The present study utilized longitudinal data from a high-risk community sample (n=254, 52.8% female, 47.2% children of alcoholics, 74% non-Hispanic Caucasian) to test questions concerning the effects of genetic risk, parental knowledge, and peer substance use on emerging adult substance use disorders (SUDs). Specifically, this study examined whether parental knowledge and peer substance use mediated the effects of parent alcohol use disorder (AUD) and genetic risk for behavioral undercontrol on SUD. The current study also examined whether genetic risk moderated effects of parental knowledge and peer substance use on risk for SUD. Finally, this study examined these questions over and above a genetic "control" which explained a large proportion of variance in the outcome, thereby providing a stricter test of environmental influences.

Analyses were performed in a path analysis framework. To test these research questions, the current study employed two polygenic risk scores. The first, a theory-based score, was formed using single-nucleotide polymorphisms (SNPs) from receptor systems implicated in the amplification of positive effects in the presence of new/exciting stimuli and/or pleasure derived from using substances. The second, an empirically-based score, was formed using a data-driven approach that explained a large amount of variance in SUDs. Together, these scores allowed the present study to test explanations for the relations among parent AUD, parental knowledge, peer substance use, and SUDs.

Results of the current study found that having parents with less knowledge or an AUD conferred greater risk for SUDs, but only for those at higher genetic risk for behavioral undercontrol. The current study replicated research findings suggesting that peer substance use mediated the effect of parental AUD on SUD. However, it adds to this literature by suggesting that some mechanism other than increased behavioral undercontrol explains relations among parental AUD, peer substance use, and emerging adult SUD. Taken together, these findings indicate that children of parents with AUDs comprise a particularly risky group, although likelihood of SUD within this group is not uniform. These findings also suggest that some of the most important environmental risk factors for SUDs exert effects that vary across level of genetic propensity.

Low-income Mexican American women face significant risk for poor health during the postpartum period. Chronic stressors are theorized to negatively impact mental and physical health outcomes. However, physiological factors associated with increased self-regulatory capacity, such as resting heart rate variability, may buffer the impact of stress. In a sample of 322 low-income Mexican American women (mother age 18-42; 84% Spanish-speaking; modal family income $10,000-$15,000), the interactive influence of resting heart rate variability and three chronic prenatal stressors (daily hassles, negative life events, economic stress) on maternal cortisol output, depressive symptoms, and self-rated health at 12 weeks postpartum was assessed. The hypothesized interactive effects between resting heart rate variability and the chronic prenatal stressors on the health outcomes were not supported by the data. However, results showed that a higher number of prenatal daily hassles was associated with increased postpartum depressive symptoms, and a higher number of prenatal negative life events was associated with lower postpartum cortisol output. These results suggest that elevated chronic stress during the prenatal period may increase risk for poor health during the postpartum period.

The current study delineated the developmental trajectories of early childhood externalizing and internalizing symptoms reported by mothers and fathers, and examined the role of the 18-month observed parenting quality × Respiratory Sinus Arrhythmia

(RSA) interaction in predicting these trajectories. Child sex was tested as a covariate and moderator. It was found that children's low baseline RSA or high RSA reactivity , in comparison to high baseline RSA or low RSA reactivity , was more reactive as a function

of early parenting quality when predicting the development of early childhood problem symptoms. Differential patterns of the interaction between parenting quality and RSA were detected for mothers' and fathers' reports. Mother-reported models showed a diathesis-stress pattern, whereas the father-reported model showed a vantage-sensitivity pattern, especially for internalizing symptoms. This may imply the potential benefit of fathers' active engagement in children's early development. In addition, the effect of the parenting quality × RSA interaction in predicting the mother-reported models was found

to be further moderated by child sex. Specifically, the parenting quality × baseline RSA interaction was significantly predictive of girls' 54-month internalizing, and the parenting quality × RSA reactivity interaction significantly predicted boys' internalizing slope. Girls with low baseline RSA or boys with high RSA reactivity were vulnerable to the less positive parenting, exhibiting high levels of 54-month internalizing symptoms or slow decline in internalizing over time, respectively. Future research directions were discussed in terms of integrating the measures of SNS and PNS in psychopathology study,

exploring the mechanisms underlying the sex difference in parenting quality × RSA interaction, and comparing the findings of children's typical and atypical development.

