To our knowledge, this is the first study to simultaneously investigate hypothetical mechanisms linking CSA to adult PSS and a BI in a community sample of disadvantaged urban ethnic minority women. We found partial support for our conceptual model of two distinct pathways from CSA to negative outcomes. As shown by the outward arrows in , the first pathway from peri-trauma variables to negative outcomes was driven by CSA severity, was not mediated by post-trauma variables, predicted avoidance/numbing symptoms, and was associated with greater biomarker risk. The second pathway involved moderate CSA only, was mediated by post-trauma disclosure experiences, predicted re-experiencing symptoms, and was not associated with BI risk.
Specifically, severe CSA was associated with greater PSS relative to moderate CSA, after controlling for chronic stress and childhood adversity. Importantly, this relationship was not mediated by whether the incident was disclosed, a negative response if disclosed, or self-blame. Examination of separate PSS clusters indicated that the relationship between severe CSA and increased PSS was particularly strong with avoidance/numbing.
Disclosure experiences mediated the relationship of CSA and PSS only in women who experienced moderate severe CSA. Among women with moderate CSA, PSS symptoms were lowest in non-disclosers, higher in disclosers who experienced a low negative response, and highest for disclosers who experienced a highly negative response. Counter-intuitively, a high negative response to disclosure after moderately severe CSA was associated with greater PSS than among women with severe CSA who disclosed and received high negative responses. Other peri-trauma variables (age at the time, duration of the incident and perpetrator) were not directly linked to PSS and were not related to post-trauma disclosure or self-blame.
A greater BI among AA women was predicted by interactions between CSA severity, age at the time, and the perpetrator characteristics. For moderately severe CSA, incidents perpetrated by a family member when the victim was of elementary school age showed nearly double the BI as other low severity categories. For high severity CSA, the BI was nearly doubled for pre-kindergarten survivors victimized by a familiar, but non-family member perpetrator. The significance of a BI score above 4 among these women who average 35 years of age is illustrated by reference to population means on a similar BI obtained via a national survey (Geronimous, Hicken, Keene & Bound, 2006
). White and black women aged 35–44 had mean BI’s of 2.36 and 3.00, respectively and rose to mean BI’s of 4.29 and 4.99 at the 55–64 age groups. Thus, some CSA survivors in this sample are showing BI levels similar to women 20 years older.
We replicated previous work and showed that severe CSA was associated with significantly greater PSS overall, after controlling for childhood adverse experiences other than CSA and adult chronic stress. The latter is a strength of our study, contributing to the literature by showing that the effect of CSA severity on PSS was not modified by the victim’s age at the time of the first CSA incident, the duration of the incident, or by the relationship to the perpetrator. This could mean that there is a ceiling effect of penetrative CSA on PSS, and that additional abuse characteristics that predict adult distress (i.e., younger age, longer duration, closeness to the perpetrator) are not associated with more severe symptoms.
We also found that the relationship between CSA severity and adult PSS was mostly accounted for by the effect of CSA severity on the avoidance/numbing symptom cluster. This is consistent with previous findings that a general tendency to avoid or escape from unpleasant internal experiences may be a specific factor that exacerbates psychological distress among women with a history of childhood (Rosenthal, Rassmussen, Palm, et al, 2005
) or adolescent sexual victimization (Polusny et al, 2004
). In addition, cumulative adverse childhood experiences (including multiple types of abuse) are associated with increased reliance on avoidant coping strategies (Leitenberg, Gibdon & Novy, 2004
On the other hand, disclosure effects among those who experienced moderate CSA incidents were evident for re-experiencing symptoms and not for avoidance/numbing symptom clusters. In other words, variables that preceded or coincided with the abuse (e.g., penetration) are more likely associated with the PSS cluster of avoidance/numbing, whereas post-trauma variables (e.g., negative reactions to abuse disclosure) are more likely to impact the re-experiencing and possibly the hyperarousal cluster. Since re-experiencing, avoidance and dissociation seem to engage distinct neural circuits (Hopper, Frewen, van der Kolk & Lanius, 2007
), we speculate that these circuits are preferentially activated in sequence, some during the abuse and others in its aftermath, to result in the pattern of associations we found.
