Introduction
Many studies have revealed associations between childhood adversities and mental health problems later in life, suggesting that these adversities often have long-term effects on functioning and well-being [
1‐
5]. Yet, the mere existence of such an association is not very informative about the chain of events linking the adversities experienced as a child to psychopathology during adulthood [
6,
7]. The existing evidence has made clear that this chain involves a highly complex interplay of multiple personal and environmental factors. In a recently published extensive review on childhood determinants of adult psychiatric disorder [
8], Fryers and Brugha stated that “Definitions of childhood adversity are truly problematic: they inevitably overlap with apparently more specific variables such as negative life events, child abuse or family conflict, and must be expected to inter-relate with variables such as divorce of parents, child behaviour and child psychological disturbance.” (p.3). A further complicating factors concerns the large time lag between childhood and adulthood; the longer the period between determinant and outcome, the larger the number of possible intermediate pathways. Investigating the mental health consequences of childhood adversities during the intermediate period, adolescence, may help to elucidate the link between childhood adversities and adult mental health problems, and to finetune the risk associated with childhood adversities in a dynamic way. The more is known about the short-term and longer-term aftermath of childhood adversities, the better we will be able to estimate the prognosis of an individual with a history of childhood adversities, and to adjust and improve the accuracy of the prognosis over time. Longitudinal surveys offer excellent opportunities to better understand and predict the development of mental health problems after exposure to childhood adversities [
8]. This article describes an attempt to do so based on a Dutch longitudinal population survey of adolescents, TRAILS.
That childhood adversities are associated with an increased risk to have mental health problems in adolescence and adulthood does not necessarily imply that they are associated with an equally increased risk to develop such problems later in life. The few studies that accounted for problem levels in the period in-between suggest that this may not always be true. Appleyard et al. [
9] found that the association between maternal support in early childhood and internalizing problems at age 16 was mediated by internalizing problems at school entry. Consistent with that, a recent study in our own cohort TRAILS indicated that the effect of childhood family instability on internalizing and externalizing problems in late adolescence was mediated by early-onset mental health problems rather than continued family instability [
10].
These prior findings provide a rationale to hypothesize that the risk of an incident onset of psychiatric disorder after exposure to childhood adversities attenuates over time. Indeed, in the US National Comorbidity Survey (NCS), associations of childhood adversities with first onsets of psychiatric disorders declined with lifecourse stage [
11]; a finding that was replicated in the World Mental Health Survey and NCS Replication survey [
7,
12]. A drawback of these studies is that they included respondents with a wide age range, implying that both the childhood adversities and the onset of psychiatric disorders could have occurred a long time ago, which provides a potential source of recall bias [
12,
13]. The TRAILS study allowed to reduce the time lag between the occurrence of these events and their measurement and to use multiple informants, which will enhance the validity of the measures.
The present study was conducted to test the hypothesis of decreasing effects of childhood adversities over time by means of a Cox proportional hazards regression model with separate risk estimates for childhood and adolescence, that is, during and after exposure to the childhood adversities. Specific aims were: (1) to investigate similarities and differences between three major groups of disorders: depressive disorders, anxiety disorders, and disruptive disorders; (2) to compare the effects of different kinds of childhood adversities; and (3) to explore gender differences in any of the effects.
The aim to investigate similarities and differences between depressive, anxiety, and disruptive behavior disorders was inspired by the fact that these three groups of disorders often occur in concert and have all been related to childhood adversities [
3,
6,
7,
12,
14], but are also assumed to have partly diverging etiologies [
15‐
17] and associated endophenotypes (e.g., [
18,
19]). In the Adolescent Supplement of the National Comorbidity Survey, childhood adversities were found to predict disruptive behavior disorders most strongly and anxiety disorders least strongly [
3]. Although these findings do not provide a solid basis for specific hypotheses with regard to time-dependent effects of childhood adversities, they do indicate that differential effects are well conceivable.
