactive aggression's intercept (21%) and slope (26%) and uncorrelated shared environmental factors were also associated with reactive aggression's slope (14%). Common nonshared environmental factors explained most of the remaining variability of proactive and reactive aggression slopes.A genetic differentiation hypothesis common to both phenotypes was supported by common genetic factors associated with the developmental heterogeneity of proactive and reactive aggression in childhood. A genetic maturation hypothesis common to both phenotypes, albeit stronger for proactive aggression, was supported by common genetic factors associated with proactive and reactive aggression slopes. A shared environment set point hypothesis for proactive aggression was supported by shared environmental factors associated with proactive aggression baseline and slope. Although there are many common features to proactive and reactive aggression, the current research underscores the advantages of differentiating them when studying aggression.

SUBMITTER: Paquin S

PROVIDER: S-EPMC5718601 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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Heterogeneity in the development of proactive and reactive aggression in childhood: Common and specific genetic - environmental factors.

Paquin Stéphane S Lacourse Eric E Brendgen Mara M Vitaro Frank F Dionne Ginette G Tremblay Richard Ernest RE Boivin Michel M

PloS one 20171206 12

<h4>Background</h4>Few studies are grounded in a developmental framework to study proactive and reactive aggression. Furthermore, although distinctive correlates, predictors and outcomes have been highlighted, proactive and reactive aggression are substantially correlated. To our knowledge, no empirical study has examined the communality of genetic and environmental underpinning of the development of both subtypes of aggression. The current study investigated the communality and specificity of g ...[more]

PMID: 29211810

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Project description:The Taylor Aggression Paradigm (TAP) has been widely used to measure reactive aggression following provocation during competitive interactions. Besides being reactive, aggression can be goal-directed (proactive aggression). Our study presents a novel paradigm to investigate proactive aggression during competitive interactions. Sixty-seven healthy participants competed in two modified versions of the TAP against an ostensible opponent while skin conductance responses (SCRs) were recorded. During the proactive TAP (pTAP), only the participant could interfere with the ostensible opponent's performance by blurring the screen. In the reactive TAP (rTAP), the opponent repeatedly provoked the participant by blurring the screen of the participant, impeding their chance to win. In both versions, the blurriness levels chosen by the participant served as a measure of aggression (unprovoked in the pTAP and provoked in the rTAP). In the pTAP, trial-by-trial mixed model analyses revealed higher aggression with higher self-reported selfishness. SCRs decreased with increasing proactive aggression. An interaction effect between gender and proactive aggression for the SCRs revealed increased SCRs at higher aggression levels in females, but lower SCRs at higher aggression levels in males. In the rTAP, SCRs were not associated with reactive aggression but aggression increased with increasing provocation and especially after losing against the opponent when provoked. While males showed higher aggression levels than females when unprovoked, reactive aggression increased more strongly in females with higher provocation. Mean levels of aggression in both tasks showed a high positive correlation. Our results highlight that, despite being intercorrelated and both motivated by selfishness, proactive and reactive aggression are differentially influenced by gender and physiological arousal. Proactive aggression is related to lower physiological arousal, especially in males, with females showing the opposite association. Reactive aggressive behavior is a result of individual responses to provocation, to which females seem to be more sensitive.

