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Although maternal stress during pregnancy and even before conception shapes offspring risk for mental health problems, relatively little is known about the mechanisms through which these associations operate. In theory, preconception and prenatal stress may affect offspring mental health by influencing child responses to postnatal caregiving. To address this knowledge gap, this study had two aims. First, we examined associations between preconception and prenatal stress with child temperament profiles at age four using multilevel assessment of maternal perceived stress and stress physiology. Second, we tested child temperament profiles as moderators of associations between observed parenting behaviors during a parent-child free-play interaction when children were 4 years old and child behavior problems 1 year later. Latent profile analyses yielded four distinct child temperament profiles: inhibited, exuberant, regulated low reactive, and regulated high reactive. Consistent with hypotheses, preconception, and prenatal stress each independently predicted the likelihood of children having temperament profiles characterized by higher negative emotionality and lower regulation. Specifically, preconception perceived stress and prenatal cortisol predicted likelihood of children having an exuberant temperament, whereas prenatal perceived stress predicted likelihood of children having an inhibited temperament. Contrary to hypotheses, temperament profiles did not moderate predictions of child behavior problems from observed parenting behaviors; however, responsive parenting behaviors inversely predicted child behavior problems independently of child temperament. These findings add to growing evidence regarding effects of preconception factors on child outcomes and underscore a central role for responsive parenting behaviors in predicting more favorable child mental health independent of child temperament. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Given that noncompliance is the most common externalizing problem during middle childhood and reliably predicts significant conduct problems, innovations in elucidating its etiology are sorely needed. Evaluation of in-the-moment antecedents and consequences of child noncompliance improves traction on this goal, given that multiple theories contend that child noncompliance and parent behavior mutually influence each other through negative reciprocation as well as contingent praise processes. Among a sample of 140 families (child age: 6-10 years; 32.1% female), the present study capitalized on intensive repeated measures of observed child noncompliance and parent negative talk and praise objectively coded during three unique tasks. We employed dynamic structural equation modeling to evaluate within-dyad parent-child behavioral dynamics and between-dyad differences therein. Results provided mixed support for hypotheses and suggested that antecedents and consequences of child noncompliance differed according to task demands and child ADHD symptoms. Contrary to models of coercive cycles, during child-led play, parent negative talk was more likely following prior child noncompliance, but child noncompliance was less likely following prior parent negative talk. As expected, during parent-led play, parent praise was less likely following prior child noncompliance, which was also less likely following prior parent praise. Relative to youth with fewer symptoms, for children with elevated ADHD symptoms, during a challenging clean-up task, child noncompliance was less stable and less contingent on prior parent negative talk. Results are discussed in terms of their implications of real-time parent-child interactions for typical and atypical development of externalizing problems.

Early life adversity is a potent risk factor for poor mental health outcomes across the lifespan, including offspring vulnerability to psychopathology. Developmentally, the prenatal period is a sensitive window in which maternal early life experiences may influence offspring outcomes and demarcates a time when expectant mothers and offspring are more susceptible to stressful and salutary influences. This prenatal plasticity constituted the focus of the current study where we tested the association of maternal early life adversity with infant stress regulation through maternal prenatal internalizing symptoms and moderation by prenatal social support. Mother-infant dyads (n = 162) were followed prospectively and mothers completed assessments of social support and depressive and anxiety symptoms across pregnancy. Infants completed standardized stress paradigms at one month and six months. There were several key findings. First, maternal prenatal depressive symptoms significantly mediated predictions of infant cortisol reactivity to the heel stick at one month from maternal early life adversity: specifically, maternal early life adversity positively predicted depressive symptoms in pregnancy, which in turn predicted dampened infant cortisol reactivity. Second, prenatal social support did not significantly moderate predictions of depressive or anxiety symptoms in pregnancy from maternal early life adversity nor did it alter the associations of maternal depressive or anxiety symptoms with infant stress regulation. These results suggest that maternal prenatal mental health is a key mechanism by which maternal early life adverse experiences affect offspring risk for psychopathology. We discuss potential clinical and health implications of dysregulated infant cortisol reactivity with respect to lifespan development.

