Beyond dual systems: A genetically-informed, latent factor model of behavioral and self-report measures related to adolescent risk-taking.

The dual systems model posits that adolescent risk-taking results from an imbalance between a cognitive control system and an incentive processing system. Researchers interested in understanding the development of adolescent risk-taking use a diverse array of behavioral and self-report measures to index cognitive control and incentive processing. It is currently unclear whether different measures commonly interpreted as indicators of the same psychological construct do, in fact, tap the same underlying dimension of individual differences. In a diverse sample of 810 adolescent twins and triplets (M age=15.9years, SD=1.4years) from the Texas Twin Project, we investigated the factor structure of fifteen self-report and task-based measures relevant to adolescent risk-taking. These measures can be organized into four factors, which we labeled premeditation, fearlessness, cognitive dyscontrol, and reward seeking. Most behavioral measures contained large amounts of task-specific variance; however, most genetic variance in each measure was shared with other measures of the corresponding factor. Behavior genetic analyses further indicated that genetic influences on cognitive dyscontrol overlapped nearly perfectly with genetic influences on IQ (rA=-0.91). These findings underscore the limitations of using single laboratory tasks in isolation, and indicate that the study of adolescent risk taking will benefit from applying multimethod approaches.

Sensation seeking, peer deviance, and genetic influences on adolescent delinquency: Evidence for person-environment correlation and interaction.

Both sensation seeking and affiliation with deviant peer groups are risk factors for delinquency in adolescence. In this study, we use a sample of adolescent twins (n = 549), 13 to 20 years old (M age = 15.8 years), in order to test the interactive effects of peer deviance and sensation seeking on delinquency in a genetically informative design. Consistent with a socialization effect, affiliation with deviant peers was associated with higher delinquency even after controlling for selection effects using a co-twin-control comparison. At the same time, there was evidence for person-environment correlation; adolescents with genetic dispositions toward higher sensation seeking were more likely to report having deviant peer groups. Genetic influences on sensation seeking substantially overlapped with genetic influences on adolescent delinquency. Finally, the environmentally mediated effect of peer deviance on adolescent delinquency was moderated by individual differences in sensation seeking. Adolescents reporting high levels of sensation seeking were more susceptible to deviant peers, a Person × Environment interaction. These results are consistent with both selection and socialization processes in adolescent peer relationships, and they highlight the role of sensation seeking as an intermediary phenotype for genetic risk for delinquency. (PsycINFO Database Record

A Twin Study of Objective and Subjective Pubertal Timing and Peer Influence on Risk-Taking.

The current study used a behavioral genetic design to test whether three measures of pubertal timing moderated peer influence on risk-taking in a sample of 248 female adolescent twin pairs (Mage =16.0, SD=1.5) from the National Longitudinal Study of Adolescent Health. Peer influence was operationalized as the quasi-causal association between girls' self-reported risk-taking and the risk-taking reported by their friends. Girls with earlier ages at menarche and who perceived themselves as more developed than peers were more susceptible to peer influence on risk-taking. However, age-standardized ratings of body changes did not moderate peer influence. This study highlights distinctions between multiple measures of pubertal timing, using an innovative synthesis of genetically informative data and peer nomination data.

Peer Group Similarity in Perceptions of Pubertal Timing.

Self-report measures of perceived pubertal timing correspond only weakly with clinical measures of "objective" physical development. Peer and school contexts shape adolescents' self-perceptions of pubertal timing. The current study examined associations between perceived pubertal timing and the pubertal timing reported by nominated friends and schoolmates. Participants included 2817 adolescents (Mage = 16.6; 49 % female; 16 % Black; 20 % Hispanic) from the National Longitudinal Study of Adolescent Health. Three measures of pubertal timing were included: age-standardized ratings of body changes, comparisons of development relative to peers (relative timing), and, in females, age at menarche. It was hypothesized that relative timing, which explicitly asks adolescents to compare themselves to their peers, would be related to the age-standardized pubertal timing of nominated friends and schoolmates. Surprisingly, there were no associations between relative timing and age-standardized pubertal timing reported by peers, suggesting that pubertal self-perceptions do not fluctuate in response to the average level of development in a friend group. Instead, males were similar to nominated friends and schoolmates in age-standardized ratings of body changes, and females were similar to nominated friends in relative timing, controlling for race, ethnicity, and age. Different self-report measures of pubertal timing index different underlying constructs, and the social processes that influence adolescents' perceptions of pubertal maturation may differ between genders.

Interactions between DRD4 and developmentally specific environments in alcohol-dependence symptoms.

