The role of perceived parent drinking motives on alcohol use among adolescents with and without childhood attention-deficit/hyperactivity disorder.

OBJECTIVE: Parent history of alcohol-related problems and antisocial behaviors contribute to adolescent alcohol use and are associated with offspring attention-deficit/hyperactivity disorder (ADHD). Youth with ADHD may be susceptible to intergenerational transmission of alcohol-related cognitions, which may model drinking motives that enhance risk for adolescent alcohol use. We examined whether childhood ADHD and parent history of alcohol use disorder, with or without antisociality, were associated with adolescents' perceptions of their parents' drinking motives and whether these perceptions predicted their alcohol use behaviors. METHOD: Adolescents (N = 199; 56% with ADHD; Mage = 15.73) completed the Drinking Motives Questionnaire regarding perceptions of their parents' drinking motives. Participants subsequently reported their past-year alcohol use behaviors (Mage = 16.95). Parents reported their history of alcohol-related problems and antisocial symptoms. Covariates included adolescent gender (7% girls), race (9% self-identified Black), and parental education and marital status. RESULTS: Perceived parent drinking motives were highest for social and lowest for conformity motives, consistent with adult self-reports in the literature. Parent alcohol use and antisociality history predicted perceptions of parent drinking motives, and child ADHD only predicted perceptions of parent social drinking motives. Perceived parent drinking motives predicted adolescent alcohol use, but only among youth without ADHD. CONCLUSION: Findings reflect the potential importance of assessing adolescent perceptions of parent drinking motives for adolescents without ADHD and a possible need for supporting parents in communicating about their own alcohol use. Future research should consider alternative strategies (e.g., assessing implicit cognitions) for studying the link between alcohol-related cognitions and behaviors for adolescents with ADHD. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Heritable Composite Phenotypes Defined by Combinations of Conduct Problem, Depression, and Temperament Features: Contributions to risk for Alcohol Problems.

The genetic architectures underlying symptoms of conduct problems and depression have largely been examined separately and without incorporating temperament, despite evidence for their genetic overlap. We examined how symptoms and temperament dimensions were transmitted together in families to identify highly heritable composite phenotypes, and how these composite phenotypes predicted alcohol outcomes in young adulthood. Participants (N = 486) were drawn from the third generation of families oversampled for alcohol use disorder in the first generation. Conduct problems, depression, and temperament were reported at 11-19 years old and alcohol outcomes at 18-26 years old. Using principal components of heritability analysis, we found seven highly heritable composite phenotypes, five of which predicted alcohol outcomes: three characterized by co-occurring conduct problems and depression and two by conduct problems. Novel composite phenotypes that were characterized by both conduct problems and depression showed different types of symptoms, temperament features, and genetic underpinnings. Children manifesting differing composite phenotypes might benefit from distinct treatments based on their unique etiologies.

The role of early intervention for adolescent mental health and polydrug use: Cascading mediation through childhood growth in the general psychopathology (p) factor.

This study is a secondary data analysis that extends knowledge about the effects of the early childhood Family Check-Up (FCU) intervention to trajectories of general psychopathology problems (p factor) across early and middle childhood, and effects on adolescent psychopathology and polydrug use. The Early Steps Multisite study (ClinicalTrials.gov Identifier NCT00538252) is a randomized controlled trial of the FCU and consists of a large, racially and ethnically diverse sample of children who grew up in low-income households in Pittsburgh, Pennsylvania; Eugene, Oregon; and Charlottesville, Virginia (n = 731; 49% female; 27.6% African American, 46.7% European American, 13.3% Hispanic/Latinx). To represent a comorbid presentation of internalizing and externalizing problems, we fit a bifactor model that included a general psychopathology (p) factor at eight ages in early childhood (ages 2-4), middle childhood (ages 7.5-10.5), and adolescence (age 14). Latent growth curve modeling was conducted to examine trajectories of the p factor across ages within the developmental periods of early and middle childhood. The effects of FCU on the reductions in growth in the childhood p factor had cascading effects on adolescent p factor (i.e., within-domain effect) and polydrug use (i.e., across-domain effect). Findings underscore the utility of the early FCU in preventing a host of maladaptive adolescent outcomes across diverse settings and populations. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Polygenic risk score for problematic alcohol use predicts heavy drinking and alcohol use disorder symptoms in young adulthood after accounting for adolescent alcohol use and parental alcohol use disorder.

