Altruism is a prosocial tendency that has developed through long-term evolutionary selection. The present study adopts social comparison and evolutionary psychology theories to examine how benign/malicious envy can affect altruism and how altruism can affect the two types of envy in turn, respectively. In Study 1, 513 adolescents participated in a three-wave longitudinal survey to explore the relationships between dispositional altruistic tendency and dispositional benign/malicious envy. The cross-lagged analysis showed a long-term and stable negative bidirectional relationship between dispositional altruistic tendency and dispositional malicious envy and a short-term positive bidirectional relationship between dispositional altruism and dispositional benign envy. In Study 2, 109 adolescents kept a weekly diary for seven consecutive weeks to record state levels of altruistic tendency and benign/malicious envy in their daily lives. The hierarchical linear model demonstrated that weekly altruistic tendency and weekly benign envy could positively predict each other, and weekly altruistic tendency presented a negative bidirectional relationship with weekly malicious envy. These findings offer an effective way to study the relationship between human behavior and emotions from perspectives of social comparison and evolutionary psychology theories. Meanwhile, it also has practical significance for the harmonious development of society.

The stress-vulnerability model has been repeatedly highlighted in relation to the risk, onset and course of psychosis, and has been independently studied in clinical high-risk (CHR) and first-episode psychosis (FEP) populations. Notable in this literature, however, is that there are few studies directly comparing markers of stress response across progressive stages of illness. Here we examined the psychobiological response to the Trier Social Stress Test in 28 CHR (mean age 19.1) and 61 FEP (age 23.0) patients, in order to understand the stage(s) or trajectories in which differences in subjective stress or physiological response occur. The overall clinical sample had greater perceived stress and blunted cortisol (FEP + CHR, n = 89, age 21.7) compared with healthy controls (n = 45, age 22.9). Additional analyses demonstrated elevated heart rate and systolic blood pressure in FEP compared with CHR, but there were no further differences in physiological parameters (cortisol, heart rate, or blood pressure) between stage- or trajectory-based groups. Together, this suggests that individual stress response markers may differentially emerge at particular stages en route to psychosis – and demonstrates how stage-based analyses can shed light on the emergence and evolution of neurobiological changes in mental illness.

The present work sought to confirm the factor structure and examine longitudinal strengths-based and mental health correlates of the dysregulation profile (DP) in children of at-risk fragile families of diverse ethnoracial backgrounds. The data came from the Fragile Families and Child Wellbeing Study (N = 2125 families). Mothers (Mage = 25.3) were mostly unmarried (74.6%), and children (51.4% boys) were identified as Black (47.0%), Hispanic (21.4%), White (16.7%), or multiracial or other backgrounds. Childhood DP was constructed using mother reports of the Child Behavior Checklist at age 9. Mothers’ in-home parent–child interactions and depressive symptoms were assessed at child age 5. At age 15, children responded about their own mental health, social skills, and other strengths-focused outcomes. A bifactor DP structure fit well to the data, with the DP factor representing difficulties in self-regulation. Using SEM, we found that mothers who were more depressed and used less warm parenting at child age 5 had children who presented with higher DP at age 9. DP was in turn associated with less social skills, perseverance, optimism, and more anxiety, depression, and impulsivity at adolescence. Childhood DP appears to be relevant and applicable for at-risk, diverse families, and may also impede on children’s future positive functioning.

The current study evaluated risk factors in adolescence on problem drinking and emotional distress in late adolescence and emerging adulthood, and meeting criteria for diagnosed disorders in adulthood. The study included 501 parents and their adolescent who participated from middle adolescence to adulthood. Risk factors in middle adolescence (age 18) included parent alcohol use, adolescent alcohol use, and parent and adolescent emotional distress. In late adolescence (age 18), binge drinking and emotional distress were assessed, and in emerging adulthood (age 25), alcohol problems and emotional distress were examined. Meeting criteria for substance use, behavioral, affective, or anxiety disorders were examined between the ages of 26 and 31. Results showed parent alcohol use predicted substance use disorder through late adolescent binge drinking and emerging adulthood alcohol problems. Behavioral disorders were indirectly predicted by adolescent and emerging adult emotional distress. Affective disorders were indirectly predicted by parent emotional distress through adolescent emotional distress. Finally, anxiety disorders were predicted by parent alcohol use via adolescent drinking; parent emotional distress via adolescent emotional distress, and through adolescent alcohol use and emotional distress. Results provided support for the intergenerational transmission of problem drinking and emotional distress on meeting criteria for diagnosed psychiatric disorders in adulthood.