Social experiences may moderate genetic influences on alcohol dependence (AD) symptoms. Consistent with this hypothesis, Park, Sher, Todorov, and Heath (2011) previously reported interactions between the dopamine D4 receptor gene (DRD4) and developmentally specific environments in the etiology of AD symptoms during emerging and young adulthood. Using a longitudinal cohort of n = 367 White participants followed from ages 18 to 27 years, we examine a series of similar interactions between DRD4 and developmentally sensitive contexts including childhood adversity and work and family roles. In contrast to previous results, we observed no significant interactions between DRD4 and childhood adversity. Overall, results further highlight the need for longitudinal studies of Gene × Environment interaction in the behavioral sciences and the difficulty of identifying candidate Gene × Environment interaction effects that are consistent across studies.

Person × Environment Interactions on Adolescent Delinquency: Sensation Seeking, Peer Deviance and Parental Monitoring.

Sensation seeking is a personality trait that is robustly correlated with delinquent behavior in adolescence. The current study tested specific contextual factors hypothesized to facilitate, exacerbate or attenuate this risk factor for adolescent delinquency. Individual differences in sensation seeking, peer deviance, parental monitoring and self-reported delinquent behavior were assessed in a sample of 470 adolescents. Peer deviance partially mediated the effects of sensation seeking and parental monitoring on adolescent delinquency. We also found evidence for a three-way interaction between sensation seeking, peer deviance and parental monitoring, such that the highest rates of delinquency occurred from the concurrence of high sensation seeking, high peer deviance, and low levels of parental monitoring. Results highlight the importance of considering peer- and family-level processes when evaluating personality risk and problematic adolescent behavior.

Developmental changes in genetic and environmental influences on rule-breaking and aggression: age and pubertal development.

BACKGROUND: Antisocial behavior (ASB) can be meaningfully divided into nonaggressive rule-breaking versus aggressive dimensions, which differ in developmental course and etiology. Previous research has found that genetic influences on rule-breaking, but not aggression, increase from late childhood to mid-adolescence. This study tested the extent to which the developmental increase in genetic influence on rule-breaking was associated with pubertal development compared to chronological age. METHOD: Child and adolescent twins (n = 1,031), ranging in age from 8 to 20 years (M age = 13.5 years), were recruited from public schools as part of the Texas Twin Project. Participants reported on their pubertal development using the Pubertal Development Scale and on their involvement in ASB on items from the Child Behavior Checklist. Measurement invariance of ASB subtypes across age groups (≤12 years vs. >12 years old) was tested using confirmatory factor analyses. Quantitative genetic modeling was used to test whether the genetic and environmental influences on aggression and rule-breaking were moderated by age, pubertal status, or both. RESULTS: Quantitative genetic modeling indicated that genetic influences specific to rule-breaking increased as a function of pubertal development controlling for age (a gene × puberty interaction), but did not vary as a function of age controlling for pubertal status. There were no developmental differences in the genetic etiology of aggression. Family-level environmental influences common to aggression and rule-breaking decreased with age, further contributing to the differentiation between these subtypes of ASB from childhood to adolescence. CONCLUSIONS: Future research should discriminate between alternative possible mechanisms underlying gene × puberty interactions on rule-breaking forms of antisocial behavior, including possible effects of pubertal hormones on gene expression.

Childhood Sexual Abuse and Impulsive Personality Traits: Mixed Evidence for Moderation by DRD4 Genotype.

This project examines associations between childhood sexual abuse (CSA) and two dimensions of impulsivity (sensation seeking and premeditation), and tests whether CSA-personality associations are moderated by the DRD4 exon III VNTR polymorphism. Sample 1 is from a longitudinal study of university students measured at 10 waves over ages 18-24 years (n = 500). Sample 2 is from a national sample of young adult sibling pairs, ages 18-24, from the National Longitudinal Study of Adolescent Health (n = 2,559). In both samples, CSA was associated with elevated sensation seeking. In Sample 1, the association between CSA and sensation seeking was moderated by DRD4 genotype; this gene × environment interaction effect, however, was not replicated in Sample 2. Results suggest new avenues for research on CSA in the area of normal-range personality variation.

Descriptive review: hormonal influences on risk for eating disorder symptoms during puberty and adolescence.

OBJECTIVE: Puberty is an important period of risk for the onset of eating pathology in adolescent females. This review focuses on changes in reproductive hormones during puberty as one specific psychopathogenic mechanism. METHOD: Studies of puberty and eating disorder-related phenotypes were identified using search databases and the reference sections of previous literature. RESULTS: Correlational studies of adult women and experimental studies of animals provide evidence for the effects of reproductive hormones on eating disorder symptoms. Very few studies of puberty, however, have directly measured or tested the effects of hormonal change in samples of human adolescents. Commonly used measures of pubertal development, such as menarche or self-reported pubertal status, are relatively poor indicators of individual differences in hormones. The extent to which puberty-related hormonal change accounts for elevated risk for disordered eating remains unclear. DISCUSSION: Future research is necessary to elucidate the specific relations between hormonal change during puberty and risk for disordered eating. In particular, there is a need for longitudinal studies with multivariate measurement of pubertal development, including direct measures of change in reproductive hormones.

