AbstractGene–environment interaction effects in predicting antisocial behavior in late childhood were investigated among maltreated and nonmaltreated low-income children (N= 627,Mage = 11.27). Variants in three genes were examined: tryptophan hydroxylase 1 (TPH1), serotonin transporter linked polymorphic region (5-HTTLPR), and monoamine oxidase A (MAOA) upstream variable number tandem repeat. In addition to child maltreatment status, we considered the impact of maltreatment subtypes, developmental timing of maltreatment, and chronicity. Indicators of antisocial behavior were obtained from self-, peer, and adult counselor reports. In a series of analyses of covariance, child maltreatment and its parameters demonstrated strong main effects on early antisocial behavior as assessed by all report forms. Genetic effects operated primarily in the context of gene–environment interactions, moderating the impact of child maltreatment on outcomes. Across the three genes, among nonmaltreated children no differences in antisocial behavior were found based on genetic variation. In contrast, among maltreated children specific polymorphisms ofTPH1,5-HTTLPR, andMAOAwere each related to heightened self-report of antisocial behavior; the interaction of5-HTTLPRand developmental timing of maltreatment also indicated more severe antisocial outcomes for children with early onset and recurrent maltreatment based on genotype.TPH1and5-HTTLPRinteracted with maltreatment subtype to predict peer reports of antisocial behavior; genetic variation contributed to larger differences in antisocial behavior among abused children. TheTPH1and5-HTTLPRpolymorphisms also moderated the effects of maltreatment subtype on adult reports of antisocial behavior; again, the genetic effects were strongest for children who were abused. In addition,TPH1moderated the effect of developmental timing of maltreatment and chronicity on adult reports of antisocial behavior. The findings elucidate how genetic variation contributes to identifying which maltreated children are most vulnerable to antisocial development.

A model examining the effects of an increasing number of maltreatment subtypes experienced on antisocial behavior, as mediated by impulsivity and moderated by a polygenic index of dopaminergic genotypes, was investigated. An African American sample of children (N = 1012, M age = 10.07) with and without maltreatment histories participated. Indicators of aggression, delinquency, and disruptive peer behavior were obtained from peer and counselor rated measures to form a latent variable of antisocial behavior; impulsivity was assessed by counselor report. Five genotypes in four dopaminergic genes (DRD4, DRD2, DAT1, and COMT) conferring heightened environmental sensitivity were combined into one polygenic index. Using SEM, a first-stage, moderated-mediation model was evaluated. Age and sex were entered as covariates, both as main effects and in interaction with maltreatment and the gene index. The model had excellent fit: χ2(32, N =1012) = 86..51, p<0.001; CFI = 0.982; TLI = 0.977; RMSEA = 0.041; SRMR = 0.022. The effect of maltreatment subtypes on antisocial behavior was partially mediated by impulsivity (β= 0.173, p<0.001), and these relations were moderated by the number of differentiating dopaminergic genotypes. Specifically, a significant GxE interaction (b = 0.016, p = 0.013) indicated that the relation between maltreatment and impulsivity was stronger as children evinced more differentiating genotypes, thereby strengthening the mediational effect of impulsivity on antisocial behavior. These findings elucidate the manner by which maltreated children develop early signs of antisocial behavior, and the genetic mechanisms involved in greater vulnerability for maladaptation in impulse-control within context of child maltreatment.

This study used a structural equation mixture model to examine associations between child maltreatment, polygenic risk, and indices of adaptive functioning. Children aged 6 to 13 years (N = 1,004), half maltreated, half nonmaltreated, were recruited to attend a research day camp. Multi-informant indicators of prosocial behavior, antisocial behavior, withdrawn behavior, and depression were collected and used in a latent class analysis. Four classes emerged, characterizing “well-adjusted,” “externalizing,” “internalizing,” and “socially dominant” groups. Twelve genetic variants, previously reported in the Gene × Environment literature, were modeled as one weighted polygenic risk score. Large main effects between maltreatment and adaptive functioning were observed (Wald = 35.3, df = 3, p &lt; .0001), along with evidence of a small Gene × Environment effect (Wald = 13.5, df = 3, p = .004), adjusting for sex, age, and covariate interaction effects.

Preventive interventions that target high-risk youth, via one-size-fits-all approaches, have demonstrated modest effects in reducing rates of substance use. Recently, substance use researchers have recommended personalized intervention strategies. Central to these approaches is matching preventatives to characteristics of an individual that have been shown to predict outcomes. One compelling body of literature on person × environment interactions is that of environmental sensitivity theories, including differential susceptibility theory and vantage sensitivity. Recent experimental evidence has demonstrated that environmental sensitivity (ES) factors moderate substance abuse outcomes. We propose that ES factors may augment current personalization strategies such as matching based on risk factors/severity of problem behaviors (risk severity (RS)). Specifically, individuals most sensitive to environmental influence may be those most responsive to intervention in general and thus need only a brief-type or lower-intensity program to show gains, while those least sensitive may require more comprehensive or intensive programming for optimal responsiveness. We provide an example from ongoing research to illustrate how ES factors can be incorporated into prevention trials aimed at high-risk adolescents. Keywords Substance use, Prevention, Environmental sensitivity, R i s k s e v e r i t y, D i ff e r e n t i a l s u s c e p t i b i l i t y, PersonalizationAlcohol and other drug use among adolescents is a serious public health concern in the USA. For example, by late adolescence, over 78 % of teens will have experimented with alcohol, over 47 % will be engaged in regular drinking habits, and over 14 % will have met criteria for lifetime abuse [1]. Despite herculean efforts over the previous five decades to stem the rising tide of substance use, treatment approaches (largely based on behavioral parent training and cognitive behavioral therapy principles) have been modest at best; there is considerable variability in outcomes, and no one model works similarly for all youth [2]. Even among those who experience initial success following treatment, relapse rates are high [3].

Extant research is mixed regarding the relations among lifetime exposure to stressors, adrenocortical activity, and executive function (EF), particularly in children. Aggregate measures of adrenocortical activity like hair cortisol concentration (HCC), timing of stress exposure, and age at assessment may clarify these associations. This cross‐sectional study examined the association among parent‐reported exposure to stressors, hair cortisol concentration (HCC), and children's EF via a tablet task in a community sample (n = 318, 52.5% female) of children across a wide age range (4–13 years, M = 9.4, SD = 2.3). Path analyses revealed that parent‐reported child lifetime exposure to stressors, but not past‐year stressful life events, negatively predicted HCC. There was also a marginally significant moderation by age such that HCC was associated negatively with EF for younger children (age < 9.7 years) but not older children. HCC did not significantly mediate the association between lifetime exposure to stressors and EF. Findings are consistent with the proposition that chronically high cortisol production has a neurotoxic effect on brain regions supporting EF. However, lifetime exposure to stressors predicted relatively lower cumulative cortisol production, consistent with a stress inoculation effect in this normative‐risk sample.

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