Conduct problems are increasingly prevalent in girls and they uniquely predict negative outcomes. Yet, few reliable risk factors for aggression and violence in girls and women have been identified. Although preliminary evidence suggests peer relationships may be central to the development of youth conduct problems, especially in girls, rigorous interactive models of peer risk and protective factors for conduct problems are lacking. Based on 3104 10-13-year-old girls in the Adolescent Brain and Cognitive Development study, we tested the independent associations of separate peer risk factors (i.e., relational aggression victimization, physical aggression victimization, and deviant peer affiliation) with multidimensional conduct problems, including their moderation by peer support. Being the victim of relational aggression, being the victim of physical aggression, and deviant peer affiliation were each positively associated with conduct problems and perpetration of aggression whereas peer support was negatively associated with youth report conduct problems and perpetration of physical aggression. Further, elevated peer support significantly attenuated the association of being the victim of relational aggression with teacher-rated conduct problems. These results highlight the sensitivity of conduct problems to peer risk factors and suggest that peer support designates important configurations of risk that differentially relate to conduct problems in girls.

Given the increasing prevalence of adolescent depression, identification of its early predictors and elucidation of the mechanisms underlying its individual differences is imperative. Controlling for baseline executive functioning (EF), we tested separate ADHD dimensions (i.e., inattention, hyperactivity-impulsivity) as independent predictors of early adolescent depression, including temporally-ordered causal mediation by academic functioning and social problems, using structural equation modeling. At baseline, participants consisted of 216 children (67% male) ages 6-9 years old with (n = 112) and without (n = 104) ADHD who subsequently completed Wave 2 and 3 follow-ups approximately two and four years later, respectively. Predictors consisted of separate parent and teacher ratings of childhood ADHD and laboratory-based assessments of key EF domains. At Wave 2, parents and teachers completed normed rating scales of youth academic and social functioning; youth completed standardized assessments of academic achievement. At Wave 3, youth self-reported depression. Baseline inattention positively predicted early adolescent depression whereas childhood hyperactivity-impulsivity and EF did not. Neither academic nor social functioning significantly mediated predictions of depression from baseline ADHD and EF. We consider prediction of early adolescent depression from inattention, including directions for future intervention and prevention research.

Although childhood aggression is typically associated with peer rejection, some children concurrently employ coercive and socially skilled behavior and successfully avoid negative peer outcomes. However, research on children's dual use of coercive and social behavior has largely employed cross-sectional designs with nonclinical populations and, as a result, little is known about the covariation of aggression with social skills, particularly among high-risk samples. We directly addressed this limitation by testing childhood aggression and social skills as separate time-varying predictors of prospective change in peer rejection in a sample of children with and without attention-deficit/hyperactivity disorder (ADHD). Two hundred and two 5-10-year-old children (M = 7.9 years, SD = 1.2) with and without ADHD were followed prospectively for 6 years. Key constructs, including children's overt aggression, social skills, and peer rejection, were collected at each of the three waves using multiple methods and informants. Controlling for demographic factors and time-varying ADHD symptoms, longitudinal change in child-, parent-, and teacher-reported aggression positively predicted prospective change in parent- and teacher-reported peer rejection. Importantly, predictions were moderated by parent- and teacher-reported social skills, such that aggression inversely predicted peer rejection for children with high social skills. These results demonstrate that social skills meaningfully alter trajectories of peer rejection predicted from cross-time variation in aggression. We discuss the theoretical and empirical implications of these findings within a developmental psychopathology framework, including recommendations for directions for future research.

This prospective longitudinal study evaluated multiple maternal biomarkers from the preconception and prenatal periods as time-sensitive predictors of child executive functioning (EF) in 100 mother-child dyads. Maternal glycated hemoglobin (HbA1C ), C-reactive protein (CRP), and blood pressure (BP) were assayed before pregnancy and during the second and third trimesters. Subsequently, children were followed from birth and assessed for EF (i.e. cognitive flexibility, response inhibition) at ages 4-6 years. Perinatal data were also extracted from neonatal records. Higher maternal CRP, but not maternal HbA1C or BP, uniquely predicted poorer child cognitive flexibility, even with control of maternal HbA1C and BP, relevant demographic factors, and multiple prenatal/perinatal covariates (i.e. preconception maternal body mass index, maternal depression, maternal age at birth, child birth weight, child birth order, child gestational age, and child birth/neonatal complications). Predictions from maternal CRP were specific to the third trimester, and third trimester maternal CRP robustly predicted child cognitive flexibility independently of preconception and second trimester CRP. Child response inhibition was unrelated to maternal biomarkers from all time points. These findings provide novel, prospective evidence that maternal inflammation uniquely predicts child cognitive flexibility deficits, and that these associations depend on the timing of exposure before or during pregnancy.