BACKGROUND: Genome-wide association studies (GWAS) have identified hundreds of loci associated with alcohol-related traits. GWAS permit the calculation of polygenic risk scores (PRS), which aggregate genetic risk for a trait across the genome. To evaluate the usefulness of a PRS for problematic alcohol use (PAU)-which subsumes alcohol use disorder (AUD) and alcohol-related problems-we tested whether this PRS predicted heavy drinking and alcohol problems after accounting for family history of AUD and prior drinking history, robust and established predictors of PAU. METHODS: Participants (N=665) were European-ancestry members of the Michigan Longitudinal Study, a prospective family study with high rates (65%) of parental AUD. Participants reported their frequency of alcohol use, maximum drinks consumed in a 24-hour period, and alcohol use problems at four assessments in adolescence and young adulthood (11-29 years old). We used polygenic prediction via Bayesian regression and continuous shrinkage priors to create a PAU PRS using summary statistics from a meta-GWAS of PAU. RESULTS: After adjusting for demographic covariates, parental AUD, and drinking and alcohol use problems in early and mid/late adolescence, the PAU PRS was significantly associated with alcohol-related problems in young adulthood (ß=.08, p=.047; R2=0.6%). The PAU PRS also had a significant indirect effect on alcohol use problems in young adulthood through earlier drinking and alcohol use problems (ß=.02, p=.03). CONCLUSIONS: The PAU PRS predicted alcohol problems in young adulthood after accounting for parental history of AUD and alcohol use in adolescence, providing evidence that genetic data uniquely inform the etiology of alcohol problems.

A Polygenic Risk Score Enhances Risk Prediction for Adolescents' Antisocial Behavior over the Combined Effect of 22 Extra-familial, Familial, and Individual Risk Factors in the Context of the Family Check-Up.

Possessing informative tools to predict who is most at risk for antisocial behavior in adolescence is important to help identify families most in need of early intervention. Polygenic risk scores (PRSs) have been shown to predict antisocial behavior, but it remains unclear whether PRSs provide additional benefit above more conventional tools to early risk detection for antisocial behavior. This study examined the utility of a PRS in predicting adolescents' antisocial behavior after accounting for a broad index of children's contextual and individual risk factors for antisocial behavior. Participants were drawn from a longitudinal family-based prevention study (N = 463; Ncontrol = 224; 48.8% girls; 45.1% White; 30.2% Black; 12.7% Hispanic/Latino, 10.4% biracial; 0.2% Native American). Participants were recruited from US-based Women, Infants, and Children Nutritional Supplement programs. A risk tolerance PRS was created from a genome-wide association study. We created a robust measure capturing additive effects of 22 conventional measures of a risk of antisocial behavior assessed at child age 2 (before intervention). A latent variable capturing antisocial behavior (ages 10.5-16) was created. After accounting for intervention status and the conventional risk index, the risk tolerance PRS predicted independent variance in antisocial behavior. A PRS-by-conventional risk interaction showed that the conventional risk measure only predicted antisocial behavior at high levels of the PRS. Thus, the risk tolerance PRS provides unique predictive information above conventional screening tools and, when combined with them, identified a higher-risk subgroup of children. Integrating PRSs could facilitate risk identification and, ultimately, prevention screening, particularly in settings unable to serve all individuals in need.

The interaction between infant negative emotionality and cognition predicts ADHD-related behaviors in toddlerhood.

