The purpose of this study was to examine the relationship between fathers' alcoholism and the quality of parent–infant interactions during free play. A related goal was to study the potential mediating or moderating role of comorbid parental psychopathology, such as depression and antisocial behavior, difficult infant temperament, and parental aggression. The sample consisted of 204 families with 12-month-old infants (104 alcoholic and 100 control families), recruited from New York State birth records. Results indicated that fathers' alcoholism was associated with a number of other risk factors (depression, antisocial behavior, and family aggression). Fathers' alcoholism was also associated with more negative father–infant interactions as indicated by lower paternal sensitivity, positive affect, verbalizations, higher negative affect, and lower infant responsiveness among alcoholic fathers. As expected, fathers' depression mediated the relationship between fathers' alcoholism and sensitivity, while maternal depression mediated the association between maternal alcohol problems and maternal sensitivity. Parents' psychopathology did not moderate the association between alcoholism and parent-infant interactions. The results from the present study suggest that the origins of risk for later maladjustment among children of alcoholic fathers are apparent as early as infancy and highlight the role of comorbid parental risk factors.

A number of lines of evidence converge in implicating neurodevelopmental processes in the etiology and epigenesis of schizophrenia. In this study we used a prospective, longitudinal design to examine whether adverse obstetric experiences predict schizophrenia and whether there is a deviant functional–developmental trajectory during the first 7 years of life among individuals who manifest schizophrenia as adults. The 9,236 members of the Philadelphia cohort of the National Collaborative Perinatal Project were screened for mental health service utilization in adulthood, and chart reviews were performed to establish diagnoses according to DSM-IV criteria. The risk for schizophrenia increased linearly with the number of hypoxia-associated obstetric complications but was unrelated to maternal infection during pregnancy or fetal growth retardation. Preschizophrenic cases (and their unaffected siblings who were also cohort members) manifested cognitive impairment, abnormal involuntary movements and coordination deficits, and poor social adjustment during childhood. There was no evidence of intraindividual decline in any domain, but preschizophrenic cases did show deviance on an increasing number of functional indicators with age. Together, these findings suggest that both genetic and obstetric factors participate in creating a neural diathesis to schizophrenia, the phenotypic expressions of which are age dependent, probably reflecting the maturational status of a number of interconnected brain systems.

We tested three competing models regarding the role of deviant friends in the trajectory linking early disruptiveness with later conduct problems through the use of a preventive intervention program. The program was implemented during the second and third grade. One model predicted that the program would positively affect later conduct problems by facilitating nondeviant peer association during early adolescence. The second model predicted a direct impact of the program on later conduct problems through the reduction of early disruptiveness. The third model predicted an interaction between postintervention disruptiveness and association with less deviant friends. The results showed that the program's effects on later conduct problems were mediated by the reduction in disruptiveness and by the association with less deviant friends. However, the positive effect of associating with less deviant friends depended on whether children's disruptiveness had been reduced or not by their participation in the program, thus supporting the third model. We recommend using intervention studies to test developmental models.

Recent research has suggested that there are two distinct trajectories for the development of antisocial behavior in boys: a childhood-onset pathway and an adolescent-onset pathway. After reviewing the limited available research on antisocial girls, we propose that this influential method of conceptualizing the development of severe antisocial behavior may not apply to girls without some important modifications. Antisocial girls appear to show many of the correlates that have been associated with the childhood-onset pathway in boys, and they tend to show impaired adult adjustment, which is also similar to boys in the childhood-onset pathway. However, antisocial girls typically show an adolescent-onset to their antisocial behavior. We have proposed that these girls show a third developmental pathway which we have labeled the “delayed-onset” pathway. This model rests on the assumption that many of the putative pathogenic mechanisms that contribute to the development of antisocial behavior in girls, such as cognitive and neuropsychological deficits, a dysfunctional family environment, and/or the presence of a callous and unemotional interpersonal style, may be present in childhood, but they do not lead to severe and overt antisocial behavior until adolescence. Therefore, we propose that the delayed-onset pathway for girls is analogous to the childhood-onset pathway in boys and that there is no analogous pathway in girls to the adolescent-onset pathway in boys. Although this model clearly needs to be tested in future research, it highlights the need to test the applicability of current theoretical models for explaining the development of antisocial behavior in girls.