Social skills are traditionally viewed as acquired through social environments including parenting. However, biopsychosocial models highlight the importance of genetic influences and gene-environment interactions (G×Es) in child development. Extant G×E investigations often fail to account for developmental changes in the phenotype or rigorously assess the social environment using observational measures. The present study prospectively assessed 110 children (44.5% female) and their parents to explore biologically plausible independent and interactive associations of the serotonin transporter-linked polymorphic region (5-HTTLPR) and observed positive and negative parenting in prediction of (a) initial levels of social skills at school entry (age 6 years) and (b) developmental changes in social skills across the early school years (ages 6-9 years). Overall, the SS (vs. SL/LL) 5-HTTLPR genotype inversely predicted social skills across all domains, although parenting behavior moderated these associations wherein putative G×E effects differed by developmental timing and social skills domain. Positive parenting positively predicted concurrent (age 6) overall social skills for children with SL/LL genotypes, but not the SS genotype. However, for the SS group only, age 6 positive parenting positively predicted prospective growth in social responsibility, although negative parenting positively predicted growth in social cooperation. Findings suggest that 5-HTTLPR may signal differential sensitivities to parenting styles and patterns of social development, which may help to inform targeted intervention approaches to enhance person-environment fit. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Although ADHD and negative parenting are established predictors of youth outcomes, their independent and interactive effects on youth social functioning remain unclear. We tested childhood ADHD symptoms and negative parenting as independent and interactive predictors of prospective change in social problems across a four-year follow-up. At baseline, families of 221 (33% female) children with (n = 94) and without ADHD were rigorously assessed including observed positive and negative parenting behavior, youth ADHD symptoms, as well as multi-informant ratings of youth social problems at multiple occasions. Based on multiple regression with robust standard errors and full-information maximum likelihood procedures to address missing data, ADHD symptoms positively predicted social problems, even with control of observed parenting behavior, child age and sex, oppositional defiant disorder symptoms, and baseline social problems. Additionally, a child ADHD symptoms x negative parenting interaction uniquely predicted separate parent- and teacher-rated social problems where ADHD symptoms positively predicted social problems exclusively in the context of high (+1SD) and very high (+2 SD) negative parenting, respectively. When ADHD was separated into distinct dimensions (i.e., inattention, hyperactivity), an interaction between inattention symptoms and negative parenting approached significance such that inattention symptoms positively predicted parent-rated social problems in the context of high negative parenting. We discuss the interaction between parenting and ADHD symptoms in predictions of youth social problems and implications for intervention.

ObjectiveWe tested mediation of birth weight and ADHD symptoms by multiple biologically plausible neurocognitive functions and evaluated familiality of observed indirect effects.Method647 youth from 284 multiplex families with ADHD completed the Arithmetic, Digit Span, Vocabulary, and Block Design subtests of the Wechsler Intelligence Scale for Children (WISC). Multiple mediation tested WISC subtests as mediators of birth weight and multi-informant ADHD symptoms. Familiality of indirect effects was estimated via moderated mediation comparing conditional indirect effects across siblings concordant and discordant for ADHD.ResultsControlling for IQ and demographic factors, Arithmetic uniquely mediated birth weight and ADHD symptoms. Conditional indirect effects through Arithmetic did not differ across ADHD concordant and discordant siblings.ConclusionThese cross-sectional findings support previous prospective longitudinal research implicating Arithmetic (i.e., fluid reasoning) as a preliminary causal mediator of birth weight and ADHD symptoms, and suggest that this pathway is independent of genetic influences on ADHD.

