Our findings suggest that both within-individual childhood characteristics and early environmental conditions increase risk of developing PTSD. Specifically, two sets of risk factors for PTSD at age 26 emerged. The first set of factors affected the risk of trauma exposure as well as the risk of developing PTSD once exposed. These risk factors included children’s externalizing characteristics (including difficult temperament, antisocial behavior, and hyperactivity), family history of mental-health difficulties (including maternal reports of distress), and family adversities (including loss of a parent). The second set of factors affected risk for PTSD only. These risk factors included low IQ and chronic environmental stressors such as low SES. The effect of cumulative childhood risk was substantial; over 58% of cohort members in the highest risk quartile for three developmental factors had PTSD by age 26 as compared to only 25% of those not at high risk on any factors.
One limitation of the age-26 PTSD assessment was that the interview did not ascertain the age of onset for trauma exposure or PTSD. PTSD before age 11 is rare in general population samples (Costello et al. 2003
; Ford et al. 2003
), and our risk factors were measured prior to age 11, suggesting that the risks preceded PTSD for most cases. However, to document with certainty that risks were antecedent to trauma exposure, we tested whether childhood factors predicted PTSD that occurred in relation to traumatic events between the ages of 26 and 32. The association of low IQ and externalizing behavior with PTSD was similar, albeit slightly attenuated, compared to that for the age 26 cases. In fact, both IQ at age 5 and antisocial behavior remained robust, significant predictors of PTSD, even though there were only 35 PTSD cases at the age-32 assessment. The most substantial attenuation was observed for family environmental factors, except for low SES, which remained a strong predictor of PTSD. The effect of family environment on many traits has been shown to stronger in childhood and attenuate in adulthood (Plomin et al. 2001
; Jaffee et al. 2002
). Moreover, PTSD related to childhood events was excluded from the age 26–32 data. Exclusion of childhood events has been related to attenuated associations between childhood characteristics (retrospectively assessed) and PTSD in one other study (Breslau et al. 1995
). However, the effect of cumulative childhood risk on PTSD remained substantial. For participants who experienced traumatic events between the ages of 26 and 32, over 23% of cohort members in the highest risk quartile for two or three developmental factors had developed PTSD compared to only 8% of those not at high risk on any factors.
Three findings stand out. First, whereas some research suggests that low IQ and other cognitive deficits may be PTSD sequelae (De Bellis, 2001
), the present study, along with prospective studies of military samples (Pitman et al. 1991
; Macklin et al. 1998
; Kremen et al. in press
), implicates low IQ as a risk factor. The mechanism by which low IQ increases risk of PTSD is not understood. It is possible that individuals with more cognitive resources are better able to translate their traumatic event into a narrative (Pennebaker, 1999
) and make meaning out of it (Janoff-Bulman, 1992
). In addition, low IQ is a risk factor for other forms of psychopathology (Fergusson et al. 2005
), including externalizing disorders, which are in turn associated with increased risk of trauma exposure and PTSD.
Second, the findings suggest unstable early environmental conditions may sensitize individuals to the adverse effects of later stressors. Animal models suggest that offspring reared under stressful conditions are insecurely attached, emotionally dysregulated (Rosenblum & Paully, 1984
; Coplan et al. 1998
), and show persisting alterations in functioning of the hypothalamic–pituitary–adrenal (HPA) axis (Gorman et al. 2002
; Heim & Nemeroff, 2002
). Dysregulation of the HPA axis is implicated in the etiology of PTSD and is a potential biological mechanism linking the association between early environmental conditions and the development of PTSD (Yehuda, 2002
Third, the association between children’s externalizing-spectrum problems and risk of PTSD replicates an association previously documented using retrospective data (Kulka et al. 1990
; Breslau et al. 1991
; Kessler et al. 1995
; Koenen et al. 2005
). Difficult temperament, antisocial behavior and hyperactivity are manifestations of poor self-regulation that may place the individual at increased risk of trauma exposure. Individuals with poor self-regulation, broadly defined by the inability ‘to modulate behavior according to the cognitive, emotional and social demands of a particular situation’ (Calkins & Fox, 2002
, p. 479), may be more likely to develop PTSD once exposed to trauma because they lack the affect tolerance necessary for processing the traumatic event. Instead, they are likely to angrily act out, or to engage in avoidance, strategies shown to interfere with PTSD recovery in community samples (Koenen et al. 2003
The strengths of the current study include the use of a birth cohort, prospective measures of a range of childhood characteristics, and a low attrition rate. However, the present study has several limitations. First, our ascertainment of trauma exposure asked respondents if they had had any horrible experience that gave them difficulties such as sleep disturbance or jumpiness. As a result of this protocol, our trauma-exposed group was selected for respondents who recalled at least a minor, acute reaction to the trauma. Trauma-exposed participants who experienced no acute reaction would not have been included in the trauma-exposed group. Therefore, the childhood characteristics associated with trauma exposure in this sample may not apply to individuals who experienced an event but were not bothered by it. Our definition of exposure also probably increased the similarity between the trauma-exposed no-PTSD and PTSD groups, and therefore probably attenuated differences in childhood characteristics. Second, because of time constraints it was not possible for the Dunedin team to interview participants more extensively to ascertain details about the nature of their traumatic event, the possibility of repeated trauma exposures, their age at exposure, or other contextual details. Therefore, we could not test whether the association between early childhood risk factors and the development of PTSD was mediated by trauma type. Findings from other studies support such mediation (Bromet et al. 1998
). Third, results of the present study are limited to a single, contemporary cohort of New Zealand young adults. Although lifetime rates of PTSD in this cohort (11.8% for women, 7.6% for men) are similar to those reported by the National Comorbidity Survey (NCS; Kessler et al. 1995
) for young adults in the same age range (11.2% for women, 5.6% for men), further research is required to determine whether our findings will generalize to other times and places. Fourth, studies with larger sample sizes of PTSD cases are needed to examine the interplay of childhood characteristics and sex differences in the etiology of PTSD. Fifth, our study was not a genetically sensitive design. Genetic influences account for substantial variation in PTSD (True et al. 1993
; Stein et al. 2002
). Future research is needed to determine whether the link between the childhood risk factors we studied and PTSD is environmentally or genetically mediated.
A developmental perspective on the epidemiology of PTSD has implications for research and practice. Our findings suggest that a developmental perspective should not be limited to studies of childhood PTSD. Rather, 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. Further research into the developmental epidemiology of PTSD may improve understanding of its etiology. Clinicians may find their treatment approach informed by integrating information on clients’ childhood cognitive and temperamental characteristics and other environmental experiences, particularly those related to chronic adversity, into their case conceptualization. In fact, psychotherapy that combines a developmentally informed approach to addressing deficits in clients’ emotional and interpersonal capacities with more traditional trauma-focused treatment has been shown to be highly effective in treating adult PTSD (Cloitre et al. 2006
). Finally, prevention efforts aimed at addressing some of these developmental capacities, such as antisocial behavior, or at improving conditions of chronic adversity, such as poverty, may ultimately reduce risk of PTSD.