Diana R. Samek

Considerations of Elder Sibling Closeness in Predicting Younger Sibling Substance Use: Social Learning Versus Social Bonding Explanations

Adolescent siblings are often similar in a variety of adjustment outcomes, yet little is known about the processes that explain sibling influences during adolescence. Two alternative explanations were tested, attachment (based in social bonding theory) and anaclitic identification (based in social learning theory). Hypotheses were tested with a sample of 613 adolescent sibling pairs (206 nonadopted, 407 adopted; elder sibling mean age = 16.1 years, younger sibling mean age = 13.8 years) across three sibling contexts (gender composition, age difference, and genetic similarity). Attachment explanations were supported so that the greater the perceived sibling emotional and behavioral closeness, the lower the likelihood of substance use; however, there were considerable moderating effects of sibling gender composition. Anaclitic identification explanations were not supported; closeness and elder sibling substance use did not interact to predict younger sibling substance use. Overall, this research adds to a body of work demonstrating important sibling influences on adolescent substance use.

Gene-environment interplay between parent-child relationship problems and externalizing disorders in adolescence and young adulthood.

BACKGROUND Previous studies have shown that genetic risk for externalizing (EXT) disorders is greater in the context of adverse family environments during adolescence, but it is unclear whether these effects are long lasting. The current study evaluated developmental changes in gene-environment interplay in the concurrent and prospective associations between parent-child relationship problems and EXT at ages 18 and 25 years. METHOD The sample included 1382 twin pairs (48% male) from the Minnesota Twin Family Study, participating in assessments at ages 18 years (mean = 17.8, s.d. = 0.69 years) and 25 years (mean = 25.0, s.d. = 0.90 years). Perceptions of parent-child relationship problems were assessed using questionnaires. Structured interviews were used to assess symptoms of adult antisocial behavior and nicotine, alcohol and illicit drug dependence. RESULTS We detected a gene-environment interaction at age 18 years, such that the genetic influence on EXT was greater in the context of more parent-child relationship problems. This moderation effect was not present at age 25 years, nor did parent-relationship problems at age 18 years moderate genetic influence on EXT at age 25 years. Rather, common genetic influences accounted for this longitudinal association. CONCLUSIONS Gene-environment interaction evident in the relationship between adolescent parent-child relationship problems and EXT is both proximal and developmentally limited. Common genetic influence, rather than a gene-environment interaction, accounts for the long-term association between parent-child relationship problems at age 18 years and EXT at age 25 years. These results are consistent with a relatively pervasive importance of gene-environmental correlation in the transition from late adolescence to young adulthood.

A Genetic Epidemiological Mega Analysis of Smoking Initiation in Adolescents

Introduction Previous studies in adolescents were not adequately powered to accurately disentangle genetic and environmental influences on smoking initiation (SI) across adolescence. Methods Mega-analysis of pooled genetically informative data on SI was performed, with structural equation modeling, to test equality of prevalence and correlations across cultural backgrounds, and to estimate the significance and effect size of genetic and environmental effects according to the classical twin study, in adolescent male and female twins from same-sex and opposite-sex twin pairs (N = 19 313 pairs) between ages 10 and 19, with 76 358 longitudinal assessments between 1983 and 2007, from 11 population-based twin samples from the United States, Europe, and Australia. Results Although prevalences differed between samples, twin correlations did not, suggesting similar etiology of SI across developed countries. The estimate of additive genetic contributions to liability of SI increased from approximately 15% to 45% from ages 13 to 19. Correspondingly, shared environmental factors accounted for a substantial proportion of variance in liability to SI at age 13 (70%) and gradually less by age 19 (40%). Conclusions Both additive genetic and shared environmental factors significantly contribute to variance in SI throughout adolescence. The present study, the largest genetic epidemiological study on SI to date, found consistent results across 11 studies for the etiology of SI. Environmental factors, especially those shared by siblings in a family, primarily influence SI variance in early adolescence, while an increasing role of genetic factors is seen at later ages, which has important implications for prevention strategies. Implications This is the first study to find evidence of genetic factors in liability to SI at ages as young as 12. It also shows the strongest evidence to date for decay of effects of the shared environment from early adolescence to young adulthood. We found remarkable consistency of twin correlations across studies reflecting similar etiology of liability to initiate smoking across different cultures and time periods. Thus familial factors strongly contribute to individual differences in who starts to smoke with a gradual increase in the impact of genetic factors and a corresponding decrease in that of the shared environment.