Although parenting behavior and friendship quality predict adolescent externalizing behaviors (EBs), individual differences in temperament may differentially affect susceptibility to these factors over time. In a multi-method and multi-informant study of 141 children followed prospectively from toddlerhood to adolescence, we tested the independent and interactive associations of age 3 reactive temperament (e.g., negative emotionality) and age 13 observed parenting (i.e., positive and negative behavior) and friendship (i.e., conflict and warmth), with multi-informant ratings of age 15 aggression and rule-breaking behavior. Negative parenting predicted growth in parent-rated EB, but only for adolescents with early reactive temperament. Temperament did not affect sensitivity to positive parenting or friendship. Results are discussed in the context of differential susceptibility theory and intervention implications for adolescents.

The serotonin transporter-linked polymorphic region (5-HTTLPR) is associated with caregiving in nonhuman animals and with affective and cognitive correlates of human parenting, yet its association with human parenting is largely unknown. Using a well-characterized sample of parents and offspring, we evaluated the association of parental 5-HTTLPR with observed positive and negative parenting behavior, as well as its biologically plausible moderation of child-related stress and disruptive child behavior as predictors of parenting. One hundred and sixty-two parents (86% mothers) and their 6- to 9-year-old children with and without attention-deficit/hyperactivity disorder were ascertained using multiple methods including structured interviews, rating scales, and observed parent-child interaction, yielding strong measures of key constructs. Controlling for multiple youth-level (e.g., sex, 5-HTTLPR genotype, disruptive behavior) and parent-level (e.g., demographics, depression, attention-deficit/hyperactivity disorder) factors, parents with an S allele exhibited significantly less observed positive parenting than those with the LL genotype. Significant Gene × Environment interactions were also observed: Child-related stress was negatively associated with observed parental negativity among SS/SL genotype parents but not LL genotype parents; next, observed disruptive child behavior was positively associated with parental negativity for both genotypes, but the effect was strongest in SS/SL parents. These preliminary findings suggest that parental 5-HTTLPR is uniquely associated with positive and negative parenting behavior, with more specific patterns according to child-related stress and disruptive child behavior. We consider implications for future research evaluating genetic influences on parenting as well as considerations for designing and delivering parenting-based interventions.

Individual differences in emotion regulation are central to social, academic, occupational, and psychological development, and emotion dysregulation (ED) in childhood is a risk factor for numerous developmental outcomes. The present study aimed to (a) describe the developmental trajectory of ED across early childhood (3-6 years) and (b) examine its sensitivity to youth serotonin transporter genotype, positive and negative parenting behaviors, and their interaction. Participants were 99 families in the Collaborative Family Study, a longitudinal study of children with or without developmental delays. Child ED and early parenting were coded from parent-child interactions. To examine serotonin transporter genotype as a moderator between parenting and child emotion dysregulation (ED), children with the homozygous short (SS) genotype were compared to children with the homozygous long (LL) or heterozygous (SL) genotype. We used latent growth curve modeling (LGCM) to model yearly change in ED from child age 3 to 6 years. LGCM revealed that ED decreased overall across early childhood. In addition, we observed separate Genotype × Positive and Genotype × Negative parenting behavior interactions in predictions of ED growth curves. Children with the SL/LL genotype had ED trajectories that were minimally related to positive and negative parenting behavior, whereas ED decreased more precipitously among children with the SS genotype when exposed to low negative parenting or high positive parenting. These findings provide evidence for Gene × Environment interactions (G×Es) in the development of ED in a manner that is conceptually consistent with vantage sensitivity, and they improve inferences afforded by prospective designs.

