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Depression and Abdominal Pain in IBS Patients: The Mediating Role of Catastrophizing

From the Department of Medicine (J.M.L.), University at Buffalo School of Medicine and Biomedical Sciences, State University of New York, Buffalo, NY; Research Institute on the Addictions (B.M.Q.), University at Buffalo, SUNY Buffalo; and Department of Psychology (E.B.B.), University at Albany, State University of New York, Albany, NY.

Address correspondence and reprint requests to Jeffrey M. Lackner, PsyD, Behavioral Medicine Clinic, Department of Medicine, UB School of Medicine, SUNY, ECMC, 462 Grider Street, Buffalo, NY, 14215. E-mail: lackner{at}buffalo.edu

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION ACKNOWLEDGMENTS REFERENCES

 
OBJECTIVE: Depression has been linked to irritable bowel syndrome (IBS), but the mechanism underlying this relationship is unknown. This cross-sectional study explores the possibility that negatively skewed beliefs patients hold regarding abdominal pain (ie, catastrophizing) mediate the relationship between depression and pain severity.

METHODS: The sample included 244 consecutively evaluated individuals who met Rome II diagnosis for IBS without comorbid gastrointestinal disease and completed measures of pain severity, trait anxiety, catastrophizing, maladaptive beliefs, and depression as part of baseline assessment of an National Institutes of Health–funded randomized controlled trial of 2 nondrug treatments.

RESULTS: Using a mediational model involving a series of linear regressions, results indicated that pain catastrophizing partially mediated the link between depression and abdominal pain severity. Depression, catastrophizing, and control variables accounted for 21% of the variance in pain severity. The finding that patients with IBS with greater depression reported greater pain severity can be partially explained by their tendency to engage in more catastrophic thinking specific to pain.

CONCLUSIONS: The relation between depression and pain is not, as psychogenic models predict, strictly a direct and linear one but works partly through patients’ beliefs regarding their pain in general and pain catastrophizing in specific. Implications of the findings for understanding and investigating the depression–IBS link from a biopsychosocial perspective are discussed.

Key Words: irritable bowel syndrome, • depression, • cognition, • visceral pain, • catastrophizing, • chronic pain.

Abbreviations: IBS = irritable bowel syndrome;; BP = Bodily Pain;; BDI = Beck Depression Inventory;; CBT = cognitive behavioral therapy;; DAS = Dysfunctional Attitudes Scale;; DSM = Diagnostic and Statistical Manual for Mental Disorders;; SF-36 = Short Form-36 Health Survey;; STAI = State-Trait Anxiety Inventory.

	INTRODUCTION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION ACKNOWLEDGMENTS REFERENCES

 
Irritable bowel syndrome (IBS) is a prevalent, painful, often disabling functional gastrointestinal disorder whose key pathophysiological features include disordered gut motility, visceral sensitivity, and psychological dysfunction. Psychological factors have a profound influence on the onset, expression, and course of IBS, particularly in more severely affected patients (1). One psychosocial variable often elevated in patients with IBS is depression. The frequent occurrence of depression is confirmed by studies showing that treatment-seeking patients have higher levels of depressive symptoms than normal controls (2,3) and high rates of diagnosable mood disorders (4).

Although there is general consensus that IBS is often accompanied by states of clinical depression, the manner by which it influences core symptoms of IBS is unknown (5). At least 3 lines of research suggest that the influence of depression is not necessarily direct. First, research that has sought to establish the prevalence of IBS in mood-disordered patients (ie, primary Diagnostic and Statistical Manual for Mental Disorders [DSM] diagnosis of major depression) not seeking treatment for IBS finds that only 25% meet criteria for IBS (6). Second, not all treatment-seeking patients with IBS report clinical levels of depressive symptoms (7). Third, the severity of IBS symptoms does not necessarily correspond with the severity of depressive symptoms. In 1 of the few studies that has explored the depression–IBS symptom link, Drossman (8) found that although levels of depression distinguished patients classified as severe on the basis of their scores on the Functional Bowel Severity Scale, depression did not predict symptom severity. Because their data analysis strategy was not designed to assess complex (eg, indirect) relationships involving 3 or more variables, Drossman’s findings do not necessarily exclude the possibility that depression influences IBS symptoms by working through a third (ie, mediator) variable. Identifying biobehavioral factors that underlie the relation between depression and IBS is important to enhancing our understanding of IBS and developing more effective treatments for patients whose comorbid mood problems (eg, depression) puts them at risk for poor outcome of pharmacological and behavioral treatments (9).

