Kristine Marceau

Although specific parenting behaviors have been identified as protective factors for adolescent substance use (SU), the relationship between parents’ beliefs about the risks associated with SU and their adolescent’s SU remains unclear. Associations between parental characteristics and adolescent SU may reflect both environmental and genetic influences. Using data from a prospective longitudinal adoption study, we investigated whether parents’ substance-related risk perceptions when their adolescent was 15 years old predicted adolescent SU frequency at age 18, whether parents’ lifetime history of problematic SU predicted their risk perceptions and indirectly predicted adolescent SU, and whether these associations differed by biological relatedness. The sample included 432 parent-adolescent dyads (53.0% of adolescents were male and 58.6% were White), of whom 324 were not biologically related. We hypothesized that greater perceived risk would predict less frequent adolescent SU and that associations would be stronger among biologically related dyads. Contrary to hypotheses, parents’ alcohol- and cannabis-related risk perceptions did not predict adolescents’ subsequent alcohol or cannabis use frequency, and biological relatedness did not moderate these associations. Parents with a lifetime history of problematic SU perceived less risk associated with cannabis use, but there was no significant indirect association with adolescent cannabis use. By leveraging an adoption design to distinguish shared genetic from environmental influences, these findings suggest that parents’ substance-related risk perceptions alone may have limited influence on adolescent SU and that more proximal parenting behaviors may be important prevention targets.

Adolescents are more likely to use alcohol if close friends are characterized as majority other-sex. The extent to which the association between proportion of other-sex close friends and adolescent alcohol use is directional and/or reciprocal is unclear. Although evidence is mixed for male adolescents, higher proportion of other-sex close friends is associated with increased risk of alcohol use for female adolescents. This study examined whether proportion of other-sex close friends and alcohol use predicted each other longitudinally and if associations differed by sex. Participants were 1021 adolescents (M_age = 12.22 years), 52.20% female, 71.36% White non-Hispanic, from a cohort-sequential study. Adolescent alcohol use was measured via progression on alcohol use milestones. Proportion of other-sex close friends was calculated via adolescent report of their three closest friends' sex. A random-intercept cross-lagged panel model tested for reciprocal, longitudinal association between other-sex close friends and alcohol use across six timepoints. Sex differences were examined via a multigroup framework. Alcohol use and proportion of other-sex close friends were relatively stable traits, with other-sex close friends' autoregressive accumulation more pronounced at later timepoints. There were no observed concurrent nor cross-lagged associations, indicating no reciprocal association within individuals. However, there was a positive between-person association, wherein adolescents with a higher proportion of other-sex close friends had, on average, greater alcohol involvement. Results suggest that the influence of other-sex close friends on alcohol use is a between-, not within-, person process. Thus, theory purporting a within-person reciprocal mechanism may not be pertinent within the context of other-sex close friendships.

Family-based longitudinal studies are increasingly used to investigate psychological and behavioral processes, and it is imperative to understand the power to detect effects in increasingly complex statistical models. The Discordant-Sibling Random Intercept Cross-Lagged Panel Model (DS RI-CLPM) extends the Random Intercept Cross-Lagged Panel Model to estimate longitudinal bidirectional associations by separating within- and between family-level components to control stable traits and sibling-shared family-level confounding. To inform study design in family-based research, we conducted a simulation-based power analysis varying the number of families and waves, sibling discordance, random intercept variance proportion, effect sizes, and variable’s non-normality. Power increased with both increase in families and waves, although effect size was the strongest determinant. Within-family cross-lagged effects were easier to detect than between-family effects, and joint detection required most conservative designs. Practical recommendations for numbers of families and waves are provided for longitudinal research on psychological and behavioral phenomena using the DS RI-CLPM.

Maternal tobacco smoking during pregnancy (MSDP) is associated with an increased risk of child externalizing problems. It remains unclear whether these associations are externalizing-specific, or better explained by comorbidity between externalizing and internalizing domains, or vary by age and sex. To address comorbidity and differentiation between domains, we leveraged the severity-directional model of psychopathology. Severity reflects the overall level of psychopathology symptoms across both domains (high levels of severity can only be reached by having symptoms of both types simultaneously), whereas directionality captures the balance/differentiation of internalizing vs. externalizing symptoms regardless of number of total symptoms. Participants included 16,335 children aged 1–19 years old (47.78% female, 58.17% White, 75.46% non-Hispanic) from 55 U.S.-based cohorts within the Environmental Influences on Child Health Outcomes (ECHO) consortium. MSDP predicted differentiation toward externalizing problems in 2-year age bins 1–2 through 7–8 and 13–14 years; remaining (non-significant) age bins had similar magnitudes. MSDP predicted higher symptom severity in all age bins. Findings likely reflect a combination of MSDP associations with comorbid symptom severity and specificity toward externalizing problems, with little evidence of age or sex differences. Additional analyses explored e-cigarette use, other prenatal substance use, and postnatal smoke exposure; associations were sparse and unsystematic.