IntroductionExternalizing disorders are more prevalent in rural than urban settings and account for disproportionately high mental health service costs for rural adolescents. Although cultural stressors such as discrimination have been associated with externalizing problems in ethnic minority youth broadly, this relationship is understudied in Latinos, particularly those in rural settings. Further, though the associations of family processes such as familism and family conflict have been studied in relation to youth externalizing symptoms, whether these processes change in the face of adolescent discrimination stress remains unknown.MethodsA moderated multiple mediation model was used to examine the association between perceived discrimination, externalizing symptoms, and the indirect effect of family factors (familism, and family conflict) in a large sample (n = 455) of rural Latino youth. We also evaluated whether indirect and direct effects of discrimination on externalizing symptoms differed in boys versus girls.ResultsFamilism and family conflict each independently mediated the relationship between discrimination related stress and externalizing symptoms. However, discrimination had a direct effect on externalizing symptoms for boys only. In girls, this association held only when family factors were accounted for. Post-hoc analyses reveal that the moderating effect of sex on discrimination is driven by differences in rule-breaking behavior, as opposed to aggressive behavior.ConclusionFindings suggest that discrimination is associated with changes in the family environment which in turn invoke elevated risk for externalizing problems. Further, family-focused interventions that address externalizing problems may be especially effective for adolescent girls.

Although birth weight is a potential causal risk factor for attention-deficit/hyperactivity disorder (ADHD) symptoms, both the specificity of this association and its mediating pathways are largely unknown. We carefully assessed youth with and without ADHD (i.e., Wave 1), and followed them prospectively for 2 years (i.e., Wave 2). We (a) tested the association of birth weight with Wave 2 ADHD symptoms, and (b) evaluated biologically plausible neurocognitive functions from Wave 1 as temporally ordered mediators of birth weight and Wave 2 ADHD symptoms in a multiple mediation framework. At Wave 1, 222 ethnically diverse youth (30% female; ages 5-10) completed the Digit Span, Vocabulary, Symbol Search, and Arithmetic subtests of the Wechsler Intelligence Scale for Children-IV. At both Wave 1 and Wave 2 (ages 7-13), multiple informants (i.e., parents, teachers) rated youth ADHD symptoms and co-occurring psychopathology using multiple methods (i.e., structured interview, rating scale). Controlling for demographic factors, gestational age, and co-occurring externalizing and internalizing psychopathology, birth weight inversely predicted Wave 2 ADHD symptoms across multiple methods and informants. Additionally, controlling for Wave 1 ADHD symptoms and relevant covariates, Wave 1 Arithmetic uniquely mediated the association of birth weight with multi-method/informant Wave 2 ADHD symptoms. These findings suggest that birth weight is a relatively specific risk factor for youth ADHD symptoms and they implicate individual differences in fluid reasoning as a preliminary causal mediator of this association. We discuss implications for future research evaluating causal mechanisms underlying risk factors for ADHD.

Although gene × environment interactions contribute to youth attention-deficit/hyperactivity disorder (ADHD) symptoms, the pathways mediating these influences are unknown. We tested genetic moderation of indirect effects from parenting behavior to youth ADHD symptoms through multiple neurocognitive factors. Two hundred and twenty-nine youth with and without ADHD were assessed at baseline (Wave 1; ages 5-10) and at a 2-year follow-up (Wave 2; ages 7-13). At Wave 1, youth completed a neurocognitive battery including measures of response inhibition, visuospatial working memory, and fluid reasoning, and a standardized parent-child interaction task yielding observational measures of positive and negative parenting. At Wave 2, youth psychopathology was rated by parents and teachers using multiple methods (i.e., structured interview, rating scale). We employed moderated multiple mediation and compared conditional indirect effects across youth genotypes at two biologically plausible genetic loci. Controlling for parent ADHD symptoms as well as youth demographic factors and co-occurring externalizing symptoms, these genetic factors moderated the indirect effect from Wave 1 parenting to multi-method/informant Wave 2 ADHD symptoms through Wave 1 neurocognitive functioning. This preliminary study is the first to identify genetic moderation of mediated effects underlying ADHD symptoms and suggests that specific gene × parenting interactions may underlie neurocognitive functioning deficits and subsequent ADHD.