For mother-infant health especially, the pandemic has brought multiple stressors inside a susceptible psychobiological system. We study the longitudinal associations between maternal prenatal and postpartum: (a) COVID-19 stressful events exposure, (b) pandemic psychological stress, and (c) mental health and infants’ negative affect. A sample of 643 Italian pregnant women completed a web-based survey from April 8th to May 4th, 2020 and a follow-up at 6 months after delivery. Maternal assessment covered prenatal and postpartum measures for: COVID-19 stressful events exposure, pandemic psychological stress, mental health symptoms (i.e., depression, anxiety, posttraumatic stress disorder) and postpartum, social support and report of infants’ negative affect. Maternal mental health symptoms during pregnancy, at the peak of pandemic, is longitudinally associated with infant negative affect, with postpartum mental health mediating this association. Also, maternal COVID-19 stressful events exposure in postpartum is associated with negative affect at 6 months mediated by postpartum mental health symptoms. Maternal pandemic psychological stress during pregnancy predicted mental health symptoms in postpartum. The study supports the association between pandemic-related maternal health across pregnancy and postpartum and offspring’s development (i.e., negative affect). It also puts the spotlight on mental health risk in women experiencing lockdown during pregnancy, especially when feeling high psychological stress in pregnancy or when directly exposed to COVID-19 stressful events postpartum.

Female adolescents have a greatly increased risk of depression starting at puberty, which continues throughout the reproductive lifespan. Sex hormone fluctuation has been highlighted as a key proximal precipitating factor in the development of mood disorders tied to reproductive events; however, hormone-induced affective state change is poorly understood in the pubertal transition. The present study investigated the impact of recent stressful life events on the relationship between sex hormone change and affective symptoms in peripubertal female participants. Thirty-five peripubertal participants (ages 11–14, premenarchal, or within 1 year of menarche) completed an assessment of stressful life events, and provided weekly salivary hormone collections [estrone, testosterone, dehydroepiandrosterone (DHEA)] and mood assessments for 8 weeks. Linear mixed models tested whether stressful life events provided a context in which within-person changes in hormones predicted weekly affective symptoms. Results indicated that exposure to stressful life events proximal to the pubertal transition influenced the directional effects of hormone change on affective symptoms. Specifically, greater affective symptoms were associated with increases in hormones in a high stress context and decreases in hormones in a low stress context. These findings provide support for stress-related hormone sensitivity as a diathesis for precipitating affective symptoms in the presence of pronounced peripubertal hormone flux.

Internalizing and externalizing problems that emerge during adolescence differentially increase boys’ and girls’ risk for developing psychiatric disorders. It is not clear, however, whether there are sex differences in the intrinsic functional architecture of the brain that underlie changes in the severity of internalizing and externalizing problems in adolescents. Using resting-state fMRI data and self-reports of behavioral problems obtained from 128 adolescents (73 females; 9–14 years old) at two timepoints, we conducted multivoxel pattern analysis to identify resting-state functional connectivity markers at baseline that predict changes in the severity of internalizing and externalizing problems in boys and girls 2 years later. We found sex-differentiated involvement of the default mode network in changes in internalizing and externalizing problems. Whereas changes in internalizing problems were associated with the dorsal medial subsystem in boys and with the medial temporal subsystem in girls, changes in externalizing problems were predicted by hyperconnectivity between core nodes of the DMN and frontoparietal network in boys and hypoconnectivity between the DMN and affective networks in girls. Our results suggest that different neural mechanisms predict changes in internalizing and externalizing problems in adolescent boys and girls and offer insights concerning mechanisms that underlie sex differences in the expression of psychopathology in adolescence.