We examined the effect of various measures and types of adversities because, although different kinds of childhood adversities tend to co-occur [
3,
7,
20], some adversities have been found to be stronger associated with later mental health outcomes than others (e.g., [
3,
7,
8,
12]). Only by studying a variety of childhood adversities in the same sample can we make comparative statements about their impact in the short and longer term.
Gender differences were explored because of various indications that the short-term and long-term effects of childhood adversities might be different for boys and girls. To start with, the prevalence of these disorders is known to be different for boys and girls, with boys being overrepresented in the disruptive behavior disorders, and girls in anxiety and depressive disorders (e.g., [
21]). Furthermore, Rutter and colleagues [
22] pointed to the fact that boys tend to predominate in neurodevelopmental disorders with an early onset, and girls in emotional disorders with an adolescent onset, and related these differences to genetic gender differences, the biological and psychosocial consequences of these differences, and gender differences in the distribution of more proximal risk factors. Not only the risk of disorder itself, but also the sensitivity to interpersonal stressors might develop differentially for boys and girls over time [
23‐
25], possibly as a result of differential actions of male and female sex hormones [
26]. Cyranowski et al. [
27] provided a theoretical model for these developmental differences by postulating that girls become increasingly sensitive to interpersonal stressors during adolescence, due to a combination of puberty-related changes in oxytocin levels and social pressures to behave in a feminine way. In the context of the present study, it is particularly relevant that this increased sensitivity occurs mainly in at-risk girls, that is, girls with pre-existing vulnerabilities, according to the model, and that childhood adversities are a likely cause of such vulnerabilities. These notions might imply that the assumed decrease in the onset risk associated with childhood adversities in adolescence is stronger in boys than in girls, or even that girls experience an increase rather than a decrease. In a prior study, we found that parental divorce in childhood was associated with an increase in girls’, but not boys’, depressive symptoms during early adolescence [
28], suggesting that adolescence is a period that can enhance preexisting susceptibilities in a gender-specific way indeed.
To sum up, we aimed to investigate whether and how childhood adversities, as assessed with a variety of different measures, affected the risk of developing an incident psychiatric disorder in childhood and adolescence, with the expectation that it would decrease over time. In addition to an assessment of overall risk, we examined depressive, anxiety, and disruptive behavior disorders separately, as well as gender differences in any of the effects under study. More knowledge about the dynamics of the impact of childhood adversities on the risk of onset of psychiatric disorders, or their non-occurrence, can help to improve prediction models, and allow them to be extended and refined continuously, with every increasing year.
Discussion
This study was conducted to test the hypothesis that the effect of exposure to childhood adversities on the risk of onset of a psychiatric disorder decreases over time, that is, was lower during adolescence than during childhood. Depressive, anxiety and disruptive behavior disorders each appeared to have their own, characteristic, pattern of associations with childhood adversities across childhood and adolescence, which was maintained after adjustment for comorbid disorders.
For depressive disorders, the overall pattern found was as expected, that is, a high excess risk during childhood, which decreased during adolescence. This pattern was by and large comparable for all measures of childhood adversities used, though not always statistically significant. For anxiety disorders, the pattern found suggested a moderately increased risk during childhood, lower than that of depressive and disruptive behavior disorders, which remained approximately stable over time. Disruptive behavior disorders took an intermediate position with regard to the effect of childhood adversities on risk of onset during childhood. The relatively few first onsets of disruptive behavior disorder during adolescence precluded reliable statements about the long-term effects of childhood adversities. The size and direction of the regression coefficients suggest that, with regard to the onset of disruptive behaviors, the long-term effects of childhood adversities depend to a larger extent on the nature of the adversity than with regard to depressive and anxiety disorders.