Attention-deficit/hyperactivity disorder (ADHD) is a highly prevalent disorder commonly identified in childhood. Affective and cognitive characteristics that are identifiable as early as infancy could be signals of risk for developing ADHD. Specifically, the interplay between emotionality and cognition may be important in predicting early symptoms of ADHD. This study examined the independent and interactive effects of infant negative emotionality and cognition on the development of inattention and hyperactivity/impulsivity in toddlerhood among infants at high and low familial likelihood for ADHD. Participants were 64 infants (M = 8.7, SD = 1.8) at high (n = 32) and low (n = 32) familial likelihood for ADHD, defined as at least one parent with ADHD or two parents without ADHD, respectively. Negative emotionality and cognition in infancy were assessed using the Infant Behavior Questionnaire and the Bayley's Scales of Infant and Toddler Development, and ADHD symptoms were assessed at toddler follow-up (M= 20.0, SD= 3.2) using the Child Behavior Checklist. Accounting for the quality of parent-child interaction, infants' negative emotionality (ß = .033, p = .938) and cognition (ß = .006, p = .884) did not independently predict toddlers' ADHD-related behaviors, but their interaction did (ß = .110, p = .019). For infants with higher levels of cognition (>95th percentile), higher negative emotionality predicted more ADHD-related behaviorss. For infants with lower levels of cognition (<11th percentile), higher negative emotionality predicted fewer ADHD-related behaviors. There may be two affective-cognitive pathways to inattention and hyperactivity/impulsivity in toddlerhood. The combination of higher levels of negative emotionality and cognition may result in greater frustration when goals are blocked, resulting in the expression of dysregulated behaviors (i.e., ADHD symptoms). Alternatively, low levels of negative emotionality and cognition combined may lead to dysregulation that is primarily cognitive in nature (such as the inattention symptoms of ADHD). Investigating affective and cognitive processes simultaneously may be important for increasing understanding of the early signals of ADHD risk.

Persistent attention-deficit/hyperactivity disorder predicts socially oriented, but not physical/physiologically oriented, alcohol problems in early adulthood.

BACKGROUND: Although individuals with histories of childhood attention-deficit/hyperactivity disorder (ADHD) report more alcohol-related problems in adulthood than those without ADHD, it is unknown whether there are group differences in certain types of alcohol problems. We tested whether the nature of alcohol problems differed for individuals with and without childhood ADHD, as well as adulthood-persistent ADHD, to facilitate a personalized medicine approach for alcohol problems in this high-risk group. METHODS: Data were drawn from a prospective, observational study. Children diagnosed with ADHD and demographically similar individuals without childhood ADHD were followed prospectively through young adulthood (N = 453; 87.6% male). ADHD symptom persistence was assessed using self-reports and parent reports. Alcohol problems and heavy drinking were assessed repeatedly from 18-30 years old to construct lifetime measures. RESULTS: Full-sample confirmatory factor analyses identified 5 alcohol problem "types:" interpersonal problems/risky behaviors, occupational/academic impairment, impaired control/treatment seeking, tolerance/withdrawal, and drinking to blackout. Latent class analyses of items within each type yielded the best fit for 3-class solutions for all sets of items except blackout drinking, for which 2 classes emerged. Children with ADHD were more likely than those without ADHD to belong to high-risk latent classes for interpersonal problems/risky behaviors, occupational/academic problems, and impaired control (the high-risk class that indexed treatment-seeking behavior). These effects were driven by individuals whose ADHD symptoms persisted into adulthood. Few group differences emerged for tolerance/withdrawal and blackout drinking, except that individuals with only childhood ADHD (no persistence) were more likely to belong to the low-risk groups than those with adulthood-persistent ADHD and without ADHD. CONCLUSIONS: Individuals with ADHD histories whose symptoms persist into adulthood may be more likely to experience socially oriented alcohol problems and impaired control/treatment seeking than individuals without an ADHD history and those with childhood ADHD only. Tailored alcohol prevention and treatment programs may benefit this high-risk population.

Correction to: Heterogeneous Trajectories of Problematic Alcohol Use, Depressive Symptoms, and their Co-Occurrence in Young Adults with and without Childhood ADHD.

The original version of this article unfortunately contained a mistake.

Heterogeneous Trajectories of Problematic Alcohol Use, Depressive Symptoms, and their Co-Occurrence in Young Adults with and without Childhood ADHD.