Although individual differences in fluid reasoning reliably mediate predictions of attention-deficit/hyperactivity disorder (ADHD) symptoms from birth weight in youth with typical cognitive development (TD), it is unknown if this indirect effect operates similarly in the development of ADHD symptoms secondary to intellectual disability (ID). Thus, we evaluated mediation by fluid reasoning in a longitudinal sample of 163 youth (45% female) with (n = 52) or without (n = 111) ID who were followed prospectively from age 5 to age 13. At age 9, youth completed the Arithmetic subtest of the Wechsler Intelligence Scale for Children, a measure of fluid reasoning. At ages 9 and 13, mothers and teachers separately rated youth ADHD symptoms and mothers completed a diagnostic interview. Mediation was tested via path analysis with bootstrapped confidence intervals, and moderated mediation estimated whether indirect effects differed between ID and TD youth or based on youth IQ. Controlling for demographic factors and age 9 ADHD symptoms, age 9 Arithmetic mediated birth weight and multi-method/informant age 13 ADHD symptoms, such that birth weight positively predicted Arithmetic, which negatively predicted ADHD symptoms. Neither ID status nor IQ moderated the observed indirect effect through Arithmetic, suggesting that it was similar for ID and TD youth as well as across the range of youth IQs. These findings support previous evidence that fluid reasoning, as measured by Arithmetic, may causally mediate birth weight and ADHD symptoms, and suggest that this pathway operates similarly with respect to the development of ADHD symptoms in youth with ID.

Item response theory (IRT) was separately applied to parent- and teacher-rated symptoms of attention-deficit/hyperactivity disorder (ADHD) from a pooled sample of 526 six- to twelve-year-old children with and without ADHD. The dimensional structure ADHD was first examined using confirmatory factor analyses, including the bifactor model. A general ADHD factor and two group factors, representing inattentive and hyperactive/impulsive dimensions, optimally fit the data. Using the graded response model, we estimated discrimination and location parameters and information functions for all 18 symptoms of ADHD. Parent- and teacher-rated symptoms demonstrated adequate discrimination and location values, although these estimates varied substantially. For parent ratings, the test information curve peaked between -2 and +2 SD, suggesting that ADHD symptoms exhibited excellent overall reliability at measuring children in the low to moderate range of the general ADHD factor, but not in the extreme ranges. Similar results emerged for teacher ratings, in which the peak range of measurement precision was from -1.40 to 1.90 SD Several symptoms were comparatively more informative than others; for example, is often easily distracted ("Distracted") was the most informative parent- and teacher-rated symptom across the latent trait continuum. Clinical implications for the assessment of ADHD as well as relevant considerations for future revisions to diagnostic criteria are discussed.

ContextAlthough children with attention-deficit/hyperactivity disorder (ADHD) are at elevated risk for comorbid psychopathology, the clinical correlates of ADHD in girls are far less understood relative to boys, despite ADHD being one of the most common childhood disorders in girls.ObjectiveTo meta-analytically summarize rates of comorbid internalizing (anxiety, depression) and externalizing (oppositional defiant disorder [ODD], conduct disorder [CD]) psychopathology among girls with and without ADHD.Data sourcesLiterature searches (PubMed, Google Scholar) identified published studies examining comorbid psychopathology in girls with and without ADHD.Study selectionEighteen studies (1997 participants) met inclusion criteria and had sufficient data for the meta-analysis.Data extractionOdds ratios for each comorbid disorder were calculated from available data. Demographic (eg, age, race/ethnicity) and study characteristics (eg, referral source, diagnostic method) were also coded.ResultsCompared with girls without ADHD, girls with ADHD were significantly more likely to meet Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria for each comorbid disorder assessed. Relative odds were higher for externalizing (ODD: 5.6×; CD: 9.4×) relative to internalizing disorders (anxiety: 3.2×; depression: 4.2×). Meta-regression revealed larger effect sizes of ADHD on anxiety for studies using multiple diagnostic methods, featuring younger children, and including clinic-referred (versus community-referred) girls; the effect of ADHD on ODD varied based on diagnostic informant.LimitationsFindings were derived from cross-sectional studies, precluding causal inferences.ConclusionsGirls with ADHD frequently exhibit comorbid externalizing and internalizing disorders. We discuss future research priorities and consider intervention implications for ADHD and comorbid psychopathology in girls.