Genetic and environmental influences on testosterone in adolescents: evidence for sex differences.

The current study investigated genetic and environmental influences on salivary testosterone during adolescence, using data from 49 pairs of monozygotic twins and 68 pairs of dizygotic twins, ages 14-19 years (M = 16.0 years). Analyses tested for sex differences in genetic and environmental influences on testosterone and its relation to pubertal development. Among adolescent males, individual differences in testosterone were heritable (55%) and significantly associated with self-reported pubertal status (controlling for age) via common genetic influences. In contrast, there was minimal heritable variation in testosterone for females, and testosterone in females was not significantly associated with pubertal status after controlling for age. Rather, environmental influences shared by twins raised together accounted for nearly all of the familial similarity in female testosterone. This study adds to a small but growing body of research that investigates genetic influences on individual differences in behaviorally relevant hormones.

Academic achievement as a moderator of genetic influences on alcohol use in adolescence.

Prior research suggests a link between academic performance and alcohol use during adolescence, but the degree to which this association reflects actual protective effects continues to be debated. We investigated the role of genetic factors in the association between academic achievement and adolescent alcohol use and whether achievement might constrain the translation of genetic influences on drinking into actual behavior (a Gene × Environment interaction). Analysis of twin data from Add Health (n = 399 monozygotic and dizygotic twin pairs) revealed not only common genetic factors underlying the association between achievement and alcohol consumption but also evidence for a gene-environment interaction. Specifically, the protective effect of achievement operated by moderating heritability of alcohol use, which was particularly salient for adolescents at high genetic risk for alcohol use.

Screening for unhealthy alcohol and other drug use by health educators: do primary care clinicians document screening results?

OBJECTIVES: Health educators are increasingly being used to deliver preventive care including screening and brief intervention (SBI) for unhealthy substance use (SU) (alcohol or drug). There are few data, however, about the "handoff" of information from health educator to primary care clinician (PCC). Among patients identified with unhealthy SU and counseled by health educators, the objective of this study was to examine (1) the proportion of PCC notes with documentation of SBI and (2) the spectrum of SU not documented by PCCs. METHODS: Before the PCC-patient encounter, health educators screened for SU, assessed severity (Alcohol, Smoking, and Substance Involvement Screening Test), and counseled patients. They also conveyed this information to the PCC before the PCC-patient encounter. Researchers reviewed the electronic medical record for PCC documentation of SBI performed by the health educator and/or the PCC. RESULTS: Among patients with the health educator-identified SU, only 69% (342/495) of PCC notes contained documentation of screening by the health educator and/or the PCC. Documentation was found in all encounters with patients with likely dependent SU, but only 62% and 59% of encounters with patients with risky alcohol and drug use, respectively. Documentation of cocaine or heroin use was higher than that of alcohol or marijuana use but still not universal. Although all SU-identified patients had received a brief intervention (from a health educator and possibly a PCC), only 25% of PCC notes contained documentation of a brief intervention. CONCLUSIONS: Among patients screened and counseled by health educators for unhealthy SU, SBI was often not documented by PCCs. These results suggest that strategies are needed to integrate SBI by primary care team members to advance the quality of care for patients with unhealthy SU.

Collaborative care of opioid-addicted patients in primary care using buprenorphine: five-year experience.

BACKGROUND: Opioid addiction is a chronic disease treatable in primary care settings with buprenorphine hydrochloride, but this treatment remains underused. We describe a collaborative care model for managing opioid addiction with buprenorphine hydrochloride-naloxone hydrochloride dihydrate sublingual tablets. METHODS: Ours is a cohort study of patients treated for opioid addiction using collaborative care between nurse care managers and generalist physicians in an urban academic primary care practice during a 5-year period. We examine patient characteristics, 12-month treatment success (ie, retention or taper after 6 months), and predictors of successful outcomes. RESULTS: From September 1, 2003, through September 30, 2008, 408 patients with opioid addiction were treated with buprenorphine. Twenty-six patients were excluded from analysis because they left treatment owing to preexisting legal or medical conditions or a need to transfer to another buprenorphine program. At 1 year, 196 of 382 patients (51.3%) underwent successful treatment. Of patients remaining in treatment at 12 months, 154 of 169 (91.1%) were no longer using illicit opioids or cocaine based on urine drug test results. On admission, patients who were older, were employed, and used illicit buprenorphine had significantly higher odds of treatment success; those of African American or Hispanic/Latino race had significantly lower odds of treatment success. These outcomes were achieved with a model that facilitated physician involvement. CONCLUSION: Collaborative care with nurse care managers in an urban primary care practice is an alternative and successful treatment method for most patients with opioid addiction that makes effective use of time for physicians who prescribe buprenorphine.