In this 2-year prospective study, psychopathology and competence among drug abusers' offspring were examined in relation to characteristics of their neighborhoods. The sample consisted of 77 children of cocaine and opioid addicts with a mean age of 12.3 years at baseline and 14.2 years at follow-up. Outcomes examined included psychiatric diagnoses, dimensional symptom indices, and aspects of everyday behavioral competence. Links involving neighborhood variables varied by gender, wherein boys reflected greater deterioration than girls when neighborhoods had high crime rates and high proportions of low-income households. Conversely, girls appeared to benefit more than boys from the presence of professional adults in the community. Overall, neighborhood indicators accounted for more variability in changes in child adjustment over time than did indices of maternal psychopathology. Findings are discussed in terms of developmental changes in the salience of exosystemic and familial forces, and implications for interventions are outlined.

Attentional deficits are well-established characteristics of patients with schizophrenia and their at-risk offspring, suggesting a biological connection between attention and schizophrenia. The goal of this study is to clarify the developmental role of attention in the illness. Data has been collected from 87 subjects at high and low risk for schizophrenia who have participated in the New York High-Risk Project from 1977 to the present. Individuals are considered to be at high risk if either or both of their parents has schizophrenia. Analyses of attention and global behaviors, measured at intervals from about 12 to 26 years of age, indicate (a) attentional deficits can be reliably detected in high-risk children who will develop future schizophrenia-spectrum disorders (the prespectrum [PSP] group); (b) these deficits are stable, enduring over time, and appear to reflect a compromised attentional capacity; (c) attention is not affected by the onset of illness in the PSP group; (d) for all subjects, attention and global behaviors follow independent developmental pathways; and (e) behavioral difficulties, but not attention deficits, appear to be highly sensitive to environmental factors, especially rearing by a mentally ill parent. It is concluded that in PSP individuals impaired attention probably results from prenatal developmental abnormalities (possibly on the cellular level) and is likely to be a marker of a biological vulnerability to schizophrenia. In addition, attentional deficits, as opposed to early behavioral difficulties, are concluded to be a useful first step in screening for youngsters in need of early intervention.

A three-wave longitudinal study design with two 6-month intervals was used to examine the stability and change in Internalizing, Externalizing, and Total Problem behavior among children and adolescents referred to outpatient mental health services. Our results indicated high stabilities for parent ratings of child psychopathology across a 1-year interval. Additionally, we found decreases in the level of problem behavior. Interindividual differences in change were found for Total Problems and Externalizing behavior but not for Internalizing. While both the child's temperament and intelligence level and family relations were related to the initial level of parent-rated problem behavior, only intermediary stressful life events had an influence on the rate of change of child psychopathology.

The relationship between conduct problems at age 8 years and teenage pregnancy by the age of 18 years was analyzed in a birth cohort of 491 girls. A statistically significant association was found between early conduct problems and later risk of teenage pregnancy, with girls in the most disturbed 10% of the cohort having a pregnancy rate that was 5.3 times higher (p < .001) than the rate found in the least disturbed 50% of the cohort. The elevated risk of teenage pregnancy amongst girls with early conduct problems was in part, explained by social and family factors that were correlated with early conduct problems, and in part, by a causal chain process in which early conduct problems were associated with increased rates of risk taking behaviors in adolescence, which in turn led to an increased risk of teenage pregnancy. These results suggest that the higher rate of teenage pregnancy among girls with early conduct problems reflected both their relatively disadvantaged family backgrounds and their tendencies to risk taking behavior in adolescence.