The literature is inconsistent regarding whether childhood ADHD confers risk for adulthood problematic alcohol use, depressive symptoms, and their co-occurrence. These inconsistencies could be due to meaningful heterogeneity in the adulthood outcomes of children with ADHD that were obscured in traditional group-based analyses. The current study tested this possibility, as well as the contribution of adulthood ADHD symptom persistence, in order to clarify long-term risk in this population. Children diagnosed with ADHD and demographically-similar children without ADHD were followed longitudinally into adulthood and repeatedly assessed on heavy drinking, alcohol problems, and depressive symptoms from ages 21-29 (84.1% White (not Hispanic); 86.9% male; 51.2% childhood ADHD; 14.7% adulthood-persistent ADHD; N = 320). Group-based multi-trajectory modeling identified six groups with different combinations of trajectories across these variables. Heterogeneous longitudinal outcomes for those with ADHD were found. Some children with ADHD showed increased risk as typically predicted, with a higher likelihood of membership in a group with stable-moderate alcohol outcomes and stable-severe depression (adulthood persistent ADHD also predicted this group), whereas some children with ADHD were more likely to belong to a group with virtually no alcohol outcomes and low depression. Additionally, adulthood persistent ADHD predicted membership in a group with stable-severe alcohol outcomes and stable-moderate depression. Given the severity associated with co-occurring alcohol and depressive disorders, studies of early risk and protective factors and long-term outcomes for these disparate trajectory patterns are needed, particularly for those with childhood and persisting ADHD.

Evidence for two genetically distinct pathways to co-occurring internalizing and externalizing problems in adolescence characterized by negative affectivity or behavioral inhibition.

Unique pathways to adolescents' co-occurring internalizing/externalizing problems, a severe and common form of psychopathology, remain poorly delineated; this paucity of knowledge impedes the development of personalized interventions. We examined established measures of genetic risk and early childhood temperamental dimensions to clarify potentially distinct pathways to adolescents' co-occurring internalizing/externalizing problems. Participants were drawn from a longitudinal randomized controlled trial of a family-based intervention. The study employed multiple informants and methods, including observer ratings of toddlers' negative affectivity and behavioral inhibition, and primary caregiver ratings of toddlers' inhibitory control; internalizing and aggression polygenic risk scores (PRS) based on prior meta-genome-wide association studies (GWAS); and parents' and teachers' reports of adolescents' internalizing and externalizing problems. Higher levels of the aggression PRS indirectly predicted primary caregiver- and teacher-reported co-occurring problems relative to all other groups through greater early childhood negative affectivity. Lower levels of the aggression PRS and higher levels of the internalizing PRS indirectly predicted co-occurring problems relative to the externalizing "only" and low problem groups (primary caregivers only) through greater early childhood behavioral inhibition. Findings suggest two different genetic pathways to co-occurring problems that could lead to distinct prevention and intervention efforts. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Early Childhood Trajectories of Conduct Problems and Hyperactivity/Attention Problems: Predicting Adolescent and Adult Antisocial Behavior and Internalizing Problems.

Although conduct problems (CP) and hyperactivity/attention problems (HAP) are thought to covary with regularity, few studies have traced the probability of co-occurring CP and HAP longitudinally, particularly beginning in the toddler period. Further, there is little research examining how early co-occurring trajectories of CP and HAP predict functioning across several domains through late adolescence and early adulthood. Using a cohort of 284 low-income boys, we examined whether separate developmental trajectories of overt CP and HAP symptomatology from ages 2 to 10 relate to violent behavior, established correlates of antisocial behavior, impulsivity, and internalizing problems in adolescence and early adulthood. Co-occurring trajectory patterns of CP and HAP from ages 2 to 10 were also investigated in relation to later maladjustment. Findings indicated that trajectories of CP beginning in early childhood were related to violent behavior in adolescence and adulthood, adolescent correlates of antisocial behavior (i.e., deviant talk with peers), and internalizing problems in adulthood. Early HAP trajectories were also related to later problem behaviors when considered in isolation. However, when examining trajectories of CP and HAP simultaneously, children with chronic CP + chronic HAP, but not HAP-only, were most at risk for multiple types of problem behaviors in adolescence and early adulthood, including violent behavior and depressive and anxiety symptoms. Thus, HAP symptomatology was no longer predictive of adolescent and adult functioning once co-occurring CP was accounted for. Findings extend prior research with older children of HAP and/or CP, highlighting the predictive value of trajectories of CP beginning in the toddler period.