Adoptees’ curiosity and information-seeking about birth parents in emerging adulthood Context, motivation, and behavior

The Adoption Curiosity Pathway (ACP) model was used to test the potential mediating effect of curiosity on adoption information-seeking in a sample of 143 emerging adult adoptees (mean age = 25.0 years) who were adopted as infants within the United States by parents of the same race. Adoptees were interviewed about their intentions and actions taken to gather new information about their birth mothers and fathers. As expected, level of curiosity was positively associated with information-seeking behavior. Moreover, level of curiosity was influenced by adoptees’ perceptions of barriers and facilitators toward information-seeking. In fact, curiosity partially mediated the impact of internal and external barriers on information-seeking about birth mothers. Curiosity fully mediated the impact of external barriers and partially mediated external facilitators on birth father information-seeking. This study provides important support for the ACP, which describes context, motivation, and behavior relating to seeking new adoption-related information.

Antisocial peer affiliation and externalizing disorders in the transition from adolescence to young adulthood: Selection versus socialization effects.

Prior research has demonstrated both socialization and selection effects for the relationship between antisocial peer affiliation and externalizing problems in adolescence. Less research has evaluated such effects postadolescence. In this study, a cross-lagged panel analysis was used to evaluate the extent of socialization (i.e., the effect of antisocial peer affiliation on subsequent externalizing disorders) and selection (i.e., the effect of externalizing disorders on subsequent antisocial peer affiliation) in the prospective relationships between antisocial peer affiliation and externalizing disorders from adolescence through young adulthood. Data from a community sample of 2,769 individuals (52% female) with assessments at ages 17, 20, 24, and 29 were used. Analyses with a latent externalizing measure (estimated using clinical symptom counts of nicotine dependence, alcohol use disorder, illicit drug use disorder, and adult antisocial behavior) and self-reported antisocial peer affiliation revealed significantly stronger socialization effects from age 17 to 20, followed by significantly stronger selection effects from age 20 to 24 and 24 to 29. To better understand the impact of college experience, moderation by college status was evaluated at each developmental transition. Results were generally consistent for those who were in or were not in college. Results suggest selection effects are more important in later developmental periods than earlier periods, particularly in relation to an overall liability toward externalizing disorders, likely due to more freedom in peer selection postadolescence. (PsycINFO Database Record

Identity Development in a Transracial Environment: Racial/Ethnic Minority Adoptees in Minnesota

It has been argued that transracially adopted children have increased risk of problems related to self-esteem and ethnic identity development. We evaluated this hypothesis across four groups of transracial adoptees: Asian (n = 427), Latino (n = 28), Black (n = 6), mixed/other (n = 20), and same-race White adoptees (n = 126) from 357 adoptive families. No mean differences were found in adoptees’ ratings of affect about adoption or of curiosity about birth parents. Some differences were found in general identity development and adjustment. There were notable differences in communication about race/ethnicity across groups and between parent and child report.

A Test-Replicate Approach to Candidate Gene Research on Addiction and Externalizing Disorders: A Collaboration Across Five Longitudinal Studies

This study presents results from a collaboration across five longitudinal studies seeking to test and replicate models of gene–environment interplay in the development of substance use and externalizing disorders (SUDs, EXT). We describe an overview of our conceptual models, plan for gene–environment interplay analyses, and present main effects results evaluating six candidate genes potentially relevant to SUDs and EXT (MAOA, 5-HTTLPR, COMT, DRD2, DAT1, and DRD4). All samples included rich longitudinal and phenotypic measurements from childhood/adolescence (ages 5–13) through early adulthood (ages 25–33); sample sizes ranged from 3487 in the test sample, to ~600–1000 in the replication samples. Phenotypes included lifetime symptom counts of SUDs (nicotine, alcohol and cannabis), adult antisocial behavior, and an aggregate externalizing disorder composite. Covariates included the first 10 ancestral principal components computed using all autosomal markers in subjects across the data sets, and age at the most recent assessment. Sex, ancestry, and exposure effects were thoroughly evaluated. After correcting for multiple testing, only one significant main effect was found in the test sample, but it was not replicated. Implications for subsequent gene–environment interplay analyses are discussed.