Most previous research has assumed that adolescent alcohol use and problem use represent a continuum and are influenced by the same psychosocial factors, with problem use representing more severe psychosocial impairment. The current study evaluated this assumption by identifying the correlates of adolescent alcohol use and those of problem use. Using a community sample of adolescent children of alcoholics (COAs) and a demographically matched comparison group (non-COAs), a typology of adolescent alcohol use was created, and alcohol use groups were compared on variables chosen from nine psychosocial domains. The correlates of problem alcohol use were different from those of moderate use. Problem use was associated with fundamental family disruptions and poor psychological functioning. In contrast, the determinants of moderate alcohol use reflected unconventionality and socialization specific to alcohol. Few psychosocial variables distinguished abstainers from light drinkers. Intervention and methodological implications of these findings are discussed.

Motor dysfunction is associated with schizophrenia, and recent longitudinal studies indicate that it precedes the onset of clinical symptoms. Of particular interest is the heightened occurrence of involuntary movements, which are apparent as early as infancy and suggest the presence of subcortical brain abnormalities. In this article, we present the results of a study of spontaneous movements in adolescents with schizotypal personality disorder (SPD). SPD is a syndrome that has been shown to be genetically linked with schizophrenia and is often observed prior to the early adult onset of schizophrenia. Systematic coding of videotapes of diagnostic interviews revealed that the SPD group showed significantly more involuntary movements of the head, trunk, and upper limbs than did normals and adolescents with other personality disorders. There were no diagnostic group differences in the rate of voluntary movements. Salivary cortisol, measured before the interview, was positively correlated with involuntary movements. Taken together, the findings provide further support for the hypothesized etiologic relation between SPD and schizophrenia. Based on a neural diathesis-stress model, potential underlying mechanisms are discussed.

Competent outcomes in late adolescence were examined in relation to adversity over time, antecedent competence and psychosocial resources, in order to investigate the phenomenon of resilience. An urban community sample of 205 (114 females, 90 males; 27% minority) children were recruited in elementary school and followed over 10 years. Multiple methods and informants were utilized to assess three major domains of competence from childhood through adolescence (academic achievement, conduct, and peer social competence), multiple aspects of adversity, and major psychosocial resources. Both variable-centered and person-centered analyses were conducted to test the hypothesized significance of resources for resilience. Better intellectual functioning and parenting resources were associated with good outcomes across competence domains, even in the context of severe, chronic adversity. IQ and parenting appeared to have a specific protective role with respect to antisocial behavior. Resilient adolescents (high adversity, adequate competence across three domains) had much in common with their low-adversity competent peers, including average or better IQ, parenting, and psychological well-being. Resilient individuals differed markedly from their high adversity, maladaptive peers who had few resources and high negative emotionality. Results suggest that IQ and parenting scores are markers of fundamental adaptational systems that protect child development in the context of severe adversity.

This study examined the developmental associations between substance use and violence. We examined the trends in each behavior throughout adolescence, how the behaviors covaried over time, and the symmetry of associations taking into account frequency and severity of each behavior. We also examined whether changes in one behavior affected changes in the other behavior over time. Six years of annual data were analyzed for 506 boys who were in the seventh grade at the first assessment. Concurrent associations between frequency of substance use and violence were relatively strong throughout adolescence and were somewhat stronger for marijuana than alcohol, especially in early adolescence. Type or severity of violence was not related to concurrent alcohol or marijuana frequency, but severity of drug use was related to concurrent violence frequency. Depending, to some degree, on the age of the subjects, the longitudinal relationships between substance use and violence were reciprocal during adolescence and slightly stronger for alcohol and violence than for marijuana and violence. Further, increases in alcohol use were related to increases in violence; however, when early alcohol use was controlled, increases in marijuana use were not related to increases in violence. Only in early adolescence was the longitudinal relationship between marijuana use and later violence especially strong. The strength of the longitudinal associations between violence and substance use did not change when common risk factors for violence and substance use were controlled. Overall, the data lend more support for a reciprocal than for a unidirectional association between substance use and violence. Prevention efforts should be directed at aggressive males who are multiple-substance users in early adolescence.