Family-based prevention of adolescents' co-occurring internalizing/externalizing problems through early childhood parent factors.

OBJECTIVE: We evaluated whether initiating the Family Check-Up (FCU) during early childhood prevented a severe form of psychopathology in adolescence-co-occurring internalizing and externalizing problems-and whether effects operated indirectly through early childhood maternal depression and parents' positive behavior support. METHOD: Participants were drawn from a randomized controlled trial of the FCU (50.2% FCU; 49.5% girls; 46.6% Caucasian, and 27.6% Black; 13.4% Hispanic/Latino). At Ages 2 and 3, mothers self-reported depression, and primary caregivers' (PCs') positive behavior support was coded by trained observers. PCs, alternate caregivers (ACs), and teachers reported on 14-year-olds' problem behaviors. Latent profile analyses (LPAs) identified problem behavior groups for each reporter, which were outcomes in multinomial logistic regressions (PC, n = 672; AC, n = 652; teacher, n = 667). RESULTS: LPAs identified a low-problem, internalizing-only, externalizing-only, and co-occurring-problem group for each reporter. For PC- and AC-reported outcomes, the FCU predicted a lower likelihood that adolescents belonged to the co-occurring group relative to the low-problem, externalizing-only (p < .05), and internalizing-only (p < .05 for PC, p < 0.10 for AC) groups; these effects operated through maternal depression (p < .05). For teacher-reported outcomes, the FCU predicted a lower likelihood that adolescents belonged to the co-occurring group relative to the low-problem, internalizing-only, and externalizing-only (p < 0.05) groups; effects operated through positive behavior support (p < 0.05). CONCLUSIONS: Early delivery of the FCU indirectly prevented adolescents' co-occurring internalizing/externalizing problems in both home and school contexts by improving the quality of the early home environment. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Role of ADHD in the Co-Occurrence Between Heavy Alcohol Use and Depression Trajectories in Adulthood.

BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) is associated with greater heavy alcohol use and depressive symptoms in adulthood. Yet, few studies have investigated whether childhood ADHD predicts an increased association between heavy drinking and depression in adulthood when this co-occurrence becomes more common. We examined associations among heavy alcohol use and depression longitudinally from ages 21 to 29 and whether these associations differed for those with or without childhood ADHD, as well as for those with or without persistent ADHD in adulthood. METHODS: Data were from the Pittsburgh ADHD Longitudinal Study, a prospective cohort of children diagnosed with ADHD and demographically similar individuals without ADHD histories. ADHD symptoms in adulthood were self- and parent reported; depressive symptoms and frequency of drinking 5 or more drinks in a single drinking occasion were self-reported and measured at 5 time-points from ages 21 to 29. Depression and alcohol use were modeled in a multiple-group, parallel process longitudinal growth model. RESULTS: The slopes of heavy alcohol use and depression were significantly and positively associated from ages 25 to 29 but not at the younger ages. Although the strength of these associations did not differ by group (with or without ADHD, childhood or adulthood), the slopes of depression and heavy drinking at the older ages were highly variable and individuals with ADHD showed significantly faster growth in depression from ages 25 to 29. CONCLUSIONS: Due to the strengthening association between heavy drinking and depression for adults in their late 20s, and increasing depression for adults with ADHD histories, individuals with ADHD may be at greater risk for co-occurring depression and binge drinking. Negative reinforcement-related alcohol use may strengthen as these individuals age toward the fourth decade of life. More rigorous testing of this possibility is warranted.

Bifactor model of effortful control and impulsivity and their prospective prediction of ego resiliency.

