The aim of this study was to use longitudinal population-based data to examine the associations between childhood sexual abuse (CSA) and risk for adverse outcomes in multiple life domains across adulthood. In 937 individuals followed from birth to age 45y, we assessed associations between CSA (retrospectively reported at age 26y) and the experience of 22 adverse outcomes in seven domains (physical, mental, sexual, interpersonal, economic, antisocial, multi-domain) from young adulthood to midlife (26 to 45y). Analyses controlled for sex, socioeconomic status, prospectively reported child harm and household dysfunction adverse childhood experiences, and adult sexual assault, and considered different definitions of CSA. After adjusting for confounders, CSA survivors were more likely than their peers to experience internalizing, externalizing, and thought disorders, suicide attempts, health risk behaviors, systemic inflammation, poor oral health, sexually transmitted diseases, high-conflict relationships, benefit use, financial difficulties, antisocial behavior, and cumulative problems across multiple domains in adulthood. In sum, CSA was associated with multiple persistent problems across adulthood, even after adjusting for confounding life stressors, and the risk for particular problems incremented with CSA severity. The higher risk for most specific problems was small to moderate, but the cumulative long-term effects across multiple domains reflect considerable individual and societal burden.

Neuropsychological evidence supports the developmental taxonomy theory of antisocial behavior, suggesting that abnormal brain development distinguishes life-course-persistent from adolescence-limited antisocial behavior. Recent neuroimaging work confirmed that prospectively-measured life-course-persistent antisocial behavior is associated with differences in cortical brain structure. Whether this extends to subcortical brain structures remains uninvestigated. This study compared subcortical gray-matter volumes between 672 members of the Dunedin Study previously defined as exhibiting life-course-persistent, adolescence-limited or low-level antisocial behavior based on repeated assessments at ages 7–26 years. Gray-matter volumes of 10 subcortical structures were compared across groups. The life-course-persistent group had lower volumes of amygdala, brain stem, cerebellum, hippocampus, pallidum, thalamus, and ventral diencephalon compared to the low-antisocial group. Differences between life-course-persistent and adolescence-limited individuals were comparable in effect size to differences between life-course-persistent and low-antisocial individuals, but were not statistically significant due to less statistical power. Gray-matter volumes in adolescence-limited individuals were near the norm in this population-representative cohort and similar to volumes in low-antisocial individuals. Although this study could not establish causal links between brain volume and antisocial behavior, it constitutes new biological evidence that all people with antisocial behavior are not the same, supporting a need for greater developmental and diagnostic precision in clinical, forensic, and policy-based interventions.

Cognitive impairment has been identified as an important aspect of major depressive disorder (MDD). We tested two theories regarding the association between MDD and cognitive functioning using data from longitudinal cohort studies. One theory, the cognitive reserve hypothesis, suggests that higher cognitive ability in childhood decreases risk of later MDD. The second, the scarring hypothesis, instead suggests that MDD leads to persistent cognitive deficits following disorder onset. We tested both theories in the Dunedin Study, a population-representative cohort followed from birth to midlife and assessed repeatedly for both cognitive functioning and psychopathology. We also used data from the Environmental Risk Longitudinal Twin Study to test whether childhood cognitive functioning predicts future MDD risk independent of family-wide and genetic risk using a discordant twin design. Contrary to both hypotheses, we found that childhood cognitive functioning did not predict future risk of MDD, nor did study members with a past history of MDD show evidence of greater cognitive decline unless MDD was accompanied by other comorbid psychiatric conditions. Our results thus suggest that low cognitive functioning is related to comorbidity, but is neither an antecedent nor an enduring consequence of MDD. Future research may benefit from considering cognitive deficits that occur during depressive episodes from a transdiagnostic perspective.

The purpose of the present study is to identify child and adult correlates that differentiate (a) individuals with persistent alcohol dependence from individuals with developmentally limited alcohol dependence and (b) individuals with adult-onset alcohol dependence from individuals who never diagnose. There are 1,037 members of the Dunedin Longitudinal Study, which is a birth cohort followed prospectively from birth until age 32. Past-year DSM-IV alcohol dependence diagnoses are ascertained with structured diagnostic interviews at ages 18, 21, 26, and 32. Individuals are classified as developmentally limited, persistent, or adult-onset subtypes based on their time-ordered pattern of diagnoses. The persistent subtype generally exhibits the worst scores on all correlates, including family psychiatric history, adolescent and adult externalizing and internalizing problems, adolescent and adult substance use, adult quality of life, and coping strategies. The prospective predictors that distinguished them from the developmentally limited subtype involved family liability, adolescent negative affectivity, daily alcohol use, and frequent marijuana use. Furthermore, young people who develop the persistent subtype of alcohol dependence are distinguished from the developmentally limited subtype by an inability to reduce drinking and by continued use despite problems by age 18. The adult-onset group members are virtually indistinguishable from ordinary cohort members as children or adolescents; however, in adulthood, adult-onset cases are distinguished by problems with depression, substance use, stress, and strategies for coping with stress. Information about age of onset and developmental course is fundamental for identifying subtypes of alcohol dependence. Subtype-specific etiologies point to targeted prevention and intervention efforts based on the characteristics of each subtype.