The central feature of schizophrenia is its onset in adolescence. Although this clinical observation is consistent with the view that schizophrenia may be a neurodevelopmental disorder, debate has focused on when the proposed brain maturational deviations may begin and what might be the nature of such defective development. Conflicting models of this illness (e.g., the early and late neurodevelopmental models) have been proposed. In this paper, we will first review concepts from basic developmental neurobiology pertinent to these issues; we then summarize aspects of the neurobiology of schizophrenia that have a particular bearing on the adolescent onset of this illness. We propose that the schizophrenic syndrome may result from early brain adversity and late maturational processes of brain development interacting with adverse humoral, biochemical, and psychosocial factors during adolescence and early adulthood. The onset of schizophrenia in adolescence may be related to the “plasticity switch” secondary to the peripubertal brain maturational changes, perhaps involving an alteration in glutamate receptor function. This loss of plasticity could result in social and nonsocial cognitive deficits that are central to the pathophysiology of schizophrenia; the vulnerable person may therefore utilize prepubertal processing styles that are insufficient to the adaptive and “gistful” abstraction requirements of adult cognition. Schizophrenia onset might occur in the context of psychosocial developmental challenges to a delayed social cognitive capacity among neurodevelopmentally compromised individuals. We review therapeutic implications as well as testable predictions generated by this model, and discuss research strategies that might further our understanding of the brain maturational abnormalities in schizophrenia.

Although a majority of adolescent mothers are graduating from high school, the processes that enhance the educational attainment of adolescent mothers are not well understood. With a sample of 93 African American and Puerto Rican adolescent mothers, we assessed the effects of material support from family (i.e., child care assistance from grandmother and residence with grandmother) and emotional support from family over and above pre- and postpregnancy risk factors (i.e., maternal age at first birth, delayed grade placement before pregnancy, ethnicity, depressive symptoms, stressful life events, and repeat pregnancy) during the first year postpartum on educational attainment at 6 years postpartum. Significant contributors to the explained variance in educational attainment included: delayed grade placement before pregnancy, maternal age at first birth, depressive symptoms, emotional support from family, and residence with grandmother. Unexpectedly, higher perceived emotional support from family and living with grandmother predicted lower educational attainment. Post hoc analysis of qualitative data suggested reasons for these latter findings and point to the need to reconceptualize and broaden the elements of social support that constitute protective factors for adolescent mothers.

The reliability and validity of a comprehensive, integrative strategy for assessing adversity exposure in childhood and adolescence was examined in a community-based longitudinal study of 205 children. Extensive data from multiple measures completed by adolescents and their parents regarding chronic and acute life experiences were aggregated into a Life Chart record of lifetime adversity exposure. Severity of adversity in three nonoverlapping time spans was rated by trained judges with excellent interrater reliability. As hypothesized, Family adversity predominated over all other types of adversity in childhood, remained salient into midadolescence, and showed considerable stability over time. Adversity related to an individual's own behavior and psychological functioning rose to equal prominence by late adolescence. Adversity arising from physical ailments that were independent of the individual's psychological functioning declined over time, while adversity arising from the community rose; physical and community events were uncommon for most individuals but substantial for some. Results suggest that coherent developmental trends in adversity exposure may be identified effectively through judges' ratings of severity of adversity over multiple-year time spans.

Epidemiological research shows some ethnic-group differences in the prevalence of substance use. This approach does not address the question of whether there are ethnic-group differences in the models that are needed to understand the development of substance use. For this question we need to understand the relations between psychological constructs and their trajectories over time. In this paper we describe some approaches to studying ethnic-group differences in the predictors of substance use that illustrate probing for mediators, multisample analyses of structural models, and an experimental trial of a preventive intervention. Our studies found some ethnic-group differences in the structure of constructs and the relations between variables, but many similarities. The challenge for researchers is using appropriate research methods for studying ethnicity, uncovering the basis for ethnic-group differences when they occur, knowing when statistical differences are meaningful, and acknowledging when developmental models are comparable.