OBJECTIVE: Children's effortful control and impulsivity are important predictors of the personality trait, ego resiliency (i.e., resiliency). Most researchers have not considered the fact that effortful control and impulsivity share substantial conceptual and empirical overlap, yet they also have been shown to be distinct. We tested a bifactor model of effortful control and impulsivity to characterize their shared and unique variance, the prospective prediction of resiliency by the factors of the bifactor model, and moderation by sex and age. METHOD: In a longitudinal study of children (N = 214; 76.5% non-Hispanic Caucasian, 12.2% Hispanic, 11.3% other race/ethnicity), parent- and teacher-reported effortful control and impulsivity, as well as behavioral measures of effortful control, were assessed on two occasions (T1: 4.5-8 years; T2: 6-10 years). Parent-reported resiliency was used as a covariate (T1) and the outcome (T3: 8-12 years). RESULTS: The bifactor model yielded a common effortful inhibitory control factor, pure attentional control factor, and pure impulsivity factor. Pure impulsivity and pure attentional control positively predicted resiliency, but only for girls. Effortful inhibitory control did not uniquely predict resiliency. CONCLUSION: Disentangling the shared and unique aspects of effortful control and impulsivity could clarify the roles they play in important outcomes, such as resiliency.

Negative Urgency Mediates the Relation between Genetically-Influenced Serotonin Functioning and Alcohol Problems.

Serotonin (5-HT) functioning is associated with alcohol problems. However, the mechanisms underlying this association remain unclear. The current study tested whether five separate dimensions of impulsivity (UPPS-P) mediated the relation between a polygenic score indexing 5-HT functioning and alcohol problems and whether any of these paths were moderated by age. Results showed that a 5-HT polygenic score predicted alcohol problems indirectly through negative urgency, but not any other facet of impulsivity. The 5-HT polygenic score also directly predicted alcohol problems. No age moderation was found. Findings suggest that negative urgency might be one important mechanism underlying the relation between genetically-influenced 5-HT functioning and alcohol problems. However, genetically-influenced 5-HT functioning likely influences alcohol problems through additional mechanisms. More broadly, results suggest that the previously observed transdiagnostic nature of 5-HT functioning on diverse types of psychopathology might be, in part, explained by its effect on negative urgency.

Serotonin functioning and adolescents' alcohol use: A genetically informed study examining mechanisms of risk.

The current study used data from two longitudinal samples to test whether self-regulation, depressive symptoms, and aggression/antisociality were mediators in the relation between a polygenic score indexing serotonin (5-HT) functioning and alcohol use in adolescence. The results from an independent genome-wide association study of 5-hydroxyindoleacetic acid in the cerebrospinal fluid were used to create 5-HT polygenic risk scores. Adolescents and/or parents reported on adolescents' self-regulation (Time 1), depressive symptoms (Time 2), aggression/antisociality (Time 2), and alcohol use (Time 3). The results showed that 5-HT polygenic risk did not predict self-regulation. However, adolescents with higher levels of 5-HT polygenic risk showed greater depression and aggression/antisociality. Adolescents' aggression/antisociality mediated the relation between 5-HT polygenic risk and later alcohol use. Deficits in self-regulation also predicted depression and aggression/antisociality, and indirectly predicted alcohol use through aggression/antisociality. Pathways to alcohol use were especially salient for males from families with low parental education in one of the two samples. The results provide insights into the longitudinal mechanisms underlying the relation between 5-HT functioning and alcohol use (i.e., earlier aggression/antisociality). There was no evidence that genetically based variation in 5-HT functioning predisposed individuals to deficits in self-regulation. Genetically based variation in 5-HT functioning and self-regulation might be separate, transdiagnostic risk factors for several types of psychopathology.

Roles of Response Inhibition and Gene-Environment Interplay in Pathways to Adolescents' Externalizing Problems.

This study used two waves of data to investigate pathways through which adolescents' response inhibition related to later externalizing problems. A polygenic risk score indexed genetic risk for poor response inhibition. Adolescents' performance on a response inhibition task mediated the relation between adolescents' polygenic risk scores and mother's inconsistent parenting (i.e., evocative rGE), even after controlling for mothers' genetic risk (i.e., passive rGE). Mothers' inconsistent parenting subsequently prospectively predicted adolescents' externalizing problems. Adolescents' response inhibition also prospectively predicted later externalizing behaviors. These findings were subgroup-specific, with greater risk for non-Hispanic Caucasian boys with substance-disordered parents. Results suggest that poor response inhibition may increase risk for adolescents' externalizing problems both directly and by evoking certain environmental conditions.