Using data from an eight-year longitudinal study of 214 children's social and emotional development, I conducted three studies to (1) examine patterns of agreement for internalizing (INT) and externalizing (EXT) symptomatology among different informants (mothers, fathers, teachers, and adolescents) using a recently developed structural equation modeling approach for multi-trait, multi-method data; (2) examine the developmental trajectories for INT and EXT and predict individual differences in symptom development using temperament and parenting variables; and (3) describe patterns of INT and EXT co-occurrence and predict these patterns from temperament and parenting. In Study 1, longitudinal invariance was established for mothers', fathers' and teachers' reports over a six-year period. Sex, age, and SES did not substantially moderate agreement among informants, although both sex and age were differentially related to symptomatology depending on the informant. Agreement among teachers and mothers, but not among mothers and fathers, differed by domain of symptomatology, and was greater for EXT than for INT. In Study 2, latent profile analysis, a person-centered analytic approach, did not provide easily interpretable patterns of symptom development, a failure that is likely the result of the relatively modest sample size. Latent growth curve models, an alternative analytic approach, did provide good fit to the data. Temperament and parenting variables were examined as predictors of the latent growth parameters in these models. Although there was little prediction of the slope, effortful control was negatively related to overall levels of EXT, whereas impulsivity and anger were positively related. Mutually responsive orientation, a measure of the parent-child relationship, was a more consistent predictor of EXT than was parental warmth. Furthermore, the relation between mutually responsive orientation and EXT was partially mediated by inhibitory control. Across informants, there were few consistent predictors of INT. In Study 3, latent profile analysis was used to classify individuals into different patterns of INT and EXT co-occurrence. In these models, a similar class structure was identified for mothers and for teachers. When temperament and parenting were examined as predictors of co-occurring symptomatology, few significant interactions were found and results largely replicated prior findings from this data set using arbitrary symptom groups.

Several decades of research have concluded that child social functioning is a critical predictor of wellbeing across various developmental domains. Most scientists agree that both genetic and environmental influences play defining roles in social behavior; the processes by which they concurrently affect child development, however, has been the subject of less research. This work examines distinct mechanisms that shape child prosociality by examining genetic and environmental influences on development, via two empirical studies. The first study analyzed the evocative-reactive and the evocative-socially-mediated hypotheses as gene-environment correlation (rGE) mechanisms connecting the arginine vasopressin receptor 1a (AVPR1a) and dopamine receptor D2 (DRD2) genes, child prosocial behavior, and parent differential treatment (PDT). Findings present modest evidence for the evocative-reactive rGE hypothesis; specifically, AVPR1a marginally influenced child prosociality, which subsequently predicted mother preference in adolescence. The second study examined several gene-environment interactions (GxEs) in exploring how social environmental variables- positive and negative parenting- predicted child prosociality, as moderated by socially-implicated child genes, DRD2 and dopamine receptor D4 (DRD4). Findings indicated that while positive parenting was predictive of child prosociality regardless of genetic variants, the effects of negative parenting on child prosociality were dependent on child genetic variants. Together, findings from these studies suggest modest genetic and environmental influences on child behavior in middle childhood and adolescence, consistent with previous research and theory. Directions for future research are offered, and intervention and policy implications are discussed.

The hypothalamus pituitary adrenal (HPA) axis and the human genome are important components of the biological etiology of externalizing disorders. By studying the associations between specific genetic variants, diurnal cortisol, and externalizing symptoms we can begin to unpack this complex etiology. It was hypothesized that genetic variants from the corticotropine releasing hormone receptor 1 (CRHR1), FK506 binding protein 51 (FKBP5), catechol-O-methyl transferase (COMT), and dopamine transporter (DAT1) genes and diurnal cortisol intercepts and slopes would separately predict externalizing symptoms. It was also hypothesized that genetic variants would moderate the association between cortisol and externalizing. Participants were 800 twins (51% boys), 88.5% Caucasian, M=7.93 years (SD=0.87) participating in the Wisconsin Twin Project. Hierarchical Linear Modeling (HLM) was used to separate the variance associated with state and trait cortisol measured across three consecutive days and trait cortisol measures were used. There were no main effects of genes on externalizing symptoms. The evening cortisol intercept, the morning cortisol slope and the evening cortisol slope predicted externalizing, but only in boys, such that boys with higher cortisol and flatter slopes across the day also had more externalizing symptoms. The morning cortisol intercept and CRHR1 rs242924 interacted to predict externalizing in both boys and girls, with GG carriers significantly higher compared to TT carriers at one standard deviation below the mean of morning cortisol. For boys only there was a significant interaction between the DAT1 variable number tandem repeat (VNTR) and the afternoon slope and a significant slope for 9/9 carriers and 9/10 carriers such that when the slope was more steep, boys carrying a nine had fewer externalizing symptoms but when the slope was less steep, they had more. Results confirm a link between diurnal trait cortisol and externalizing in boys, as well as moderation of that association by genetic polymorphisms. This is the first study to empirically examine this association and should encourage further research on the biological etiology of externalizing disorder symptoms.