The term self-organization has at least two meanings for developmental psychopathologists: the spontaneous emergence of order in developing systems and the consolidation of that part of the person called the self. The first meaning is shared across the sciences at large, and it denotes a general model of change and growth in complex systems. We review principles of self-organization from the natural sciences and discuss their application to the study of human development. We then suggest possible sources and consequences of terminological confusion in developmental psychology and offer some potential resolutions. The “self” in self-organization seems a special case of this confusion, and it can be addressed by modeling the self as both autonomous agent and emergent form. We outline preliminary directions for this modeling and then go on to a more general discussion of how principles of self-organization can help bring developmental psychopathology closer to its goals.

Recent studies have focused on the behavioral and neurobiological sequella of exposure to early adverse events. We hypothesize that early adverse experiences result in an increased sensitivity to the effects of stress later in life and render an individual vulnerable to stress-related psychiatric disorders. This vulnerability may be mediated by persistent changes in corticotropin-releasing-factor (CRF)-containing neurons, the hypothalamic–pituitary–adrenal axis, and the sympathetic nervous system. We therefore present an overview of the CRF system and its role as a mediator in the development of the stress response, major depression, and posttraumatic stress disorder. The literature pertaining to behavioral and neurobiological alterations associated with exposure to early adverse life events in rodents, nonhuman primates, and humans is reviewed. We focus on animal models that precipitate depressive and anxiety symptoms while producing neuroendocrine alterations that mimic those seen in adults with those disorders. The literature integrating neurobiological and behavioral consequences of early life stress is also reviewed, focusing primarily on infants born to mothers with depression and on infants who were abused or neglected.

This study of over 1,000 adolescents focused on common and distinctive correlates of four subgroups—no problem, depressed only, heavy drinking only, and mixed (depressed and heavy drinking). Correlates were evaluated from the domains of personal dispositions (e.g., temperament), interpersonal relations (e.g., parent and peer), stressful life events, and other problem behaviors (e.g., delinquency, substance use). The no-problem subgroup differed from the other three subgroups in the direction of healthier functioning on almost all measures. The mixed subgroup reported the most pervasive, low levels of functioning, with the highest levels of childhood externalizing problems and stressful life events, the lowest levels of family social support, and high levels of delinquency and substance use. The depressed-only subgroup reported a more internalized pattern characterized by childhood avoidance problems, a difficult temperament (e.g., inflexibility, withdrawal, low task orientation), interpersonal stressors, and poor coping strategies. The heavy-drinking-only subgroup was characterized by higher drinking levels by primary caregivers and lower levels of family cohesion as reported by primary caregivers. The 1-year prospective findings were generally consistent with the concurrent findings in that variables that were associated with transitions toward and away from depression and heavy drinking were associated with specific transitions (e.g., childhood externalizing problems were associated with the transition from no problem to heavy drinking).

Objectives in this research were to examine contextual differences in correlates of substance use among high school students. The focus was on two broad categories of adjustment indices: personal psychopathology (internalizing and externalizing problems) and behaviors reflecting social competence (academic achievement, teacher-rated classroom behaviors, and peer acceptance or rejection). Associations between drug use and each of these constructs were examined in two sociodemographically disparate groups: teens from affluent, suburban families (n = 264), and low socioeconomic status adolescents from inner-city settings (n= 224). Results indicated that suburban youth reported significantly higher levels of substance use than inner-city youth. In addition, their substance use was more strongly linked with subjectively perceived maladjustment indices. Comparable negative associations involving grades and teacher-rated behaviors were found in both groups, and among suburban males only, substance use showed robust positive associations with acceptance by peers. Results are discussed in terms of developmental perspectives on adolescent deviance, contextual socializing forces, and implications for preventive interventions and treatment.