This study examined the etiology and course of anxiety symptoms from infancy through adolescence in a longitudinal high-risk community sample. One hundred fifty-five subjects were assessed using a variety of observational, projective, and objective measures. Results of path analyses revealed the following: (a) anxiety symptoms showed moderate stability during childhood and adolescence; (b) heightened neonatal biobehavioral reactivity and poor regulation predicted emotion regulation difficulties in preschool, which predicted anxiety symptoms in childhood; (c) developmental incompetence in childhood predicted anxiety symptoms in preadolescence, and anxiety symptoms in preadolescence predicted incompetence in adolescence; (d) insecure attachment relationships in infancy predicted negative peer relationship representations in preadolescence, and these representations predicted anxiety symptoms in adolescence; (e) compared to males, females showed similar rates of anxiety symptoms in childhood but greater and more stable rates in adolescence; however, males and females showed similar patterns of association between risk factors and anxiety symptoms across childhood and adolescence; and (f) the model tested was specific in predicting anxiety symptoms and not psychopathology in general. The results support a developmental model of the etiology and maintenance of anxiety symptoms in childhood and highlight factors to consider in efforts to prevent and treat childhood anxiety.This article is based on a doctoral dissertation completed by the first author. The research was supported by a Philanthropic Educational Organization Scholarship to the first author and by funds provided by grants to the second author from the Maternal and Child Health Service (MC-R-270416); the William T. Grant Foundation, New York; and the National Institute of Mental Health (MH-40864). This study is currently supported by the National Institute of Mental Health (MH-40864-18). The authors thank Manfred van Dulmen for the invaluable statistical guidance he provided in the preparation of this manuscript and the families and teachers whose generation donation of time made this project possible.

Evidence for the intergenerational transmission of posttraumatic stress disorder (PTSD) is documented in the literature, although the underlying mechanisms are poorly understood. Attachment theory provides a framework for elucidating the ways in which maternal PTSD may increase offspring PTSD vulnerability. The current study utilized two independent prospective data sets to test the hypotheses that (a) maternal PTSD increases the probability of developing an insecure mother–infant attachment relationship and (b) an insecure mother–infant attachment relationship increases the risk of developing PTSD following trauma exposure in later life. In the first study of urban, primarily low-income ethnic/racial minority mothers and infants (N= 45 dyads), elevated maternal PTSD symptoms at 6 months were associated with increased risk for an insecure, particularly disorganized, mother–infant attachment relationship at 13 months. In the second birth cohort of urban, low-income mothers and children (N= 96 dyads), insecure (avoidant or resistant) attachment in infancy was associated in a dose–response manner with increased lifetime risk for a diagnosis of PTSD by adolescence. A history of disorganized attachment in infancy predicted severity of PTSD symptoms, including reexperiencing, avoidance, hyperarousal, and total symptoms, at 17.5 years. In both studies, associations between attachment and PTSD were not attributable to numerous co-occurring risk factors. The findings suggest that promoting positive mother–child relationships in early development, particularly in populations at high risk for trauma exposure, may reduce the incidence of PTSD.

While adult hypothalamic-pituitary-adrenocortical (HPA) axis functioning is thought to be altered by traumatic experiences, little data exist on the effects of cumulative stress on HPA functioning among pregnant women or among specific racial and ethnic groups. Individuals may be increasingly vulnerable to physiological alterations when experiencing cumulative effects of multiple stressors. These effects may be particularly relevant in urban poor communities where exposure to multiple stressors is more prevalent. The goal of this study was to explore the effects of multiple social stressors on HPA axis functioning in a sample of urban Black (n = 68) and Hispanic (n = 132) pregnant women enrolled in the Asthma Coalition on Community, Environment, and Social Stress (ACCESS). Pregnant women were administered the Revised Conflict Tactics Scale (R-CTS) survey to assess interpersonal violence, the Experiences of Discrimination (EOD) survey, the Crisis in Family Systems-Revised (CRISYS-R) negative life events survey, and the My Exposure to Violence (ETV) survey, which ascertains exposure to community violence. A cumulative stress measure was derived from these instruments. Salivary cortisol samples were collected five times per day over three days to assess area under the curve (AUC), morning change, and basal awakening response in order to characterize diurnal salivary cortisol patterns. Repeated measures mixed models, stratified by race/ethnicity, were performed adjusting for education level, age, smoking status, body mass index and weeks pregnant at time of cortisol sampling. The majority of Hispanic participants (57%) had low cumulative stress exposure, while the majority of Black participants had intermediate (35%) or high (41%) cumulative stress exposure. Results showed that among Black but not Hispanic women, cumulative stress was associated with lower morning cortisol levels, including a flatter waking to bedtime rhythm. These analyses suggest that the combined effects of cumulative stressful experiences are associated with disrupted HPA functioning among pregnant women. While the etiology of racial/ethnic differences in stress-induced HPA alterations is not clear, this warrants further research.

Background Childhood trauma exposure has been associated with deficits in cognitive functioning. The influence of timing of exposure on the magnitude and persistence of deficits is not well understood. The impact of exposure in early development has been especially under-investigated. This study examined the impact of interpersonal trauma exposure (IPT) in the first years of life on childhood cognitive functioning. Methods Children (N=206) participating in a longitudinal birth cohort study were assessed prospectively for exposure to IPT (physical or emotional abuse or neglect, sexual abuse, witnessing maternal partner violence) between birth and 64 months. Child intelligent quotient (IQ) scores were assessed at 24, 64 and 96 months of age. Race/ethnicity, gender, socioeconomic status, maternal IQ, birth complications, birth weight and cognitive stimulation in the home were also assessed. Results IPT was significantly associated with decreased cognitive scores at all time points, even after controlling for socio-demographic factors, maternal IQ, birth complications, birth weight and cognitive stimulation in the home. IPT in the first 2 years appeared to be especially detrimental. On average, compared with children not exposed to IPT in the first 2 years, exposed children scored one-half SD lower across cognitive assessments. Conclusion IPT in early life may have adverse effects on cognitive development. IPT during the first 2 years may have particular impact, with effects persisting at least into later childhood.