Project description:ImportanceKnowledge about factors associated with persistence of atopic dermatitis (AD) during childhood is sparse.ObjectiveTo explore heritable, environmental, and clinical factors associated with persistent AD based on 13 years' follow-up of an at-risk birth cohort.Design, setting, and participantsIn the Copenhagen Prospective Study on Asthma in Childhood 2000 (COPSAC2000) clinical birth cohort study, 411 children born to mothers with asthma were followed up until the age of 13 years at a clinical research unit in Copenhagen, Denmark, from August 1998 to June 2015. Atopic dermatitis was diagnosed prospectively during close clinical follow-up according to the criteria of Hanifin and Rajka. Data were gathered on parental history, social circumstances, and environmental factors through parent interviews. The cohort was followed up with biannual visits to the clinic until the age of 7 years and were seen again at age 13 years. Data were analyzed from August 2015 to January 2018.Main outcomes and measuresAtopic dermatitis was diagnosed using Hanifin and Rajka major and minor criteria, and severity was determined by Scoring Atopic Dermatitis (SCORAD) index, with possible scores from 0 to 83, with higher scores indicating more severe AD.ResultsOf the 411 children in the cohort, 203 (49.4%) were male and 186 (45.3%) were diagnosed with AD before the age of 13 years; 40 of 166 children (24.1%) had persistent AD at the age of 13 years, and 126 (76.0%) experienced remission. Factors associated with persistent AD to age 13 years included heritability, environmental exposures, asthma and allergic sensitization, clinical presentation at the time of diagnosis, the composition of Hanifin and Rajka diagnostic minor criteria, and AD severity according to SCORAD. A higher AD genetic risk score was associated with an increased the risk for persistent AD (multivariable odds ratio [OR], 1.8; 95% CI, 1.1-2.9; P = .02), together with paternal asthma (multivariable OR, 3.7; 95% CI, 1.2-11.5; P = .02); paternal AD (multivariable OR, 6.2; 95% CI, 1.17-23.2; P = .007), and higher social circumstances (multivariable OR, 1.6; 95% CI, 1.0-2.5; P = .05). Particular clinical presentations at time of diagnosis were also associated with specific minor criteria of Hanifin and Rajka (Dennie-Morgan and anterior neck folds, white dermographism, intolerance to wool, itching when sweating, tendency to skin infection, food intolerance, and food allergy) (OR, 2.6; 95% CI, 1.1-6.2; P = .03) as well as increased severity at diagnosis (OR, 1.1; 95% CI, 1.0-1.1; P = .007).Conclusions and relevanceIn a birth cohort of children at risk for asthma who received close clinical follow-up to age 13 years, known genetic AD risk variants, paternal asthma and AD, high social circumstances, diagnostic minor criteria, and disease severity at onset were associated with persistent AD at age 13 years. These findings may be applied in clinical practice to evaluate the likely disease course for individual patients.

Project description:Childhood aggressive behavior (AGG) has a substantial heritability of around 50%. Here we present a genome-wide association meta-analysis (GWAMA) of childhood AGG, in which all phenotype measures across childhood ages from multiple assessors were included. We analyzed phenotype assessments for a total of 328 935 observations from 87 485 children aged between 1.5 and 18 years, while accounting for sample overlap. We also meta-analyzed within subsets of the data, i.e., within rater, instrument and age. SNP-heritability for the overall meta-analysis (AGGoverall) was 3.31% (SE = 0.0038). We found no genome-wide significant SNPs for AGGoverall. The gene-based analysis returned three significant genes: ST3GAL3 (P = 1.6E-06), PCDH7 (P = 2.0E-06), and IPO13 (P = 2.5E-06). All three genes have previously been associated with educational traits. Polygenic scores based on our GWAMA significantly predicted aggression in a holdout sample of children (variance explained = 0.44%) and in retrospectively assessed childhood aggression (variance explained = 0.20%). Genetic correlations (rg) among rater-specific assessment of AGG ranged from rg = 0.46 between self- and teacher-assessment to rg = 0.81 between mother- and teacher-assessment. We obtained moderate-to-strong rgs with selected phenotypes from multiple domains, but hardly with any of the classical biomarkers thought to be associated with AGG. Significant genetic correlations were observed with most psychiatric and psychological traits (range [Formula: see text]: 0.19-1.00), except for obsessive-compulsive disorder. Aggression had a negative genetic correlation (rg = ~-0.5) with cognitive traits and age at first birth. Aggression was strongly genetically correlated with smoking phenotypes (range [Formula: see text]: 0.46-0.60). The genetic correlations between aggression and psychiatric disorders were weaker for teacher-reported AGG than for mother- and self-reported AGG. The current GWAMA of childhood aggression provides a powerful tool to interrogate the rater-specific genetic etiology of AGG.

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Heterogeneity in the development of proactive and reactive aggression in childhood: Common and specific genetic - environmental factors.

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Heterogeneity in the development of proactive and reactive aggression in childhood: Common and specific genetic - environmental factors.

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