This study examines the relations among three aspects of temperament (shyness, impulsivity, and effortful control), resting respiratory sinus arrhythmia (RSA) recorded during a calming film and RSA suppression during three behavioral measures of effortful control, and adjustment (anxiety and externalizing behavior) in a sample of 101 preschool-age children. Principal components analysis was used to create composites for effortful control, shyness, impulsivity, anxiety, and externalizing behavior, and hierarchical regression analysis was used to test the study hypotheses. As expected, baseline RSA was negatively related to effortful control in shy children, but was unrelated to effortful control in children who were not shy. It was hypothesized that high baseline RSA would reduce the relation between shyness and anxiety, and between impulsivity and externalizing behavior; this hypothesis was supported for externalizing behavior, but not for anxiety. The interaction between impulsivity and RSA as a predictor of externalizing was statistically independent of effortful control, indicating that these are unique effects. Finally, it was hypothesized that RSA suppression would be positively related to effortful control for children low, but not high, in shyness. There was a marginal interaction between shyness and RSA suppression, with RSA suppression marginally negatively related to EC for children low in shyness, but unrelated to effortful control for children high in shyness; the direction of this association was opposite predictions. These findings indicate that RSA is more strongly related to effortful control for children high in shyness, and that it consequently may not be appropriate to use RSA as an index of EC for all children. This study also draws attention to the need to consider the context in which baseline RSA is measured because a true baseline may not be obtained for shy children if RSA is measured in an unfamiliar laboratory context. The finding that high RSA moderated (but did not eliminate) the relation between impulsivity and externalizing behavior is consistent with the conceptualization of RSA as a measure of self-regulation, but further research is needed to clarify the mechanism underlying this effect.

The present study tested the factor structure of the externalizing disorders (e.g. attention-deficit hyperactivity disorder (ADHD), conduct disorder (SE), and substance experimentation (SE) ) in adolescence. In addition, this study tested the influence of the GABRA2 gene on the factors of the externalizing spectrum. Confirmatory factor analyses were used to test the factor structure of the externalizing spectrum. Specifically, three competing alternate confirmatory factor analytic models were tested: a one-factor model where all disorders loaded onto a single externalizing factor, a two-factor model where CD and SE loaded onto one factor and ADHD loaded onto another, and a three-factor model, where all three disorders loaded onto separate factors. Structural equation modeling was used to test the effect of a GABRA2 SNP, rs279858, on the factors of the externalizing spectrum. Analyses revealed that a three-factor model of externalizing disorders with correlated factors fit the data best. Additionally, GABRA2 had a significant effect on the SE factor in adolescence, but not on the CD or ADHD factors. These findings demonstrate that the externalizing disorders in adolescence share commonalities but also have separate sources of systematic variance. Furthermore, biological mechanisms may act as a unique etiological factor in the development of adolescent substance experimentation.

I examined the role of children's or teacher's effortful control (EC) in children's academic functioning in early elementary school in two separate studies. In Study 1, I tested longitudinal relations between parents' reactions to children's displays of negative emotions in kindergarten, children's EC in first grade, and children's reading or math achievement in second grade (N = 291). In the fall of each school year, parents reported their positive or negative reactions and parents and teachers reported on children's EC. Standardized achievement tests assessed achievement each spring. Results from autoregressive panel mediation models demonstrated that constructs exhibited consistency across study years. In addition, first-grade EC mediated relations between parents' reactions (i.e., a difference composite of positive minus negative reactions) at kindergarten and second-grade math, but not reading, achievement. Findings suggest that one method of promoting math achievement in early school is through the socialization of children's EC. In Study 2, I examined relations between teachers' EC, teachers' reactions to children's negative emotions, the student-teacher relationship (STR), and children's externalizing behaviors or achievement among 289 second-graders and their 116 teachers. Results from mixed-model regressions showed that negative reactions and teacher-reported STR mediated relations between teachers' EC and math achievement. In addition, teacher-reported STR mediated links between teachers' EC and externalizing problems across reporters and between teachers' EC and reading achievement. Tests of moderated mediation indicated that a high-quality STR was negatively associated with externalizing problems and high levels of teachers' negative reactions were negatively related to math achievement only for students low in EC. In tests of moderation by social competence, teachers' reports of high-quality STRs tended to be negatively associated with externalizing problems, but relations were strongest for students not high in social competence. For students low in social competence only, children's reports of a high-quality STR was related to lower reading achievement. These results highlight the utility of considering whether and how teachers' own intrinsic characteristics influence classroom dynamics and students' academic functioning outcomes.

Fibromyalgia (FM) is a chronic musculoskeletal disorder characterized by widespread pain, fatigue, and a variety of other comorbid physiological and psychological characteristics, including a deficit of positive affect. Recently, the focus of research on the pathophysiology of FM has considered the role of a number of genomic variants. In the current manuscript, case-control analyses did not support the hypothesis that FM patients would differ from other chronic pain groups in catechol-O-methyltransferase (COMT) and mu-opioid receptor (OPRM1) genotype. However, evidence is provided in support of the hypothesis that functional single nucleotide polymorphisms on the COMT and OPRM1 genes would be associated with risk and resilience, respectively, in a dual processing model of pain-related positive affective regulation in FM. Forty-six female patients with a physician-confirmed diagnosis of FM completed an electronic diary that included once-daily assessments of positive affect and soft tissue pain. Multilevel modeling yielded a significant gene X environment interaction, such that individuals with met/met genotype on COMT experienced a greater decline in positive affect as daily pain increased than did either val/met or val/val individuals. A gene X environment interaction for OPRM1 also emerged, indicating that individuals with at least one asp allele were more resilient to elevations in daily pain than those homozygous for the asn allele. In sum, the findings offer researchers ample reason to further investigate the contribution of the catecholamine and opioid systems, and their associated genomic variants, to the still poorly understood experience of FM.