ObjectivePositive alcohol expectancies and attention deficit/hyperactivity disorder (ADHD) are independent risk factors for adolescent alcohol problems and substance use disorders. However, the association of early ADHD diagnostic status, as well as its separate dimensions of inattention and hyperactivity, with alcohol expectancies is essentially unknown.MethodAt baseline (i.e., Wave 1), parents of 139 6-to 9-year-old children (71% male) with (N = 77; 55%) and without (N = 62; 45%) ADHD completed structured diagnostic interviews of child psychopathology. Approximately two years later (i.e., Wave 2), children completed a Memory Model-Based Expectancy Questionnaire (MMBEQ) to ascertain their positive and negative expectancies regarding alcohol use. All children were alcohol naïve at both baseline and follow-up assessments.ResultsControlling for age, sex, IQ, as well as the number of Wave 1 oppositional defiant disorder (ODD) and conduct disorder (CD) symptoms, the number of baseline hyperactivity symptoms prospectively predicted more positive arousing (i.e., MMBEQ "wild and crazy" subscale) alcohol expectancies at Wave 2. No predictive association was observed for the number of Wave 1 inattention symptoms and alcohol expectancies.ConclusionsChildhood hyperactivity prospectively and positively predicted expectancies regarding the arousing properties of alcohol, independent of inattention and ODD/CD symptoms, as well as other key covariates. Even in the absence of explicit alcohol engagement, youths with elevated hyperactivity may benefit from targeted intervention given its association with more positive arousing alcohol expectancies.

ObjectiveAmong Asian American young adults, variations in alcohol-metabolizing genes (i.e., aldehyde dehydrogenase [ALDH2] and alcohol dehydrogenase [ADH1B]) are protective, whereas Korean ethnicity, family history of alcohol problems (FH), and acculturation represent risk factors for alcohol misuse. This study aims to integrate these genetic and environmental factors in a sample of Asian Americans expressing a wide range of alcohol use behaviors and problems.MethodParticipants were 97 Asian American young adults (42% female) recruited as heavy and light drinkers (n = 49 and 48, respectively). Participants completed the Alcohol Use Disorders Identification Test, Timeline Followback, Vancouver Acculturation Index, and Family Tree Questionnaire. All participants provided buccal cell samples for DNA analysis.ResultsFamily history-positive (FH+) subjects reported greater alcohol use than family history-negative (FH-) subjects. A FH × ALDH2 interaction was observed such that FH- subjects demonstrated no ALDH2 effect, yet in FH+ subjects, the ALDH2*2 genotype was associated with increased alcohol use. A significant main effect of acculturation was also moderated by FH such that the positive association between acculturation and alcohol use was greater among FH+ subjects and, in particular, among FH+ men.ConclusionsAlthough preliminary, these results suggest that the potential protective effects conferred by ALDH2 and ADH1B are moderated by FH, such that a positive FH appeared to abolish the protective effect of these genes. Further, acculturation was associated with greater alcohol use in FH+ subjects only. If replicated in larger samples, these data suggest that alcohol-metabolism genes may not be protective in the context of high environmental risk.

Young adults (ages 18-26) with (n = 20) and without (n = 55) a history of child abuse (CA) completed self-report and laboratory-based measures of impulsivity and risk-taking. Relative to individuals without abuse histories, individuals with a history of CA self-reported a greater number of lifetime sexual partners as well as elevated trait impulsivity (specifically, elevated lack of premeditation and lack of perseverance). No group differences were observed for self-reported safety-related behaviors and risk-taking propensity. Notably, however, laboratory-based measures suggested that individuals with a history of CA showed significantly less impulsivity and risk-taking than individuals without abuse histories. These results suggest that self-report and laboratory measures of risk-taking and impulsivity measured in emerging adulthood may differentially relate to CA. Specifically, whereas laboratory-based measures may be influenced by hypervigilance or in the moment actions, self-report measures may assess more general behaviors related to real-world impulsivity and risk-taking.