This study’s aim was to examine whether there are negative increasing cycles of peer victimization and rejection sensitivity over time. Drawing from Social Information Processing Theory, we hypothesized that victimization leads to higher levels of rejection sensitivity, which would put adolescents at risk for higher future victimization. Data were collected in a four-wave study with 233 Dutch adolescents starting secondary education (Mage = 12.7 years), and a three-wave study with 711 Australian adolescents in the last years of primary school (Mage = 10.8 years). Random-intercept cross-lagged panel models were used to disentangle between-person from within-person effects. In each sample, a significant between-person association was found: adolescents with higher levels of victimization as compared to their peers also reported higher levels of rejection sensitivity. At the within-person level, all concurrent associations between individual fluctuations of victimization and rejection sensitivity were significant, but there were no significant cross-lagged effects (except in some sensitivity analyses). These findings demonstrate that victimization and rejection sensitivity are interrelated, but there may not be negative victimization-rejection sensitivity cycles during the early-middle adolescent years. Possibly, cycles establish earlier in life or results are due to shared underlying factors. Further research is needed examining different time lags between assessments, age groups, and contexts.

Internalizing symptoms have been linked to bullying perpetration and victimization in adolescence. However, the directions of any causal relationships remain unclear, and limited research has identified the mechanisms that explain the associations. Given the salience of peer relationships during the teenage years, we examine whether perceived support from friends is one such mechanism. By using a transactional framework and four waves of longitudinal panel data on over 900 youth, we test both cross-lagged and indirect associations between bullying perpetration, bullying victimization, internalizing symptoms, and perceived friend support. Our method represents one of the most rigorous tests to date of the mutual influences among these factors. The results show that internalizing symptoms and perceived friend support were reciprocally linked to bullying victimization, but perceived support did not predict internalizing symptoms, and bullying perpetration neither preceded nor followed perceived support or internalizing symptoms. There were no significant indirect paths between bullying involvement and internalizing symptoms through perceived friend support. The results provide only partial support for a transactional model in which bullying victimization, support, and internalizing symptoms are reciprocally related. The implications of these findings for theory, future research, and practice are discussed.

Adolescence is a time of heightened vulnerability for both peer victimization (PV) and internalizing symptoms. While the positive association between them is well established, there is little understanding of the mechanisms underpinning this relationship. To address this gap, the current study aimed to investigate sleep hygiene and school night sleep duration as individual and sequential mediators of the relationship between PV and both depressive and social anxiety symptoms during pre- to mid-adolescence. The study drew upon a community sample of 528 Australian youth aged 10–12 years at baseline (Mage = 11.19, SD = .55; 51.1% boys) and data were collected over five annual measurement occasions. Direct and indirect longitudinal and bidirectional associations were examined using cross-lagged panel analysis. There was no evidence of sequential mediation through both sleep hygiene and sleep duration to depression and social anxiety. Instead, the findings show that sleep hygiene mediated the prospective association between PV and both depressive and social anxiety symptoms, and between PV and sleep duration. Overall, sleep hygiene represents a modifiable transdiagnostic factor that can be targeted to break the cycle of PV, inadequate sleep, and internalizing symptoms.

Prenatal maternal stress and mental health problems are known to increase risk for developmental psychopathology in offspring, yet pathways leading to risk or resiliency are poorly understood. In a quasi-experimental design, we prospectively examined associations between disaster-related prenatal stress, maternal mental health symptoms, and infant temperament outcomes. Mothers who were pregnant during Hurricane Harvey (N = 527) reported on objective hardships (e.g., loss of belongings or income, evacuation, home flooding) related to the storm and subsequent mental health symptoms (anxiety/depression, posttraumatic stress) across time. At a postpartum assessment, mothers reported on their infant’s temperament (negative affect, positive affect, orienting/regulatory capacity). Greater objective hardship indirectly predicted higher levels of infant orienting/regulatory capacity through its association with increased maternal posttraumatic stress symptoms. Greater objective hardship also indirectly predicted higher levels of infant negative affect through its association with increased maternal anxiety/depression symptoms across time. Our findings suggest a psychological mechanism linking prenatal stress with specific temperamental characteristics via maternal mental health symptoms. Findings point to the importance of high-quality assessment and mental health services for vulnerable women and young children.

