The present study examined the intergenerational transmission of internalizing and externalizing symptom severity, which indexes comorbidity, and symptom directionality, which indicates differentiation toward externalizing versus internalizing problems. Data are from 854 male and female, same-sex adult twin pairs born between 1926 and 1971 (32–60 years old, M = 44.9 years, SD = 4.9 years) from the Twin and Offspring Study in Sweden and their adolescent offspring (11–22 years old, M = 15.7 years, SD = 2.4 years, 52% female). Children-of-twins models revealed additive (9%) and dominant (45%) genetic and nonshared environmental (47%) influences on twins’ symptom severity, and additive genetic (39%) and nonshared environmental (61%) influences on twins’ symptom directionality. Both comorbid problems and preponderance of symptoms of a particular – internalizing versus externalizing – spectrum were correlated across parent and child generations, although associations were modest especially for directionality (i.e., transmission of specific symptom type). By interpreting findings alongside a recent study of adolescent twins, we demonstrate that the intergenerational transmission of symptom severity and symptom directionality are both unlikely to be attributable to genetic transmission, are both likely to be influenced by direct phenotypic transmission and/or nonpassive rGE, and the intergenerational transmission of symptom severity is also likely to be influenced by passive rGE.

This research examines maternal smoking during pregnancy and risk for poorer executive function in siblings discordant for exposure. Data (N = 173 families) were drawn from the Missouri Mothers and Their Children study, a sample, identified using birth records (years 1998–2005), in which mothers changed smoking behavior between two pregnancies (Child 1 [older sibling]: Mage = 12.99; Child 2 [younger sibling]: Mage = 10.19). A sibling comparison approach was used, providing a robust test for the association between maternal smoking during pregnancy and different aspects of executive function in early-mid adolescence. Results suggested within-family (i.e., potentially causal) associations between maternal smoking during pregnancy and one working memory task (visual working memory) and one response inhibition task (color-word interference), with increased exposure associated with decreased performance. Maternal smoking during pregnancy was not associated with stop-signal reaction time, cognitive flexibility/set-shifting, or auditory working memory. Initial within-family associations between maternal smoking during pregnancy and visual working memory as well as color-word interference were fully attenuated in a model including child and familial covariates. These findings indicate that exposure to maternal smoking during pregnancy may be associated with poorer performance on some, but not all skills assessed; however, familial transmission of risk for low executive function appears more important.

Using a longitudinal design (Wave 1 n = 164, Mage = 3.57 years, 54% female, predominantly White and French-speaking), the current study sought to answer two questions: 1) does poverty influence children’s negative emotionality through heightened family-level, poverty-related stress? and 2) is negative emotionality, in turn, predictive of adolescent internalizing symptoms, externalizing behaviors, cognitive abilities, and physical health? Results confirmed an indirect pathway from family poverty to child emotionality through poverty-related stress. In addition, negative emotionality was associated with adolescent internalizing symptoms, attention difficulties, and physical health, but not externalizing symptoms, even when controlling for early poverty exposure.

Gene-environment correlations and interactions for the relationship between emotional problems (EP) and family environment in adolescents in low- to middle-income countries (LMIC) have been rarely investigated. In total, 3207 adolescent twins aged 12–18 (Mean = 14.6 ± 1.73) years attending public schools in Lagos State in Nigeria completed measures of EP and Family Chaos (FC). Model-fitting analyses suggested that genetic and non-shared environmental influences on EP were 21% and 71%, respectively, and the corresponding estimates were 23% and 71% for FC. Shared environmental influences were not significant (8% and 6% respectively). Phenotypic correlation between EP and FC was .30 (95% CI = .27–.34), which was significantly influenced by genetic (A – 49%, 95% CI: 0.01–0.97) and non-shared environmental factors (E – 32%, 95% CI: 0.10–0.54). Shared environmental influences were not significant (C – 19%, 95% CI: −0.13 to 0.50). Moderation effects were significant whereby as FC increased, A on EP decreased (βA = −0.07, 95% CI: −0.12 to −0.02) while E increased (βE = 0.06, 95% CI: 0.03–0.09). Our findings indicate that genetic and non-shared environmental risk factors may mediate the relationship between EP and FC, and that as FC increases, protective genetic influences on EP may be attenuated, whereas environmental influences may become stronger in adolescents in LMIC.

