Emotional distress during pregnancy is likely influenced by both maternal history of adversity and concurrent prenatal stressors, but prospective longitudinal studies are lacking. Guided by a life span model of pregnancy health and stress sensitization theories, this study investigated the influence of intimate partner violence (IPV) during pregnancy on the association between childhood adversity and prenatal emotional distress. Participants included an urban, community-based sample of 200 pregnant women (aged 18–24) assessed annually from ages 8 to 17 for a range of adversity domains, including traumatic violence, harsh parenting, caregiver loss, and compromised parenting. Models tested both linear and nonlinear effects of adversity as well as their interactions with IPV on prenatal anxiety and depression symptoms, controlling for potential confounds such as poverty and childhood anxiety and depression. Results showed that the associations between childhood adversity and pregnancy emotional distress were moderated by prenatal IPV, supporting a life span conceptualization of pregnancy health. Patterns of interactions were nonlinear, consistent with theories conceptualizing stress sensitization through an “adaptive calibration” lens. Furthermore, results diverged based on adversity subdomain and type of prenatal IPV (physical vs. emotional abuse). Findings are discussed in the context of existing stress sensitization theories and highlight important avenues for future research and practice.

Childhood exposure to stress can induce prolonged negative effects on health, which in turn confer risks for the next generation, but greater specificity is needed to inform intervention. A first step is to measure individual differences in emotional reactivity to stress early in life in ways that can account for heterogeneity in child exposure. The present study tested the hypothesis that mothers’ childhood exposure to stress would be differentially associated with patterns of positive and negative emotional reactivity in their offspring, suggesting transmission of stress response across generations. Participants were 268 young mothers (age 14–23 years) followed longitudinally since childhood, and their infants aged 3–9 months. Latent class analysis of infant emotions expressed before and during the still-face paradigm yielded five subgroups that varied in valence, intensity, and reactivity. After accounting for sociodemographic factors, infant temperament, and postpartum depression, multinomial regression models showed that, relative to an emotionally regulated still-face response, infants showing low negative reactivity were more likely to have mothers exposed to childhood emotional abuse, and infants showing high and increasing negative reactivity were more likely to have mothers exposed to childhood emotional neglect. Mechanisms by which early maternal stress exposure influences emotional reactivity in offspring are discussed.

Research consistently demonstrates that common polymorphic variation in monoamine oxidase A (MAOA) moderates the influence of childhood maltreatment on later antisocial behavior, with growing evidence that the “risk” allele (high vs. low activity) differs for females. However, little is known about how this Gene × Environment interaction functions to increase risk, or if this risk pathway is specific to antisocial behavior. Using a prospectively assessed, longitudinal sample of females (n = 2,004), we examined whether changes in emotional reactivity (ER) during adolescence mediated associations between this Gene × Environment and antisocial personality disorder in early adulthood. In addition, we assessed whether this putative risk pathway also conferred risk for borderline personality disorder, a related disorder characterized by high ER. While direct associations between early maltreatment and later personality pathology did not vary by genotype, there was a significant difference in the indirect path via ER during adolescence. Consistent with hypotheses, females with high-activity MAOA genotype who experienced early maltreatment had greater increases in ER during adolescence, and higher levels of ER predicted both antisocial personality disorder and borderline personality disorder symptom severity. Taken together, findings suggest that the interaction between MAOA and early maltreatment places women at risk for a broader range of personality pathology via effects on ER.

Nonsuicidal self-injury (NSSI) is a common behavior among females that has been shown to confer risk for continued self-injury and suicidal attempts. NSSI can be viewed conceptually as behavior that is pathognomonic with aggression and/or depression. Empirical research on concurrent correlates supports this concept: numerous and diverse factors are shown to be significantly associated with self-harm, including depression, emotion dysregulation, impulsivity, and aggression and other conduct problems, as well as environmental stressors such as bullying, harsh parenting, and negative life events. In the present study, we test hypotheses regarding developmental precursors (measured from ages 8 to 12 years) to NSSI in young adolescent girls (ages 13–14 years), specifically whether aggression, depression, and environmental stressors distinguish girls with and without self-harm, and whether there is evidence for multiple developmental pathways to NSSI. Data were derived from the longitudinal Pittsburgh Girls Study. In this community sample of girls, the prevalence of NSSI at ages 13 or 14 years of age was 6.0%. Initial levels in dimensions measured within the depression, aggression, and environmental stressor domains accounted for variance in NSSI in early adolescence. Changes over time in relational aggression and assertiveness were also significantly associated with risk for NSSI. To a large extent, adolescent NSSI was predicted by psychological deficits and stress exposure that began early in childhood. Risk indices were calculated using the 85th or 15th percentile. Close to 80% of girls who engaged in NSSI during adolescence were identified by at least one risk domain in childhood. A sizable proportion of adolescent girls who later engaged in NSSI had childhood risk scores in all three domains; the remaining girls with adolescent NSSI were relatively evenly distributed across the other risk domain profiles. The observation that multiple pathways to NSSI exist suggests that deficits underlying the behavior may vary and require different modes of prevention.