Maternal antenatal anxiety is an emerging risk factor for child emotional development. Both sex and epigenetic mechanisms, such as DNA methylation, may contribute to the embedding of maternal distress into emotional outcomes. Here, we investigated sex-dependent patterns in the association between antenatal maternal trait anxiety, methylation of the brain-derived neurotrophic factor gene (BDNF DNAm), and infant negative emotionality (NE). Mother–infant dyads (N = 276) were recruited at delivery. Maternal trait anxiety, as a marker of antenatal chronic stress exposure, was assessed soon after delivery using the Stait-Trait Anxiety Inventory (STAI-Y). Infants’ BDNF DNAm at birth was assessed in 11 CpG sites in buccal cells whereas infants’ NE was assessed at 3 (N = 225) and 6 months (N = 189) using the Infant Behavior Questionnaire-Revised (IBQ-R). Hierarchical linear analyses showed that higher maternal antenatal anxiety was associated with greater 6-month-olds’ NE. Furthermore, maternal antenatal anxiety predicted greater infants’ BDNF DNAm in five CpG sites in males but not in females. Higher methylation at these sites was associated with greater 3-to-6-month NE increase, independently of infants’ sex. Maternal antenatal anxiety emerged as a risk factor for infant’s NE. BDNF DNAm might mediate this effect in males. These results may inform the development of strategies to promote mothers and infants’ emotional well-being.

Sipping, an early form of alcohol initiation, is associated with aspects of psychopathology and personality that reflect long-term risk for harmful alcohol use. In the Adolescent Brain and Cognitive Development cohort (N = 11,872), sipping by age 9–10 was concurrently associated with impulsivity, other aspects of externalizing, and prodromal schizophrenia symptoms. Still, these associations were cross-sectional in nature, leaving open the possibility that these features of psychopathology and personality might not reflect long-term risk for alcohol consumption and related harm across development. Here, we attempted to replicate baseline concurrent associations across three waves of data to extend concurrent associations to prospective ones. Most cross-sectional associations replicated across waves, such that impulsivity, other aspects of externalizing, reward sensitivity (e.g., surgency, sensation seeking), and prodromal schizophrenia symptoms were associated with increased odds of having sipped alcohol by the age of 12. Nevertheless, not all concurrent associations replicated prospectively; impulsigenic features did not reflect long-term risk for sipping. Thus, some psychopathology features appeared to reflect stable risk factors, whereas others appeared to reflect state-dependent risk factors. All told, sipping might not reflect long-term risk for harmful alcohol use, and the nature of sipping may change across development.

Intimate partner violence (IPV) represents a significant public health concern. Adverse childhood experiences (ACEs) represent one risk factor for IPV, however, the results of existing research on the association between ACEs and IPV demonstrate mixed findings. The present research sought to meta-analytically examine the association between ACEs and (a) IPV perpetration and (b) IPV victimization. Moderator analyses were conducted to determine factors that may impact the association between ACEs and IPV involvement. Electronic searches were conducted in MEDLINE, Embase, and PsycINFO in August of 2021. One-hundred and twenty-three records were screened for inclusion. All studies included a measure of ACEs and IPV victimization or perpetration. Among the 27 studies and 41 samples included in the meta-analysis, 65,330 participants were included. The results of the meta-analyses demonstrated that ACEs were positively associated with IPV perpetration and victimization. Significant methodological and measurement moderators further inform our understanding of ACEs and IPV involvement. The present meta-analyses demonstrates that trauma-informed approaches to IPV screening, prevention, and intervention may be useful, given that individuals who are involved with IPV may be more likely to possess a history of ACEs exposure.

Parenting can protect against the development of, or increase risk for, child psychopathology; however, it is unclear if parenting is related to psychopathology symptoms in a specific domain, or to broad liability for psychopathology. Parenting differs between and within families, and both overall family-level parenting and the child-specific parenting a child receives may be important in estimating transdiagnostic associations with psychopathology. Data come from a cross-sectional epidemiological sample (N = 10,605 children ages 4–17, 6434 households). Parents rated child internalizing and externalizing symptoms and their parenting toward each child. General and specific (internalizing, externalizing) psychopathology factors, derived with bifactor modeling, were regressed on parenting using multilevel modeling. Less warmth and more aversive/inconsistent parenting in the family, and toward an individual child relative to family average, were associated with higher general psychopathology and specific externalizing problems. Unexpectedly, more warmth in the family, and toward an individual child relative to family average, was associated with higher specific internalizing problems in 4–11 (not 12–17) year-olds. Less warmth and more aversive/inconsistent parenting are broad correlates of child psychopathology. Aversive/inconsistent parenting, is also related to specific externalizing problems. Parents may behave more warmly when their younger children have specific internalizing problems, net of overall psychopathology.