BackgroundWell-validated models of maternal behavior in small-brain mammals posit a central role of oxytocin in parenting, by reducing stress and enhancing the reward value of social interactions with offspring. In contrast, human studies are only beginning to gain insights into how oxytocin modulates maternal behavior and affiliation.MethodsTo explore associations between oxytocin receptor genes and maternal parenting behavior in humans, we conducted a genetic imaging study of women selected to exhibit a wide range of observed parenting when their children were 4-6 years old.ResultsIn response to child stimuli during functional magnetic resonance imaging (fMRI), hemodynamic responses in brain regions that mediate affect, reward, and social behavior were significantly correlated with observed positive parenting. Furthermore, single nucleotide polymorphisms (SNPs) (rs53576 and rs1042778) in the gene encoding the oxytocin receptor were significantly associated with both positive parenting and hemodynamic responses to child stimuli in orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), and hippocampus.ConclusionsThese findings contribute to the emerging literature on the role of oxytocin in human social behavior and support the feasibility of tracing biological pathways from genes to neural regions to positive maternal parenting behaviors in humans using genetic imaging methods.

Children with attention-deficit/hyperactivity disorder (ADHD) are at increased risk for the development of depression, with evidence that peer and academic difficulties mediate predictions of later depression from ADHD. In the present study, we hypothesized that parent-child relationship difficulties may be an additional potential mediator of this association. Academic, peer, and parent-child functioning were tested as mediators of the association of attention problems and depression in two distinctly different yet complementary samples. Study 1 was a cross-sectional sample of 5- to 10-year-old children (N = 230) with and without ADHD. Study 2 was a prospective longitudinal sample of 472 youth, followed prospectively from birth to age 20 years, at risk for depression. Despite differences in age, measures, and designs, both studies implicated peer and parent-child problems as unique mediators of depressive symptoms, whereas academic difficulties did not uniquely mediate the ADHD-depression association. Furthermore, inattention symptoms, but not hyperactivity, predicted depressive symptoms via the disruption of interpersonal functioning. The inclusion of oppositional defiant disorder into models impacted results and supported its independent role in parent-child problems. Implications include support for interventions that target interpersonal competence, which may effectively reduce the risk of depression among children with ADHD.

Although genetic and environmental factors are separately implicated in the development of antisocial behavior (ASB), interactive models have emerged relatively recently, particularly those incorporating molecular genetic data. Using a large sample of male Caucasian adolescents and young adults from the National Longitudinal Study of Adolescent Health (Add Health), the association of deviant peer affiliation, the 30-base pair variable number tandem repeat polymorphism in promoter region of the monoamine oxidase-A (MAOA) gene, and their interaction, with antisocial behavior (ASB) was investigated. Weighted analyses accounting for over-sampling and clustering within schools as well as controlling for age and wave suggested that deviant peer affiliation and MAOA genotype were each significantly associated with levels of overt ASB across a 6-year period. Only deviant peer affiliation was significantly related to covert ASB, however. Additionally, there was evidence suggestive of a gene-environment interaction (G × E) where the influence of deviant peer affiliation on overt ASB was significantly stronger among individuals with the high-activity MAOA genotype than the low-activity genotype. MAOA was not significantly associated with deviant peer affiliation, thus strengthening the inference of G × E rather than gene-environment correlation (rGE). Different forms of gene-environment interplay and implications for future research on ASB are discussed.

To improve understanding about genetic and environmental influences on antisocial behavior (ASB), we tested the association of the 44-base pair polymorphism of the serotonin transporter gene (5-HTTLPR) and maltreatment using latent class analysis in 2,488 boys and girls from Wave 1 of the National Longitudinal Study of Adolescent Health. In boys, ASB was defined by three classes (Exclusive Covert, Mixed Covert and Overt, and No Problems) whereas in girls, ASB was defined by two classes (Exclusive Covert, No Problems). In boys, 5-HTTLPR and maltreatment were not significantly related to ASB. However, in girls, maltreatment, but not 5-HTTLPR, was significantly associated with ASB. A significant interaction between 5-HTTLPR and maltreatment was also observed, where maltreated girls homozygous for the short allele were 12 times more likely to be classified in the Exclusive Covert group than in the No Problems group. Structural differences in the latent structure of ASB at Wave 2 and Wave 3 prevented repeat LCA modeling. However, using counts of ASB, 5-HTTLPR, maltreatment, and its interaction were unrelated to overt and covert ASB at Wave 2 and only maltreatment was related to covert ASB at Wave 3. We discuss these findings within the context of sex differences in ASB and relevant models of gene-environment interplay across developmental periods.