Although IBD and IBS differ in that IBD is a chronic inflammatory disorder of the gut with of en serious complications, while the pathology physiology of IBS remains incompletely understood but by definition lacks evidence for structural, biochemical, or inflammatory disease (23
), GI and psychological symptoms negatively impact HRQOL in both disorders (2
). Our study is the first to use SEM to characterize the interrelationships among HRQOL, GI, and psychological symptoms in both disorders. By quantifying these relationships, our main objective was to improve our understanding of the illness processes in IBD and IBS, which may ultimately result in more effective management of disease-specific GI and psychological symptoms with improvement of overall HRQOL.
We investigated three hypotheses. First, our hypothesis that both GI symptom severity and degree of psychological distress would be directly associated with impaired HRQOL in IBS and IBD was supported. Second, our hypothesis that GI symptom severity will also indirectly impact HRQOL through its association with increased psychological distress was confirmed. Last, and in contrast to prevailing clinical dogma, our third hypothesis that GI symptom severity will have a stronger direct association with HRQOL in IBD patients, and psychological distress will be more important in IBS was not as strongly supported as both IBS and IBD demonstrated similar positive correlations.
In our study, both IBS and IBD patients demonstrated similar negative correlations between psychological symptoms and HRQOL and between GI symptoms and HRQOL. The key difference between IBS and IBD was that while both patient groups showed positive correlations between GI symptom burden and psychological distress, there was a substantially greater association in IBD compared with IBS. In IBD patients, there was a significant indirect effect of GI symptom severity on HRQOL that was mediated by increased psychological distress. In contrast, there was less of a relationship between GI symptoms and psychological distress in IBS. Psychological distress was less dependent on GI symptom severity in IBS than IBD even though the degree that psychological distress impacted HRQOL was similar. These results suggest that psychological distress is related to worsening GI symptoms in IBD patients and therefore may improve with relief of GI symptoms.
Our finding of worsening GI symptoms being associated with psychological stress in IBD is supported by previous studies (10
). These studies demonstrated a temporal relationship where psychological distress (10
) and acute life stressors (10
) or having high perceived stress (28
) resulted in worsening of IBD symptoms and subsequently a disease flare. While our study used a statistically weighted latent composite variable to measure general GI symptoms, several studies assessing IBD symptom severity with validated disease-specific tools have found a comparable association of psychological factors and GI symptoms. A potentially important issue in IBD is that disease-related concerns or fears about disabling consequences such as colectomy or ileostomy, or cancer, can impact severity and psychological distress and this may be especially true for more severe patients. This may be a more significant factor in IBD patients due to the greater actual risk of serious consequences, although IBS patients also show significant illness-related fears that are significantly associated with global symptom ratings (29
). Overall, life stress and psychological symptoms appear to positively correlate with GI symptom severity in IBD.
Interestingly, we found that psychological distress is less dependent on GI symptom severity in IBS compared with IBD. This implies that in IBS, other factors unrelated to GI symptoms probably have a stronger role in determining distress. The IBS literature suggests several possible explanations for this finding. There is an increased prevalence of psychiatric disorders in clinic patients with functional GI disorders (40–70%), such as IBS, compared with healthy controls (20%) and patients with organic GI disease, including IBD (25%) (18
). Although the psychological disorders can occur at the same time as IBS, they often precede the onset, suggesting that they should not be considered as a response to IBS (18
). Early life risk factors for the development of IBS include various forms of childhood adversity, such as increased socioeconomic stress during childhood (32
), childhood physical and sexual abuse (15
), low birth weight (39
), and poor parental relationships such as losing one parent through death (40
). This exposure to early life stress may result in persistence of childhood psychological distress into adulthood and therefore decrease the relative impact of current IBS symptoms on current psychological state. In IBD patients, there are much less data suggesting a role for early life psychological adversity, and more data showing physical risk and protective factors in IBD (38
). However, it is important to note that few studies have systematically examined hypotheses of early psychological stress in IBD. A related issue is the clearly documented higher prevalence of psychiatric diagnoses such as major depression, anxiety disorder, and somatoform disorders in IBS patients, compared with that found in IBD (41
). As with early life stress, this higher prevalence of comorbid psychiatric disorders in IBS may help explain the smaller influence of current GI symptoms on psychological distress since non-disease-related psychosocial factors may have a more significant impact on current psychological functioning in IBS compared with IBD patients for whom their symptoms may be more of the primary stressor in their life. Nonetheless, it has been shown that IBD patients are more likely to have diagnoses of mood disorders long antedating their disease diagnosis compared with healthy population controls (44
). In addition, extraintestinal symptoms, such as fatigue, sleep disturbances, and sexual disturbances are commonly reported by IBS patients (45
) and likely contribute to psychological distress, including somatization, independent of GI symptoms.
There were limitations to our study. We did not evaluate CD and UC separately, nor did we have biomarkers of IBD severity. It is questionable whether separating CD and UC would have made any difference in our study results as some previous studies show no difference in HRQOL and psychological distress between CD and UC (46
), while others do (47
). Within the IBS group, we did not separate IBS by predominant bowel habit. However, we do not suspect IBS sub-classification would have changed the final conclusions drastically as in a previous IBS study, GI and psychological symptom severity, and HRQOL did not differ in subtypes (49
). Furthermore, we have previously shown that degree of psychological symptoms, and relationship between psychological symptoms and HRQOL did not vary greatly between IBS-C and IBS-D (50
). Also, we did not test for current psychiatric diagnoses or chronicity of psychological symptoms in our two patient samples, which may have help explain the varied strength of correlation between GI and psychological symptoms. However, we assessed the presence of psychological symptoms with a validated questionnaire. Additionally, GI symptoms and HRQOL were not measured using disease-specific measures due to necessity of using a measure, which could be used in both illness groups. However, studies that used disease-specific instruments (52
) found comparable associations between GI symptoms and HRQOL in both IBS and IBD (47
). An advantage of the generic HRQOL measure is that it did not include specific GI symptoms as is true of many of the disease-specific measures in IBS and IBD and therefore it enabled a clearer examination of the relationships among the constructs.
In summary, our analysis demonstrates the importance of interrelationships among GI symptoms, psychological distress, and HRQOL in both IBD and IBS populations. The overall pattern of relationships was similar across the two groups including an important role of psychological distress as a mediator of HRQOL changes from GI symptoms. There was, however, a stronger positive correlation between GI symptoms and psychological distress in IBD than in IBS, suggesting that non-illness psychosocial variables may have a more significant role in determining HRQOL in IBS vs. IBD. These findings have several implications on the management of these two conditions. For patients with IBD, the finding of a significant role of psychological distress in determining HRQOL suggests that therapy directed at reducing intestinal inflammation and GI symptoms may result in less psychological distress and improvement of HRQOL but that also interventions directed at psychological distress may have a significant impact on HRQOL. In addition, if psychological distress remains high even with symptom improvement (for instance when there is a high degree of fear of relapse), then it would be expected that HRQOL would not improve. In IBS patients, our findings suggest that a change in GI symptoms alone may not have the desired impact on HRQOL. Following the biopsychosocial model, treatment that addresses psychological distress both related and unrelated to current GI symptom severity are indicated in order to improve overall HRQOL.