The social gradient in adolescent mental health is well established: adolescents’ socioeconomic status is negatively associated with their mental health. However, despite changes in social cognition during adolescence, little is known about whether social cognitions mediate this gradient. Therefore, this study tested this proposed mediational path using three data waves, each 6 months apart, from a socioeconomically diverse sample of 1,429 adolescents (Mage = 17.9) in the Netherlands. Longitudinal modeling examined whether three social cognitions (self-esteem, sense of control, and optimism) mediated associations between perceived family wealth and four indicators of adolescent mental health problems (emotional symptoms, conduct problems, hyperactivity, and peer problems). There was evidence of a social gradient: adolescents with lower perceived family wealth reported more concurrent emotional symptoms and peer problems and an increase in peer problems 6 months later. Results also showed evidence of mediation through social cognitions, specifically sense of control: adolescents with lower perceived family wealth reported a decrease in sense of control (though not self-esteem nor optimism) 6 months later, and lower sense of control predicted increases in emotional symptoms and hyperactivity 6 months later. We found concurrent positive associations between perceived family wealth and all three social cognitions, and concurrent negative associations between social cognitions and mental health problems. The findings indicate that social cognitions, especially sense of control, may be an overlooked mediator of the social gradient in adolescent mental health.

The early caregiving environment can have lasting effects on child mental health. Animal models suggest that glucocorticoid receptor gene (NR3C1) DNA methylation plays a mediating role in linking more responsive caregiving to improved behavioral outcomes by its impact on the stress regulatory system. In this longitudinal study, we examined whether children’s NR3C1 methylation levels mediate an effect of maternal sensitivity in infancy on levels of child internalizing and externalizing behavior in a community sample. Maternal sensitivity of 145 mothers was rated at infant age 5 weeks, 12 months, and 30 months by observing mother–infant interactions. Buccal DNA methylation was assessed in the same children at age 6 years and maternal-reported internalizing and externalizing behavior was assessed at age 6 and 10 years. Higher sensitivity at age 5 weeks significantly predicted lower DNA methylation levels at two NR3C1 CpG loci, although methylation levels at these loci did not mediate an effect of maternal sensitivity on levels of child internalizing and externalizing behavior. Overall, the study provides evidence that maternal sensitivity in early infancy is associated with DNA methylation levels at loci involved in stress regulation, but the significance of this finding for child mental health remains unclear.

This study investigates the capacity of pre/perinatal factors to predict attention-deficit/hyperactivity disorder (ADHD) symptoms in childhood. It also explores whether predictive accuracy of a pre/perinatal model varies for different groups in the population. We used the ABCD (Adolescent Brain Cognitive Development) cohort from the United States (N = 9975). Pre/perinatal information and the Child Behavior Checklist were reported by the parent when the child was aged 9–10. Forty variables which are generally known by birth were input as potential predictors including maternal substance-use, obstetric complications and child demographics. Elastic net regression with 5-fold validation was performed, and subsequently stratified by sex, race/ethnicity, household income and parental psychopathology. Seventeen pre/perinatal variables were identified as robust predictors of ADHD symptoms in this cohort. The model explained just 8.13% of the variance in ADHD symptoms on average (95% CI = 5.6%–11.5%). Predictive accuracy of the model varied significantly by subgroup, particularly across income groups, and several pre/perinatal factors appeared to be sex-specific. Results suggest we may be able to predict childhood ADHD symptoms with modest accuracy from birth. This study needs to be replicated using prospectively measured pre/perinatal data.

Developmental models of borderline personality disorder (BPD) emphasize the effects of youths’ biological vulnerabilities and their experiences of parental responses to emotion, as well as the interaction between these two elements. The current study evaluated the independent and interactive effects of two indices of autonomic nervous system response and parental responses to youth negative emotions on severity and exacerbation of youths’ BPD features during the transition to adolescence. The sample consisted of 162 psychiatric youth (10–14 years; 47.2% female) and their parents. At baseline, youth and their parents completed a lab-based conflict discussion during which parasympathetic and sympathetic nervous system response were measured and indices of sympathetic-parasympathetic balance and coactivation/coinhibition were calculated. Youth also reported on supportive and non-supportive parental responses. At baseline and after 9 months, youth self-reported on their BPD features. Results demonstrated that shifting toward sympathetic dominance independently predicted exacerbation of BPD across 9 months. Additionally, fewer experiences of supportive parental responses and more non-supportive parental responses were associated with greater severity of BPD features in youth. This study highlights the role of autonomic response to parent-child conflict as well as the significance of parental responses to youth emotion for the development of BPD during this developmental window.