A large proportion (44%) of the women in our sample did not disclose their first CSA incident, which is consistent with previous studies (Goodman-Brown et al, 2003
; Smith et al, 2000
; Wyatt et al, 1999
). Like others, we also found that the majority of those who disclose their abuse in childhood received negative reactions (Filipas & Ullman, 2001
; Jonzon & Linblad, 2004
). While some studies found that women who disclosed their abuse reported fewer PTSD symptoms in adulthood (Arata, 1998
), others have found that negative reactions to disclosure are associated with greater PTSD symptoms (Ullman, 2007
). Our results partially confirmed Ullman’s findings, where more negative reactions to CSA disclosure were associated with increased PSS, but only for women who experienced moderate CSA. For women with severe CSA, negative responses to disclosure had no significant effect on PSS in this sample.
To our knowledge, this is the first use of a BI as an outcome of exposure to CSA among adult minority women. The evidence that peri-trauma factors of age, perpetrator and CSA severity interact to affect biomarker risk with no evidence of an effect of post-trauma factors supports the conceptualization of CSA as a traumatic event with long-lasting biological dysregulation effects into adulthood. The post-trauma of responses to disclosure and self-blame may be more likely to operate on depression and other psychological symptoms which develop over time, but not to PSS in this sample. Our results also support the models of Saxe and Kaplow (Kaplow et al, 2005
; Saxe et al, 2005
), which suggest different predictors for avoidance/numbing symptoms versus anxiety/hyperarousal symptoms. Future exploration of individual biomarkers in relation to symptom clusters may be helpful in elucidating the biobehavioral mechanisms of hypothesized phenotypes.
Our results support the relevance of further research on the factors that individuals take into account when they are faced with the decision of whether or not to disclose CSA. The finding that not disclosing moderate CSA was associated with the least psychological distress runs somewhat counter to clinical judgments about the value of disclosure. It highlights the need to understand when disclosing may be disadvantageous to the victim. The factors that women (or girls) must weigh when considering whether or not to disclose and their perceptions of the reactions they will receive have not been adequately examined. Likely, the appraisal process involved will be dissimilar for children and adults. Further research is also needed to examine other abuse characteristics (i.e., the relationship of the perpetrator to the victim, the duration of the incident) that may influence the likelihood of a subsequent disclosure.
Even less is known about women whose abuse is disclosed for them; that is, the disclosure is out of their personal control (i.e., it is witnessed or interrupted by someone). Results of this study suggest that important targets for future interventions with CSA survivors may be to teach CSA victims how to disclose appropriately to receive support (Whiffen & Macintosh, 2005
). In addition, although no main effects were found for CSA severity or negative response to disclosure, their marginally significant interaction suggests the importance of testing for interactions in future studies.
The results of this study must be interpreted in light of several limitations. First, the small sample size limited power and only allowed us to examine a dichotomous definition of CSA severity and the first incident. This means that we could not examine the effect of increasingly severe CSA, or the cumulative effects of multiple incidents. We were also underpowered to test for differences between the two ethnic groups and we were only able to examine the relationship between CSA and the BI among AA women. Second, because there was no comparison group of women without CSA histories, we cannot distinguish the impact of CSA on later mental health independent of other risk factors (e.g. low SES, exposure to discrimination, other traumas, etc.). Relatedly, most of the sample did not select CSA as their “worst” traumatic experience on the PSS instrument and of the 21.7% who did, some may not have been referring to the first CSA incident, which was the focus of our analyses here. Future studies should compare CSA-specific PSS and PSS related to other traumas to examine the relative contributions of each on PSS in adult CSA survivors. Finally, assessment of self-blame was limited here and could have contributed to the absence of self-blame effects.
Despite these limitations, this is one of the first studies to address these questions in a sample of socio-economically disadvantaged, ethnic minority women. Because sample size constraints limited our ability to test for between group differences, these questions will need to be investigated with larger, more ethnically and socioeconomically diverse samples. It will also be important to recognize the diversity within each of these ethnic groups and to include samples that are large enough to permit within-group analyses as well.