Childhood adversities have been associated with risk of (first) onset of psychiatric disorder before in the US National Comorbidity Survey [
11] and associated studies from the same group, including the NCS Replication survey [
12], NCS Adolescent Supplement [
3], and World Mental Health Survey [
7]. It is noteworthy that, despite substantial differences in study design and measures used, there are notable similarities between this prior research and our findings. Consistent with these studies, we found that overall ratings of the stressfulness of the environment (in the NCS-related studies operationalized as family violence) were more strongly associated with the onset of psychiatric disorders than specific events such as parental death or divorce (included in the event index). Also consistent with these studies, childhood adversities predicted anxiety disorders less strongly than depressive and disruptive behavior disorder in childhood, and the time decay was largest for depressive disorders, while there was hardly or no decay in the onset risk of anxiety disorders. The effect sizes (relative risks generally between 1.0 and 2.0) were comparable as well. There are also differences, especially with regard to the consequences of sexual abuse and the prediction of disruptive behavior disorders. Both effects tended to be smaller in our sample than in the before-mentioned studies. With regard to sexual abuse, the extremely low prevalence in our sample may have caused inaccurate effect estimates. The NCS-related studies had considerably larger samples and included sexual abuse up until the age of 18 instead of 11; differences that might underlie their larger effects. With regard to disruptive behavior disorders, these studies included attention deficit/hyperactivity disorder, which may have inflated the association with childhood adversities. But overall, we feel that the similarities between the studies outnumber the differences by far.
To the best of our knowledge, the studies referred to in the previous paragraph are the only ones that investigated childhood adversities in relation to age-dependent onset risks of multiple psychiatric disorders. A few other reports focused on depression risk in particular. Gilman et al. [
36] used mother-reported childhood adversities collected at age 7 to predict the risk of depression onset during various life stages (as assessed between the age of 18 and 39) in 1,089 participants of the US National Collaborative Perinatal Project. Comparable to our findings, the effects of parental divorce, a main component of the event index used in the present study, was associated with depression onsets before the age of 15, and dropped below significance after that. Jaffee et al. [
37] examined etiological differences between juvenile-onset and adult-onset cases of depressive disorder in the longitudinal Dunedin Multidisciplinary Health and Development Study. Whereas the etiology of depressive disorders with an onset before the age of 16 was characterized by perinatal problems, caretaker instability, criminality, and familial psychopathology; disorders with a later onset only had an elevated prevalence of sexual abuse, compared to non-depressed controls. Sexual abuse increased the risk of juvenile onsets as well, but not statistically significant because of little power. These findings once again confirm the notion of decreasing effects of childhood adversities on depression risk over time. Moreover, it is interesting to note that sexual abuse was the only adversity in our study that did not show a significant decay in effect from childhood to adolescence, which resembles the long-term consequences of sexual abuse reported by Jaffee and colleagues.
Our study has a number of notable strengths: a population-based sample of same-aged adolescents, a follow-up period of almost ten years, several measures of childhood adversities, from multiple informants, and information about the lifetime occurrence of DSM-IV disorders and their age of onset. Also of note is the fact that our sample was relatively young. Considering that the length of recall has been suggested to inflate estimated associations, our childhood adversity measures are probably relatively valid, compared to most other studies [
12]. The combination of these factors offered unique opportunities to investigate the long-term effects of childhood adversities on later psychopathology.