Both longer term developmental changes (increases in hostility, decreases in warmth) and lability (year-to-year fluctuations) in parent-child relationship quality across childhood and adolescence have been linked to adolescent externalizing behaviors. Using a prospective longitudinal study of 561 children who were adopted into nonrelative families at birth (57% male, 56% White, 19% multiracial, 13% Black, 11% Hispanic) where parental warmth and hostility reflect environmental influences or child-evoked reactions, we examined associations between parent-child relationship measures and externalizing behaviors at age 11 and across adolescence (i.e., from age 11 to 13-15 years). Because studies considering gene-environment interplay especially in associations between lability and child externalizing behaviors are sparse and parent-child relationship measures support the intergenerational transmission of psychopathology, we also tested whether parent psychopathology of both adoptive parent (AP; environmental intergenerational transmission) and birth parents (genetic intergenerational transmission) moderated these associations in multivariate regression models. Findings generally supported more effects of fathers' than mothers' warmth and hostility. Although there were some linear associations of increased lability with externalizing behaviors, these did not persist in the context of a multivariate model. Associations between both parents' increasing hostility across childhood on age 11 externalizing behaviors and for fathers increasing hostility and decreasing warmth on increases in externalizing behaviors across adolescence more likely reflect a combination of bidirectional evocative and parenting environmental associations than purely parenting environmental transmission. Moderation by parent psychopathology was sparse, and sensitivity tests revealed no differences by child sex. (PsycInfo Database Record (c) 2025 APA, all rights reserved).

Introduction: Adolescents are particularly susceptible to peer influence and at higher risk of engaging in problematic behaviors through peer interactions, but also vary in the extent to which they are influenced by their peers. Resistance to peer influence, the tendency to refuse undesired peer pressure, is one key factor for this variation. However, how genetic and contextual influences shape the development of RPI remain unclear. Methods: The present study leveraged data from 552 family triads, collected in the U.S. between 2003 and 2022, in an adopted‐at‐birth design. Family triads included an adopted child (57.2% male; 55.3% European American, 19.6% multiracial, 13.2% African American, 10.9% Hispanic/Latinx), birth parents, and adoptive parents. Moderated mediation models were tested to examine whether: (1) child phenotypic impulsivity at age 7 mediated the association between genetic risk for impulsivity and adolescent RPI; (2) child phenotypic self‐esteem (age 6–8) mediated the association between genetic factor for self‐esteem and adolescent RPI; (3) adoptive parent responsiveness weakened the impulsivity pathway; and (4) adoptive parent responsiveness strengthened the self‐esteem pathway. Analyses were performed separately for age 11 (early adolescent; M _age = 11.39, SD _age = 0.55) and age 13–15 (middle adolescent; M _age = 14.97, SD _age = 1.24) RPI as the outcome variable. Results: Results revealed that birth parent self‐esteem positively predicted early adolescent RPI, through elevated levels of child self‐esteem. RPI was moderately stable from early to middle adolescence. Conclusions: Findings highlight the importance of nurturing children's self‐esteem to improve their skills to resist undesired peer pressure during adolescence.

Previous studies robustly link childhood peer victimization experience to the timing of substance use initiation. However, no study has investigated the contributions of genetic and environmental factors to this link. The current study focused on a sample of 779 twin pairs followed from age 9–10 to 19–20, which is racially/ethnically and socioeconomically representative of the greater Los Angeles area. The aims were to investigate (1) the associations between childhood victimization, including physical (e.g., kicking, pushing), verbal (e.g., taunting), and relational victimization (e.g., spreading rumors), and timing of substance use initiation, and (2) the contributions of genetic/environmental factors to these associations. Multinomial logistic regressions revealed several small associations, but none of these survived corrections for multiple testing. Univariate genetic models suggested genetic (A) and nonshared environmental influences (E) on verbal victimization (V_A = .43, V_E = .57), shared environmental (C) and nonshared environmental factors on relational victimization (V_C = .22, V_E = .78), and ambiguous familial influences and E on physical victimization (V_A = .34, V_E = .66; V_C = .26, V_E = .74). Timing of cigarette initiation were explained by A, C, and E (V_A = .48, V_C = .31, V_E = .21). Quantitative sex differences in contributions of A, C, and E were detected for alcohol (V_AM = .90, V_EM = .10; V_CF = .86, V_EF = .14) and marijuana initiation (V_AM = .89, V_EM = .11; V_CF = .79, V_EF = .21); however, A could be dropped for females and C could be dropped for males across both variables. Multivariate twin analyses were not feasible, due to the low cross-trait correlations. These findings call into question the robustness of links between self-reported victimization in childhood and prospectively measured timing of substance initiation across adolescence.