Using family study methodology and assessments by blind raters, this study tested hypotheses about patterns of familial association between DSM-III attention deficit disorder (ADD) and antisocial disorders (childhood conduct (CD) and oppositional disorder (OPD) and adult antisocial personality disorder) among 457 first-degree relatives of clinically referred children and adolescents with ADD (73 probands, 264 relatives), psychiatric (26 probands, 101 relatives) and normal controls (26 probands, 92 relatives). Among the 73 ADD probands, 33 (45 %) met criteria for OPD, 24 (33 %) met criteria for CD, and 16 (22 %) had no antisocial diagnosis. After stratifying the ADD sample into those with CD (ADD + CD), those with OPD (ADD + OPD) and those with neither (ADD) familial risk analysis revealed the following: (1) relatives of each ADD probands subgroup were at significantly greater risk for ADD than relatives of both psychiatric and normal controls; (2) the morbidity risk for ADD was highest among relatives of ADD + CD probands (38%), moderate among relatives of ADD + OPD (17%) and ADD probands (24%) and lowest among relatives of psychiatric and normal controls (5% for both); (3) the risk for any antisocial disorder was highest among relatives of ADD + CD (34%) and ADD + OPD (24%) which were significantly greater than the risk to relatives of ADD probands (11 %), psychiatric (7%) and normal controls (4%); and (4) both ADD and antisocial disorders occurred in the same relatives more often than expected by chance alone. Although these findings suggest that ADD with and without antisocial disorders may be aetiologically distinct disorders, they are also consistent with a multifactorial hypothesis in which ADD, ADD + OPD and ADD + CD fall along a continuum of increasing levels of familial aetiological factors and, correspondingly, severity of illness.

The concurrent and predictive influence of deviant peers on boys' disruptive and delinquent behavior was examined in a community sample of fourth- and seventh-grade boys, who were followed-up over six data waves. Analyses were conducted separately for three different types of behavior problems: authority conflict, covert, and overt disruptive behavior. Consistent with the existing literature, concurrent relations between peers' and boys' disruptive behavior were expected to be significant. A more informative test, however, was whether exposure to deviant peers resulted in boys' subsequent initiation of disruptive behavior. Although peer influences were expected in the predictive analyses, the relations were hypothesized to differ by type of behavior. The potential moderating effects of hyperactivity and poor parenting practices were also examined to test the hypothesis that boys who are already at risk for behavior problems will be more susceptible to deviant peer influence. Results supported the significant concurrent and predictive relation between exposure to deviant peers and boys' engagement in disruptive and delinquent behavior. There were no significant moderating effects of attention-deficit hyperactivity disorder (ADHD) or parenting practices on peer influence.

This study examined risk factors from infancy associated with the development of preschool disruptive behavior problems across child, parent, and sociodemographic domains. Risk factors that consistently were associated with the prediction of disruptive behavior at age 5 years included disorganized attachment classification at 12 months, and maternal personality risk and child-rearing disagreements during the second year. In addition, infants with disorganized attachment status at 12 months whose mothers perceived them as difficult in the second year showed significantly higher aggressive problems at age 5 years than those with only one of the two risk factors present. When pathways leading to clinically elevated aggression at age 5 were explored, infant disorganized attachment status, maternal personality risk, and child-rearing disagreements demonstrated equivalent predictive validity as child aggression assessed at age 3 years.

Developmental sequences in disruptive behavior from childhood to adolescence are traced retrospectively and prospectively in two community samples of boys. Three developmental pathways are distinguished: (a) an early authority conflict pathway, consisting in sequence of stubborn behavior, defiance, and authority avoidance; (b) a covert pathway, consisting of minor covert behaviors, property damage, and moderate to serious forms of delinquency; and (c) an overt pathway, consisting of aggression, fighting, and violence. The overlap among the three disruptive pathways is examined. Those boys who escalated in the overt pathway were more likely to escalate in the covert pathway than boys escalating in the covert pathway showing an escalation in the overt pathway. Escalation in the authority conflict pathway was not associated with escalation in either the overt or the covert pathways. Boys' rate of self-reported delinquency was highest for those in triple pathways (covert-overt-authority conflict) or in certain dual pathways (covert-overt, covert-authority conflict). However, by age 16 the highest rate of offending was displayed by those in the triple pathways. The rate of violent offenses was also highest for those in the triple pathways and for those in the overt and covert pathways. Results from the rate for court petitions largely supported these findings. Lowest rates of offending were observed for boys in the overt and authority conflict pathways. Implications are discussed for clinical practice and future research.