A number of limitations should be accounted for when interpreting the associations found. First, exposure to childhood adversities was assessed retrospectively. Even though the length of recall was limited compared to most other studies (see above), we cannot exclude that respondents’ (imminent) psychiatric disorders during the assessment of childhood adversities influenced the ratings of the stressfulness of their childhood and perhaps also recall of specific negative events, probably in such a way that the symptoms inflated the stressfulness ratings and hence the association between childhood adversities and psychiatric disorders. The event index used is least likely to be biased by later psychopathology, because it was based on concrete, relatively objective events as reported by the parents. A second limitation is that the childhood adversities experienced by our general population sample were, on average, mild. Severe abuse or maltreatment was, to the best of our knowledge, relatively rare among the TRAILS participants, and our findings may not generalize to extremely stressful childhood conditions. Third, we focused on broad outcome domains, which could mask important differences within those categories. Particularly anxiety disorders are notoriously heterogeneous and encompass, among other things, specific phobias, which usually have an early onset and are rarely severe; social phobias, which often emerge a bit later in life and may take serious forms; and panic disorders, which tend to have a later onset and be quite severe. Taking into account differences among these specific types of anxiety could reveal different association patterns, but is beyond the scope of the present study and not feasible due to insufficient power. Fourth, we assessed psychiatric disorders at about age 19 and hence cannot make statements about the risk of psychopathology later in life.
It is remarkable that, while the risk of onset of depressive disorders associated with childhood adversities decreased over time, no such effects were found for anxiety disorders: their initial risk was lower, but remained constant over time. Tentatively, this suggests that the onset of depression is more likely to be a direct consequence of exposure to adversities than the onset of anxiety. In case of a causal stressor-disorder relationship, one expects the effect to diminish after the stressor has subsided [
38]. The fact that the onset of anxiety did not show this pattern may indicate that these disorders did not result from the adversities directly, but rather from a common, unmeasured, cause, which was more stable over time than the adversities. Examples of possible common causes include, for instance, (parental) personality and genetic factors that may influence both the exposure to adversities and the outcome through gene-environment correlations (e.g., [
39]). Only genetically informative study designs have the potential to tear apart individual and environmental factors thoroughly.
The declining effect of childhood adversities on the onset risk of depression may be explained by selection processes rather than a decay in risk itself. Within the individuals that are exposed to (severe) childhood adversities, the most vulnerable ones are the most likely to develop a depressive disorder. After onset, these individuals are excluded from the group who is still at risk of an incident disorder, leaving an increasingly resilient group over time. In fact, we have shown that adolescents who were exposed to childhood adversities but did not develop a depressive disorder before middle adolescence were more resilient to the depressogenic effect of stressful life events than the group of adolescents who were not exposed to childhood adversities, in whom no selection process had occurred yet [
32]. From this point of view, childhood adversities can be considered a natural experiment, providing valuable information about an individual’s sensitivity or resilience to stress.
As opposed to some previous reports [
27,
28], we did not find gender differences in stress-sensitivity. Although the overall risk of depression was about twice as high in girls as in boys, the relative age at onset and the relative risk associated with exposure to childhood adversities was comparable for both genders.
We used three different measures to assess childhood adversities in this study, which ranged in their degree of objectiveness from a highly subjective stressfulness rating to a much more objective index of specific events such as parental death and divorce. The stressfulness rating reflects a mixture of the occurrence of stressful events and reactions to those events. On the one hand, this measure is preferable to more objective event indices, because it encompasses all potential sources of stress, including ones that are relatively rare and therefore likely to be overlooked in event checklists. In addition, stressful events are notoriously heterogeneous with regard to their actual meaning and threat for an individual [
40], and a measure incorporating the impact of events captures at least part of this heterogeneity. On the other hand, by including the stress experienced by the child in a measure, it may partly reflect a highly reactive temperament or (subthreshold) psychiatric symptoms, and hence lead to inflated estimations of the effects of stressful events on the outcome measure. In the present study, this may have happened with regard to anxiety disorders, which were predicted by the overall stress rating but not by the life events index, in particular.
To conclude, when individuals have been exposed to adversities early in life, the period that has passed since then without a psychiatric disorder contains useful information with regard to the probability that they will still develop that disorder, and this information is partly adversity-specific and disorder-specific. This has practical implications for, among other things, the development of prediction models, which should include not only information on exposure to childhood adversities, but also on mental health problems in the time since. By allowing prediction models to be updated by new information over time, and to use this information in a dynamic way, we might become better able to distinguish between individuals in need of prevention and those who are not.