Caregiving experiences are implicated in children’s depression risk; however, children’s neural reactivity to positive and negative feedback from mothers, a potential mediator of depression risk, is poorly understood. In a sample of 81 children (Mage = 11.12 years, SDage = 0.63), some of whom were recruited based on a maternal history of depression (n = 29), we used fMRI to characterize children’s neural responses to maternal praise and criticism. Maternal history of depression was unrelated to children’s brain activity during both the praise and criticism conditions; however, ROI analyses showed that children’s self-reported depressive symptoms were negatively associated with functional activity in the left anterior insula and right putamen while hearing maternal criticism. Whole-brain analyses showed that children’s depressive symptoms were positively associated with left inferior frontal gyrus activity while listening to maternal praise. These findings complement past work implicating these brain regions in the processing of emotionally salient stimuli, reward processing, and internal speech. Given associations between early depressive symptoms and later disorder, findings suggest that maladaptive neural processing of maternal feedback may contribute to children’s early emerging risk for depression.

Studies suggest that children who have experienced neglect are at risk for bullying which in turn increases the risk for poor mental health. Here we extend this research by examining whether this risk extends to the neglect associated with severe institutional deprivation and then testing the extent to which these effects are mediated by prior deprivation-related neuro-developmental problems such as symptoms of inattention, hyperactivity and autism. Data were collected at ages 6, 11, 15, and young adulthood (22–25 years) from 165 adoptees who experienced up to 43 months of deprivation in Romanian Orphanages in 1980s and 52 non-deprived UK adoptees (N = 217; 50.23% females). Deprivation was associated with elevated levels of bullying and neuro-developmental symptoms at ages 6 through 15 and young adult depression and anxiety. Paths from deprivation to poor adult mental health were mediated via cross-lagged effects from earlier neuro-developmental problems to later bullying. Findings evidence how deep-seated neuro-developmental impacts of institutional deprivation can cascade across development to impact social functioning and mental health. These results elucidate cascade timing and the association between early deprivation and later bullying victimization across childhood and adolescence.

Externalizing behavior in early adolescence is associated with alcohol use in adolescence and early adulthood and these behaviors often emerge as part of a developmental sequence. This pattern can be the result of heterotypic continuity, in which different behaviors emerge over time based on an underlying shared etiology. In particular, there is largely a shared genetic etiology underlying externalizing and substance use behaviors. We examined whether polygenic risk for alcohol use disorder predicted (1) externalizing behavior in early adolescence and alcohol use in adolescence in the Early Steps Multisite sample and (2) externalizing behavior in adolescence and alcohol use in early adulthood in the Project Alliance 1 (PAL1) sample. We examined associations separately for African Americans and European Americans. When examining European Americans in the Early Steps sample, greater polygenic risk was associated with externalizing behavior in early adolescence. In European Americans in PAL1, we found greater polygenic risk was associated with alcohol use in early adulthood. Effects were largely absent in African Americans in both samples. Results imply that genetic predisposition for alcohol use disorder may increase risk for externalizing and alcohol use as these behaviors emerge developmentally.

We tested whether exposure to gun or knife violence over two decades is a cause of depression in young adulthood using data from a nationally representative sample in the United States. The National Longitudinal Study of Adolescent to Adult Health is a sample of 20,745 adolescents, assessed in 1994–95 with follow-ups in 1995–1996 (n = 14,738), 2001–2002 (n = 15,197) and 2007–2008 (n = 15,701; 24 to 32 years old). At each wave, respondents reported exposure to gun or knife violence and symptoms of depression. Regression and sibling fixed effects analyses were conducted to test whether cumulative exposure to gun or knife violence was associated with depression. In fully adjusted models, greater cumulative exposure to gun or knife violence was associated with more symptoms of depression (b = 0.12, 95% C. I. = 0.05; 0.19, p < 0.01) and higher risk for clinically significant depression in young adulthood (OR = 1.07, 95% C. I. = 1.02; 1.13, p < 0.01). Results replicated in sibling fixed effects models (b = 0.21, 95% C. I. = 0.01; 0.42, p < 0.05). These quasi-experimental data suggest that exposure to gun or knife violence is a cause of depression in young adulthood.

