Our results provide empirical support for stress sensitization effects—an interaction between CA and adult stress—in liability to mood and anxiety disorders in both men and women in a national sample. Our findings are consistent with prior research suggesting that risk for MDEs among women exposed to stressful life events is heightened among those with a history of CA (Espejo et al., 2006
, Hammen et al., 2000
, Kendler et al., 2004
). We extend this literature by documenting stress sensitization effects for PTSD and other anxiety disorders, as well as among men. Although the pathways linking CAs to later stress vulnerability remain to be identified, accumulating evidence suggests that CA exposure is associated with chronic dysregulation in the physiological stress response system that may increase both reactivity to stress and risk for mood and anxiety disorders (Heim and Nemeroff, 2001
), thereby representing a generalized diathesis to psychopathology that persists across the life-course (Monroe and Simons, 1991
One of the most consistent findings in our analysis was that stress sensitization effects occurred among individuals who experienced three or more CAs. This was true for MDEs, PTSD, and ADs. To our knowledge, these findings are novel, as previous studies have not examined degree of CA exposure as a predictor of stress sensitization. Because co-occurring CAs tend to be severe and are strongly associated with poor mental health outcomes (Arata et al., 2007
, Finkelhor et al., 2007
), these results suggest that CAs may need to cross a severity threshold to impact later stress vulnerability.
The basic pattern of findings is consistent for women and men: stress sensitization effects in liability to MDEs, PTSD, and other anxiety disorders are present for both women and men exposed to three or more CAs. Gender differences were found, however, in the number of stressful life events needed to trigger such effects. Fewer major events are necessary to trigger stress sensitization effects in liability to PTSD among women compared to men. This finding may reflect differences in the severity of events experienced by women and men. For example, sexual assault is strongly associated with PTSD onset and is more prevalent among women (Kessler et al., 1995
). The opposite pattern occurred for MDEs, however, such that stress sensitization effects were evident for men with fewer past-year major events than women. It is possible that sensitization effects are triggered when there is a match between the domain of the recent stressor (e.g., interpersonal violence) and of the CA event (e.g., physical abuse) (Hammen and Goodman-Brown, 1990
, Rudolph and Flynn, 2007
), or that individuals are at greater risk for psychopathological reactions that are similar to their response to the initial CA. Either of these possibilities could have produced the observed gender differences in the magnitude of current stressors necessary to trigger sensitization effects. Because this is the first study to examine stress sensitization effects in both men and women, these findings warrant replication in future research.
One noteworthy difference between our findings and the results of prior research involves the level of current exposure to stressful life events that generates stress sensitization effects. Such effects were most commonly observed in our analysis among respondents exposed to three or more major life events. In contrast, previous studies have found increased risk for MDEs among females exposed to CAs (compared to those with no exposure) at low levels of current stress, but no difference in MDE risk at high levels of stress (Hammen et al., 2000
, Rudolph and Flynn, 2007
). These previous studies utilized smaller clinical and/or community samples of young women, which may have led to this discrepancy. It also may have resulted from differences in the way that stress was operationalized: the current study focused exclusively on stressful life events, whereas both chronic stressors and acute events were assessed in studies that reported sensitization at low levels of exposure to stressors (Hammen et al., 2000
, Rudolph and Flynn, 2007
). Consistent with our findings, however, Kendler and colleagues (2004)
also found that the difference in MDE risk between those with and without CA exposure is greater for individuals who experienced high levels of stress, using a measure of both chronic and acute stress exposure. We anticipate that advancements in the measurement of life stress (Monroe, 2008
) will facilitate the ascertainment of the level of stress exposure needed to elicit stress sensitization effects, in part, by ensuring comparability in the assessment of stress exposure across future studies.
Finally, we document an interaction between CA and adult exposure to stressful life events in predicting stress appraisal. These findings suggest that individuals exposed to CAs may be more vulnerable to mood and anxiety disorders following adult stressful events because they perceive those events to be more overwhelming or unmanageable. Moreover, they suggest that greater emotional reactivity to daily events among individuals with a history of CAs (Glaser et al., 2006
, Wichers et al., 2009
) may result from more negative appraisals of those events, a possibility that remains to be examined directly in future research.
Several limitations of the current study must be acknowledged. The first involves our use of a stress checklist rather than a stressor interview (Hammen, 1991
), which did not allow us to ascertain the severity of events or the temporal sequencing of stressors and disorder onset. We attempted to address this first concern by categorizing events as minor and major stressors, although this strategy undoubtedly involved some degree of misclassification. Moreover, because we examined associations between past-year stressors and 12-month disorders, it is possible that some disorder onsets occurred prior to stressor occurrence. Second, this study is limited by retrospective assessment of CAs. Past research suggests that recall bias of CAs primarily involves underreporting of CA (Hardt and Rutter, 2004
), and that the presence of current psychopathology does not result in reporting or memory biases that inflate estimates of the prevalence of CAs (Brewin et al., 1993
). Moreover, prior work examining the validity of retrospective reports of CAs finds that although such reports may be biased, they are sufficiently valid to be used in epidemiologic research, particularly when CAs are well-defined and do not rely on subjective interpretations (Brewin et al., 1993
, Hardt and Rutter, 2004
). Underreporting of CAs in this study would have resulted in attenuation of the associations between CAs and psychopathology, whereas over-reporting of CA occurrence among individuals with past-year disorders would have led to an overestimation of these associations. Consequently, our findings therefore warrant replication in prospective studies. Third, because measures of perceived stress have been found to overlap with measures of distress (Dohrenwend and Shrout, 1985
) our perceived stress measure may have been confounded by current mood and anxiety disorders. Our findings regarding stress sensitization effects on perceived stress should thus be interpreted with caution.
An alternative interpretation of the interactions between CAs and adult stressful life events in predicting psychopathology is that adult stressful life events act as mediators of the association between CAs and psychiatric disorders. In other words, CAs are associated with adult psychopathology because they increase the risk for stressful events in adulthood (Hazel et al., 2008
). Kraemer and colleagues (2008)
suggest that when a correlation exists between two exposures (e.g., CAs and adult stressors), a statistical interaction between those exposures in predicting an outcome should be interpreted as evidence of mediation rather than moderation. Therefore, tests of the stress sensitization hypothesis are needed that focus on adult stressors which are uncorrelated with prior adversities (e.g., so-called “independent” life events (Brown and Harris, 1978
)). Such tests would not be subject to this alternative interpretation.
Our findings have implications for theory, research and practice. First, we find that exposure to CAs increases perceived stress and vulnerability to psychopathology in the context of later stressful life events, providing support for stress sensitization as an etiological model linking CA exposure to a range of mood and anxiety disorders. Although prior research on stress-diathesis models of psychopathology have conceptualized the diathesis as an innate characteristic of the individual, such as a genetic vulnerability (Caspi et al., 2003
, Monroe and Simons, 1991
), the current findings suggest that a generalized diathesis to psychopathology may arise from environmental exposures early in life. Second, these findings point to important avenues for future research. The extent to which stress sensitization plays a role in the development of other psychiatric disorders, such as substance use disorders, represents one such area. Most importantly, the mechanisms underlying stress sensitization effects remain to be identified. It is likely that these mechanisms operate through a variety of cognitive, emotion regulation, and physiological pathways (Hammen et al., 2000
, Repetti et al., 2002
, Rudolph and Flynn, 2007
). Identification of such mechanisms is critical to the development of interventions aimed at reducing the deleterious mental health consequences of CAs. Finally, our findings suggest that individuals with a history of CA exposure represent potential targets for interventions aimed at reducing stress-related psychiatric morbidity in adulthood.