It has been shown that lower birthweight is associated with lower IQ, but it remains unclear whether this association is causal or spurious. We examined the relationship between birthweight and IQ in two prospective longitudinal birth cohorts: a UK cohort of 1116 twin pairs (563 monozygotic [MZ] pairs), born in 1994–95, and a New Zealand cohort of 1037 singletons born in 1972–73. IQ was tested with the Wechsler Intelligence Scales for Children. Birthweight differences within MZ twin pairs predicted IQ differences within pairs, ruling out genetic and shared environmental explanations for the association. Birthweight predicted IQ similarly in the twin and nontwin cohorts after controlling for social disadvantage, attesting that the association generalized beyond twins. An increase of 1000 g in birthweight was associated with a 3 IQ point increase. Results from two cohorts add to evidence that low birthweight is a risk factor for compromised neurological health. Our finding that birthweight differences predict IQ differences within MZ twin pairs provides new evidence that the mechanism can be narrowed to an environmental effect during pregnancy, rather than any familial environmental influence shared by siblings, or genes. With the increasing numbers of low-birthweight infants, our results support the contention that birthweight could be a target for early preventive intervention to reduce the number of children with compromised IQ.

This article reports on the childhood origins and adult outcomes of female versus male antisocial behavior trajectories in the Dunedin longitudinal study. Four antisocial behavior trajectory groups were identified among females and males using general growth mixture modeling and included life-course persistent (LCP), adolescent-onset, childhood-limited, and low trajectory groups. During childhood, both LCP females and males were characterized by social, familial and neurodevelopmental risk factors, whereas those on the adolescent-onset pathway were not. At age 32, women and men on the LCP pathway were engaging in serious violence and experiencing significant mental health, physical health, and economic problems. Females and males on the adolescent-onset pathway were also experiencing difficulties at age 32, although to a lesser extent. Although more males than females followed the LCP trajectory, findings support similarities across gender with respect to developmental trajectories of antisocial behavior and their associated childhood origins and adult consequences. Implications for theory, research, and practice are discussed.

Background. The close association between generalized anxiety disorder (GAD) and major depressive disorder (MDD) prompts questions about how to characterize them in future diagnostic systems. We tested whether risk factors for MDD and GAD are similar or different.

Method. The representative 1972–73 Dunedin birth cohort of 1037 males and females was followed to age 32 with 96% retention. Adult GAD and MDD were diagnosed at ages 18, 21, 26, and 32 years, and juvenile anxiety/depression were also taken into account. Thirteen prospective risk measures indexed domains of family history, adverse family environment, childhood behavior, and adolescent self-esteem and personality traits.

Results. Co-morbid MDD+GAD was antedated by highly elevated risk factors broadly across all domains. MDD+GAD was further characterized by the earliest onset, most recurrence, and greatest use of mental health services and medication. Pure GAD had levels of risk factors similar to the elevated levels for co-morbid MDD+GAD; generally, pure MDD did not. Pure GAD had risks during childhood not shared by pure MDD, in domains of adverse family environment (low SES, somewhat more maltreatment) and childhood behavior (internalizing problems, conduct problems, somewhat more inhibited temperament). Pure MDD had risks not shared by pure GAD, in domains of family history (of depression) and personality (low positive emotionality).

Conclusions. Specific antecedent risk factors for pure adult MDD versus GAD may suggest partly different etiological pathways. That GAD and co-morbid MDD+GAD share many risk markers suggests that the presence of GAD may signal a pathway toward relatively more severe internalizing disorder.

We examined neuropsychological functioning at age 13 years in adolescents who later developed schizophreniform disorder, compared with healthy controls and with adolescents diagnosed as having had a manic episode or depression or anxiety disorder. Participants were from an unselected birth cohort. Attentional, executive and motor impairments at age 13 were found in those who later fulfilled diagnostic criteria for schizophreniform disorder, suggesting that these impairments may be the earliest emerging neuropsychological impairments in schizophrenia-related disorders.

Background. Childhood factors have been associated with increased risk of developing post-traumatic stress disorder (PTSD). Previous studies assessed only a limited number of childhood factors retrospectively. We examined the association between childhood neurodevelopmental, temperamental, behavioral and family environmental characteristics assessed before age 11 years and the development of PTSD up to age 32 years in a birth cohort.

Method. Members of a 1972–73 New Zealand birth cohort (n=1037) who were assessed at ages 26 and 32 years for PTSD as defined by DSM-IV.

Results. We identified two sets of childhood risk factors. The first set of risk factors was associated both with increased risk of trauma exposure and with PTSD assessed at age 26. These included childhood externalizing characteristics and family environmental stressors, specifically maternal distress and loss of a parent. The second set of risk factors affected risk for PTSD only and included low IQ and chronic environmental adversity. The effect of cumulative childhood factors on risk of PTSD at age 26 was substantial; over 58% of cohort members in the highest risk quartile for three developmental factors had PTSD as compared to only 25% of those not at high risk on any factors. Low IQ at age 5, antisocial behavior, and poverty before age 11 continued to predict PTSD related to traumatic events that occurred between the ages of 26 and 32.

Conclusions. Developmental capacities and conditions of early childhood may increase both risk of trauma exposure and the risk that individuals will respond adversely to traumatic exposures. Rather than being solely a response to trauma, PTSD may have developmental origins.

Depression remits and recurs, but among what proportion of the population? Retrospective surveys report the lifetime risk to be around 10%. A modelling study and two prospective studies concur that close to half the population can expect one or more episodes of depression in their lifetime.