General and substance-specific predictors of young adult nicotine dependence, alcohol use disorder, and problem behavior: Replication in two samples

BACKGROUND This paper presents two replications of a heuristic model for measuring environment in studies of gene-environment interplay in the etiology of young adult problem behaviors. METHODS Data were drawn from two longitudinal, U.S. studies of the etiology of substance use and related behaviors: the Raising Healthy Children study (RHC; N=1040, 47% female) and the Minnesota Twin Family Study (MTFS; N=1512, 50% female). RHC included a Pacific Northwest, school-based, community sample. MTFS included twins identified from state birth records in Minnesota. Both studies included commensurate measures of general family environment and family substance-specific environments in adolescence (RHC ages 10-18; MTFS age 18), as well as young adult nicotine dependence, alcohol and illicit drug use disorders, HIV sexual risk behavior, and antisocial behavior (RHC ages 24, 25; MTFS age 25). RESULTS Results from the two samples were highly consistent and largely supported the heuristic model proposed by Bailey et al. (2011). Adolescent general family environment, family smoking environment, and family drinking environment predicted shared variance in problem behaviors in young adulthood. Family smoking environment predicted unique variance in young adult nicotine dependence. Family drinking environment did not appear to predict unique variance in young adult alcohol use disorder. CONCLUSIONS Organizing environmental predictors and outcomes into general and substance-specific measures provides a useful way forward in modeling complex environments and phenotypes. Results suggest that programs aimed at preventing young adult problem behaviors should target general family environment and family smoking and drinking environments in adolescence.

Increased Risk of Smoking in Female Adolescents Who Had Childhood ADHD

OBJECTIVE This study examined the effects of childhood attention deficit hyperactivity disorder (ADHD) symptoms, both inattention and hyperactivity-impulsivity, on the development of smoking in male and female adolescents. METHOD Twin difference methods were used to control for shared genetic and environmental confounders in three population-based, same-sex twin samples (N=3,762; 64% monozygotic). One cohort oversampled female adolescents with ADHD beginning in childhood. Regressions of childhood inattentive and hyperactive-impulsive symptoms were conducted to predict smoking outcomes by age 17. ADHD effects were divided into those shared between twins in the pair and those nonshared, or different within pairs. RESULTS Adolescents who had more severe ADHD symptoms as children were more likely to initiate smoking and to start smoking younger. The association of ADHD symptoms with daily smoking, number of cigarettes per day, and nicotine dependence was greater in females than in males. Monozygotic female twins with greater attentional problems than their co-twins had greater nicotine involvement, consistent with possible causal influence. These effects remained when co-occurring externalizing behaviors and stimulant medication were considered. Hyperactivity-impulsivity, while also more strongly related to smoking for female adolescents, appeared primarily noncausal. CONCLUSIONS Smoking initiation and escalation are affected differentially by ADHD subtype and gender. The association of inattention with smoking in female adolescents may be causal, whereas hyperactivity-impulsivity appears to act indirectly, through shared propensities for both ADHD and smoking.

Antisocial peer affiliation and externalizing disorders: Evidence for Gene × Environment × Development interaction.

Gene × Environment interaction contributes to externalizing disorders in childhood and adolescence, but little is known about whether such effects are long lasting or present in adulthood. We examined gene-environment interplay in the concurrent and prospective associations between antisocial peer affiliation and externalizing disorders (antisocial behavior and substance use disorders) at ages 17, 20, 24, and 29. The sample included 1,382 same-sex twin pairs participating in the Minnesota Twin Family Study. We detected a Gene × Environment interaction at age 17, such that additive genetic influences on antisocial behavior and substance use disorders were greater in the context of greater antisocial peer affiliation. This Gene × Environment interaction was not present for antisocial behavior symptoms after age 17, but it was for substance use disorder symptoms through age 29 (though effect sizes were largest at age 17). The results suggest adolescence is a critical period for the development of externalizing disorders wherein exposure to greater environmental adversity is associated with a greater expression of genetic risk. This form of Gene × Environment interaction may persist through young adulthood for substance use disorders, but it appears to be limited to adolescence for antisocial behavior.