The present study examined putative environmental predictors of adolescent substance use, using a prospective adoption design to distinguish between environmental mediation (i.e., parenting influencing adolescent substance use), passive gene–environment correlation (i.e., parental genetic predisposition influencing the association between parenting characteristics and adolescent substance use), and evocative gene–environment correlation (i.e., children’s genetic predisposition influencing parenting). Longitudinal data from the Colorado Adoption Project (395 adoptees, 491 nonadoptees, 485 adoptive parents, and 490 biological parents) were examined. Children (48% girls) were assessed at ages 1 to 17 years. Over 90% of the sample were non-Hispanic White. Associations between parenting and adolescent substance use were compared between adoptive and nonadoptive families. Positive, negative, and inconsistent parenting measures in early childhood through adolescence were not consistently associated with adolescent substance use, with only 6% of correlations being statistically significant (r = −0.152 to .207). However, parent–child relationship quality assessed from childhood to adolescence and orientation to parents assessed during adolescence were significantly, negatively associated with adolescent substance use, with 71% of correlations being statistically significant (r = −0.88 to −0.11). There was little evidence of sex differences in the associations. Environmental mediation, rather than passive or evocative gene–environment correlation, explained most associations.

The current study investigated whether prosocial behavior and emotional problems, peer problems, conduct problems, and hyperactivity and inattention problems were long-term longitudinally and bidirectionally related at inter- and or intra-individual levels from early childhood through mid-adolescence. Parents in the United Kingdom reported their child’s prosocial behavior and multidimensional psychopathology at ages 3, 5, 7, 11, and 14 years (N = 16,984, 51% male, 83% White). Four random intercepts cross-lagged panel models were fitted. Higher levels of earlier prosocial behavior were associated with greater than expected decrements in psychopathology. At an intraindividual, within-person level, prosocial behavior was negatively bidirectionally associated with peer, conduct, and hyperactivity and inattention problems. Also at an intraindividual, within-person level, prosocial behavior was unidirectionally protective against emotional problems. At an interindividual level, prosocial behavior and each dimension of psychopathology were negatively associated. Therefore, engaging in prosocial behavior can reduce psychopathological symptoms over time (and vice versa), and youth who are more prosocial also tend to experience fewer psychopathological symptoms. Intraindividual associations were small while interindividual associations were moderate to large. Implications for theory, future research, and evidence-based interventions are discussed.

Genetic factors contribute to the intergenerational transmission of alcohol misuse, but not all individuals at high genetic risk develop problems. The present study examined adolescent relationships with parents, peers, and romantic partners as predictors of realized resistance, defined as high biological risk for disorder combined with a healthy outcome, to alcohol initiation, heavy episodic drinking, and alcohol use disorder (AUD). Data were from the Collaborative Study on the Genetics of Alcoholism (N = 1,858; 49.9% female; mean age at baseline = 13.91 years). Genetic risk, indexed using family history density and polygenic risk scores for alcohol problems and AUD, was used to define alcohol resistance. Adolescent predictors included parent-child relationship quality, parental monitoring, peer drinking, romantic partner drinking, and social competence. There was little support for the hypothesis that social relationship factors would promote alcohol resistance, with the exception that higher father-child relationship quality was associated with higher resistance to alcohol initiation ( $$\hat \beta $$ = −0.19, 95% CI = −0.35, −0.03). Unexpectedly, social competence was associated with lower resistance to heavy episodic drinking ( $$\hat \beta $$ = 0.10, 95% CI = 0.01, 0.20). This pattern of largely null effects underscores how little is known about resistance processes among those at high genetic risk for AUD.

