This is the first study to examine the relationship between cancer-related trauma outcomes and QOL. Our results show that PTSD symptoms and PTG help to explain the relationship between specific antecedents and QOL. Although there is an absence of comparable studies in cancer survivors, studies of war veterans have similarly found PTSD to mediate the relationship between antecedents and QOL (Magruder et al., 2004
; Schnurr, Hayes, Lunney, McFall, & Uddo, 2006
; Zatzick et al., 1997
). Additionally, several studies conducted with cancer survivors found negative relationships between PTSD and QOL (Amir & Ramati, 2002
; Meeske, Ruccione, Globe, & Stuber, 2001
; Okamura, Yamawaki, Akechi, Taniguchi, & Uchitomi, 2005
; Santos, Kozasa, Chauffaille Mde, Colleoni, & Leite, 2006
), yet no such studies were identified in a Medline search of PTG and QOL. The dearth of literature regarding the association between PTG and QOL may be reflective of the more recent development of psychosocial models, as opposed to more traditional medical models that incorporate PTSD as a diagnostic disorder.
The Lazarus & Folkman (1984)
and Taylor and Aspinwall (1996)
theories appear to be a sound foundation to explain the relationships which resulted from the multiple linear regression, in which lower levels of resources (e.g., less social support, negative appraisals) were associated with lower QOL. In addition, the QOL model that we tested () explained a large amount of the variance in well-being (82%), indicating that it includes many key variables and is relevant to NHL survivorship. Similar to Northouse et al. (2002)
, we found that many of the clinical variables (e.g., histology) contributed little or no unique variance in the survivors’ QOL, while social support, appraisals, co-morbidity and PTSD symptoms were important components of the model. Future clinical and research activities need to consider the significant relationship of these variables to survivors’ QOL.
The testing of alternative SEM models describing the pathways between the antecedents, mediators and QOL led to a reduction in the number of paths, thereby enhancing parsimony. It also elucidated the relationship between variables; for example, we found that some had a direct path to QOL, others had an indirect path, and still others had both direct and indirect paths to QOL. It is through understanding and testing for mediation that we can begin to untangle the mechanisms and processes by which the cancer experience affects an individual’s QOL.
As stated by Baron and Kenny (1986)
, mediator variables are those that “speak to how or why such effects occur”, representing processes that could be targeted for intervention. For example, our model suggests that individuals with active disease or of an older age could be targeted for interventions aimed at enhancing PTG, while those without a college degree, more co-morbidity, more recent diagnosis or more employment and insurance issues related to cancer might benefit from treatments to reduce PTSD symptomatology as a means to improving overall QOL. In addition, individuals with less social support could benefit from interventions focused on enhancing PTG and social support, and reducing PTSD symptoms.
Several limitations warrant caution in interpreting our findings. First, since this study was cross-sectional, no definitive inferences can be made about the direction of causality between PTSD, PTG and QOL. However, our findings are consistent with the literature regarding the effects of traumatic stress on QOL and our interpretation of these findings is guided by a theoretical framework. In addition, certain variables (e.g., age and appraisals of life threat and treatment intensity at diagnosis) allow us to infer the direction of causality more than other variables (e.g., current age and level of social support). Still, longitudinal studies are needed to establish and support evidence of causality. Second, the exclusion of additional psychological variables (e.g., depression, anxiety) limits our conclusions in that these symptoms also might be important in explaining QOL. However, given the exploratory nature of this study, it was not possible to include every psychological variable of interest. Third, although several correlations reported in were statistically significant (.115<r <.300), this was attributed more to the large sample size than the actual strength of the correlation. Fourth, although our sample was representative of NHL patients treated at two major comprehensive cancer centers in North Carolina, the findings cannot be generalized beyond this specialized population. For example, replication in other geographical areas with different types of cancer diagnoses is needed to confirm the roles of PTSD and PTG in QOL. Finally, despite our finding of adequate model fit and high R2, other theoretical frameworks may yield equivalent or better fit and could be considered in future research studies. Of note, an additional model was tested (a revision of Model A’ without the social/family FACT-G domain) which yielded a good fit, RMSEA =.050, CFI=.938, TLI=.932. This would suggest that alternative measures of QOL be considered in replication studies, as the FACT-G measurement model results were weaker than those of the remaining model components.
Implications for Clinical Practice
Despite these limitations, our findings indicate that PTSD and PTG mediated the relationship between antecedents and QOL and our conceptual model accounted for a large amount of variance in the survivors’ QOL. These findings give support to using PTSD as a diagnostic framework (and PTG, to a lesser extent) in understanding symptomatology in this population. In addition, several covariates were identified that either directly or indirectly through PTSD and/or PTG relate to QOL. Furthermore, proven therapies could be modified for use with cancer survivors to include methods that enhance PTG and address the unique features of cancer-related PTSD. For example, cognitive behavioral (CBT) and prolonged exposure techniques have been shown to be effective in reducing or eliminating PTSD symptoms in survivors of sexual assault (Foa & Meadows, 1997
). Targeted treatments could be developed and implemented that minimize future-oriented intrusions (fear of recurrence, test anxiety) and enhance coping skills as survivors navigate through a range of possible aversive events such as treatments, recurrence(s), and medical surveillance.
However, given the absence of “good fit”, additional research using alternate measures and in other cancer samples is needed to improve the robustness of our findings. In addition, studies that follow patients over time are needed to help establish causality and determine if targeting PTSD symptom reduction and PTG enhancement could assist individuals in improving their QOL along the survivorship trajectory. This would help determine if efforts towards reducing PTSD symptomatology and enhancing PTG in cancer survivors as a means to improve QOL are warranted.