Affiliation with substance-using peers: Examining gene-environment correlations among parent monitoring, polygenic risk, and children's impulsivity.

Parental monitoring can buffer the effect of deviant peers on adolescents' substance use by reducing affiliation with substance-using peers. However, children's genetic predispositions may evoke poorer monitoring, contributing to negative child outcomes. We examined evocative genotype-environment correlations underlying children's genetic predisposition for behavioral undercontrol and parental monitoring in early adolescence via children's impulsivity in middle childhood, and the influence of parental monitoring on affiliation with substance-using peers a year and a half later (n = 359). Genetic predisposition for behavioral undercontrol was captured using a polygenic risk score, and a portion of passive rGE was controlled by including parents' polygenic risk scores. Children's polygenic risk predicted poorer parental monitoring via greater children's impulsivity, indicating evocative rGE, controlling for a portion of passive rGE. Poorer parental monitoring predicted greater children's affiliation with substance-using peers a year and a half later. Results are discussed with respect to gene-environment correlations within developmental cascades.

Predicting substance use in emerging adulthood: A genetically informed study of developmental transactions between impulsivity and family conflict.

Deviance proneness models propose a multilevel interplay in which transactions among genetic, individual, and family risk factors place children at increased risk for substance use. We examined bidirectional transactions between impulsivity and family conflict from middle childhood to adolescence and their contributions to substance use in adolescence and emerging adulthood (n = 380). Moreover, we examined children's, mothers', and fathers' polygenic risk scores for behavioral undercontrol, and mothers' and fathers' interparental conflict and substance disorder diagnoses as predictors of these transactions. The results support a developmental cascade model in which children's polygenic risk scores predicted greater impulsivity in middle childhood. Impulsivity in middle childhood predicted greater family conflict in late childhood, which in turn predicted greater impulsivity in late adolescence. Adolescent impulsivity subsequently predicted greater substance use in emerging adulthood. Results are discussed with respect to evocative genotype-environment correlations within developmental cascades and applications to prevention efforts.

Testing the Relations Among Family Disorganization, Delay Discounting, and Adolescent Alcohol Use: A Genetically Informed Study.

BACKGROUND: Delay discounting is a potential etiological factor in adolescents' alcohol use, making it important to understand its antecedents. Family disorganization might contribute to delay discounting, but few studies have tested this relation. Moreover, because delay discounting is heritable, the effects of family disorganization on delay discounting might be moderated by adolescents' genetic risk for delay discounting. Thus, the current study examined the role of family disorganization, in interaction with genetic risk, in predicting adolescents' delay discounting and subsequent alcohol use. METHODS: Adolescents participated in 4 waves of data collection. Adolescents self-reported their family disorganization at T1, completed a delay discounting questionnaire at T3, and self-reported their alcohol use both at T2 (covariate) and T4 (outcome). Using results from an independent sample, we created a polygenic risk score consisting of dopaminergic genes to index genetic risk for delay discounting. RESULTS: Greater family disorganization predicted adolescents' greater delay discounting, but only for adolescents with low levels of genetic risk for delay discounting. Adolescents with high and mean levels of genetic risk for delay discounting showed elevated delay discounting regardless of their family's disorganization. Greater delay discounting prospectively predicted adolescents' greater alcohol use. Finally, the effects of family disorganization on adolescents' alcohol use were mediated through delay discounting, but only for adolescents with low levels of genetic risk. CONCLUSIONS: Results suggest multiple pathways to delay discounting. Although there are genetically influenced pathways to delay discounting, family disorganization might represent an environmental pathway to delay discounting (and subsequent alcohol use) for a subset of adolescents at low genetic risk. These findings reinforce the utility of family interventions for reducing adolescents' delay discounting and alcohol use, at least for a subgroup of adolescents. Because higher family organization did not buffer against delay discounting among adolescents with high genetic risk, future research should explore other early environmental influences that could protect these high-risk adolescents from developing these risky behaviors.