Deficits in executive functioning both run in families and serve as a transdiagnostic risk factor for psychopathology. The present study employed twin modeling to examine parenting as an environmental pathway underlying the intergenerational transmission of executive functioning in an at-risk community sample of children and adolescents (N = 354 pairs, 167 monozygotic). Using structural equation modeling of multi-informant reports of parenting and a multi-method measure of child executive functioning, we found that better parent executive functioning related to less harsh, warmer parenting, which in turn related to better child executive functioning. Second, we assessed the etiology of executive functioning via the nuclear twin family model, finding large non-shared environmental effects (E = .69) and low-to-moderate heritability (A = .22). We did not find evidence of shared environmental effects or passive genotype–environment correlation. Third, a bivariate twin model revealed significant shared environmental overlap between both warm and harsh parenting and child executive functioning (which may indicate either passive genotype–environment correlation or environmental mediation), and non-shared environmental overlap between only harsh parenting and child executive functioning (indicating an effect of harsh parenting separable from genetic confounds). In summary, genetics contribute to the intergenerational transmission of executive functioning, with environmental mechanisms, including harsh parenting, also making unique contributions.

This study examined whether a key set of adolescent and early adulthood risk factors predicts problematic alcohol, cannabis, and other substance use in established adulthood. Two independent samples from the Child Development Project (CDP; n = 585; 48% girls; 81% White, 17% Black, 2% other race/ethnicity) and Fast Track (FT; n = 463; 45% girls; 52% White, 43% Black, 5% other race/ethnicity) were recruited in childhood and followed through age 34 (CDP) or 32 (FT). Predictors of substance use were assessed in adolescence based on adolescent and parent reports and in early adulthood based on adult self-reports. Adults reported their own problematic substance use in established adulthood. In both samples, more risk factors from adolescence and early adulthood predicted problematic alcohol use in established adulthood (compared to problematic cannabis use and other substance use). Externalizing behaviors and prior substance use in early adulthood were consistent predictors of problematic alcohol and cannabis misuse in established adulthood across samples; other predictors were specific to the sample and type of substance misuse. Prevention efforts might benefit from tailoring to address risk factors for specific substances, but prioritizing prevention of externalizing behaviors holds promise for preventing both alcohol and cannabis misuse in established adulthood.

In this person-centered study, we identified different profiles of resilience and vulnerability in emerging adulthood in response to previously experienced stressful life events. Additionally, we examined whether mothers’ and fathers’ parenting and participants’ personality traits in adolescence predicted these profiles. Data from the Flemish Study on Parenting, Personality, and Development (N = 346 families) were used. At T1 (2004; Mage = 11 years), T2 (2007), and T3 (2009), mothers and fathers reported on their parenting and their child’s personality. At T4 (2018; Mage = 25 years), emerging adults retrospectively self-reported the occurrence and impact of 22 stressful life events and rated current behavior problems and subjective well-being. Latent profile analysis revealed three profiles: Competent (71%; low stress, low behavior problems, high subjective well-being), Vulnerable (21%; average stress, high behavior problems, low subjective well-being), and Resilient (9%; high stress, average behavior problems, average subjective well-being). Emerging adults in the Resilient profile had experienced higher levels of maternal positive parenting and were less emotionally stable and conscientious than those in the Competent profile. Furthermore, emerging adults in the Vulnerable profile were less emotionally stable than their peers in the Competent profile. These findings reveal new insights into the heterogeneous patterns of emerging adults’ adaptation following stressful life events.

Some children are more affected by specific family environments than others, as a function of differences in their genetic make-up. However, longitudinal studies of genetic moderation of parenting effects during early childhood have not been conducted. We examined developmental profiles of child behavior problems between 18 months and age 8 in a longitudinal parent–offspring sample of 361 adopted children. In toddlerhood (18 months), observed structured parenting indexed parental guidance in service of task goals. Biological parent psychopathology served as an index of genetic influences on children’s behavior problems. Four profiles of child behavior problems were identified: low stable (11%), average stable (50%), higher stable (29%), and high increasing (11%). A multinominal logistic regression analysis indicated a genetically moderated effect of structured parenting, such that for children whose biological mother had higher psychopathology, the odds of the child being in the low stable group increased as structured parenting increased. Conversely, for children whose biological mother had lower psychopathology, the odds of being in the low stable group was reduced when structured parenting increased. Results suggest that increasing structured parenting is an effective strategy for children at higher genetic risk for psychopathology, but may be detrimental for those at lower genetic risk.

Considerable attention has been directed towards studying co-occurring psychopathology through the lens of a general factor (p-factor). However, the developmental trajectory and stability of the p-factor have yet to be fully understood. The present study examined the explanatory power of dynamic mutualism theory – an alternative framework that suggests the p-factor is a product of lower-level symptom interactions that strengthen throughout development. Data were drawn from a population-based sample of girls (N = 2450) who reported on the severity of internalizing and externalizing problems each year from age 14 to age 21. Predictions of dynamic mutualism were tested using three distinct complementary statistical approaches including: longitudinal bifactor models, random-intercept cross-lagged panel models (RI-CLPMs), and network models. Across methods, study results document preliminary support for mutualistic processes in the development of co-occurring psychopathology (that is captured in p). Findings emphasize the importance of exploring alternative frameworks and methods for better understanding the p-factor and its development.

Belonging is a basic human need, with social isolation signaling a threat to biological fitness. Sensitivity to ostracism varies across individuals and the lifespan, peaking in adolescence. Government-imposed restrictions upon social interactions during COVID-19 may therefore be particularly detrimental to young people and those most sensitive to ostracism. Participants (N = 2367; 89.95% female, 11–100 years) from three countries with differing levels of government restrictions (Australia, UK, and USA) were surveyed thrice at three-month intervals (May 2020 – April 2021). Young people, and those living under the tightest government restrictions, reported the worst mental health, with these inequalities in mental health remaining constant throughout the study period. Further dissection of these results revealed that young people high on social rejection sensitivity reported the most mental health problems at the final assessment. These findings help account for the greater impact of enforced social isolation on young people’s mental health, and open novel avenues for intervention.

This study investigated the transactional relations between vocabulary and disruptive behaviors (DB; physical aggression and opposition/rule breaking/theft and vandalism), during the transition to formal schooling, using a community sample of 572 children. Cross-lagged panel model analyses were used to examine bidirectional relationships, comparing physical aggression to non-aggressive DB. Transactional associations between vocabulary and DB were observed, coinciding with school entry. Lower vocabulary in preschool (60mo.) was predictive of higher physical aggression scores in kindergarten. In turn, higher physical aggression in kindergarten was predictive of lower vocabulary in 1st grade. For non-aggressive DB, recurrent associations were found. Lower verbal skills in preschool (42mo.) and kindergarten predicted higher non-aggressive DB scores later in preschool and in 1st grade respectively. In turn, higher non-aggressive DB in kindergarten predicted lower vocabulary scores in 1st grade. In contrast to transactional paths from vocabulary to DB, transactional paths from DB to vocabulary observed after the transition to elementary school remained significant after controlling for comorbid hyperactivity, impulsivity and inattention behaviors, suggesting these links were specific to aggressive and non-aggressive DB. Practical implications for prevention are discussed.

Substance use increases throughout adolescence, and earlier substance use may increase risk for poorer health. However, limited research has examined whether stress responses relate to adolescent substance use, especially among adolescents from ethnic minority and high-adversity backgrounds. The present study assessed whether blunted emotional and cortisol responses to stress at age 14 related to substance use by ages 14 and 16, and whether associations varied by poverty status and sex. A sample of 277 Mexican-origin youth (53.19% female; 68.35% below the poverty line) completed a social-evaluative stress task, which was culturally adapted for this population, and provided saliva samples and rated their anger, sadness, and happiness throughout the task. They also reported whether they had ever used alcohol, marijuana, cigarettes, and vaping of nicotine at age 14 and again at age 16. Multilevel models suggested that blunted cortisol reactivity to stress was associated with alcohol use by age 14 and vaping nicotine by age 16 among youth above the poverty line. Also, blunted sadness and happiness reactivity to stress was associated with use of marijuana and alcohol among female adolescents. Blunted stress responses may be a risk factor for substance use among youth above the poverty line and female adolescents.