There is reason to believe that the beliefs patients hold about symptoms mediate the relationship between depression and IBS symptoms. The importance of cognitive processes in general comes from research showing that patients with IBS are characterized by biases in central processing of visceral sensation. They show enhanced perceptual response to normal visceral events; selectively attend to and fear visceral stimuli; and mislabel in a skewed manner internal sensations that healthy controls construe as benign (10). Of different cognitive processes, the construct of "catastrophizing" has garnered much attention in the broader pain literature. Catastrophizing is a cognitive, individual difference variable characterized by a "tendency to focus on and exaggerate the threat value of painful stimuli and negatively evaluate one’s ability to deal with pain" (11, p. 2). Catastrophizing has been most extensively studied in the context of chronic pain populations but has important implications for understanding IBS, whose cardinal symptom and the one patients describe as most distressing is pain (12). In studies with heterogeneous pain samples, a tendency toward catastrophizing is associated with greater pain and functional limitations (13–17). Psychometric studies that have sought to establish the construct validity of catastrophizing indicate that it has unique properties not shared by measures of psychological distress, including depression (18,19).

While catastrophizing is empirically separable from the symptoms of depression, it is unclear whether the influence of catastrophizing on pain-related outcomes is a proxy for an enduring tendency toward negative, distorted thinking exhibited by patients with IBS (20) and other clinical samples (21). In other words, the tendency of patients with IBS to catastrophize may not necessarily be a unique, pain-specific cognitive process but a product of relatively stable cognitive schemas (ie, a general cognitive bias) used to interpret and organize experience. Schemas (22) are an internal mental "template" that consists of networks of information regarding the self, forged through early life experiences (eg, trauma) and learning history, and manifested in the form of dysfunctional attitudes and maladaptive beliefs (23). Like pain catastrophizing (17), the characteristic cognitive content of negative self-schema involves (but is not limited to) themes of negative self-evaluation and personal deficiency (18). Functionally, negative self-schemas influence information-processing tasks (expectancies, encoding, interpretation, (24)), which neuroimaging research has characterized as aberrant in patients with IBS (25,26).

Also unknown is the nature of any influence pain catastrophizing has on IBS symptoms. In the only known published study of the topic, Drossman et al. (27) found that catastrophizing measured at baseline predicted long-term illness behaviors (eg, health care utilization, activity limitation). Although these data indicate that catastrophizing affects illness behaviors, they leave unanswered the question of how it relates to core symptoms of IBS, particularly abdominal pain. One hypothesis drawn from Fields’ neurobiological model of pain and depression (28) is that affective distress influences pain by distorting in a negatively skewed manner patients’ appraisal of pain stimuli. Fields’ model suggests that depression increases pain severity by influencing pain-specific cognitive processes such as catastrophizing. That is, catastrophizing mediates the relationship between depression and pain severity. The main goal of the present study was to assess in a large sample of treatment-seeking patients with IBS symptoms the hypothesis that depression and pain severity relate to one another but do so indirectly through their relationship with catastrophizing when clinically relevant control variables (eg, trait anxiety, gender, global IBS symptom severity) were held constant. A secondary goal was to determine whether any contribution of catastrophizing to pain severity was independent of the contribution of a relatively stable tendency toward negative thinking that is not specific to pain stimuli.

	MATERIALS AND METHODS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION ACKNOWLEDGMENTS REFERENCES

 
Subjects
Subjects were 244 consecutively evaluated patients with IBS (males = 48; females = 196) referred to an academic behavioral medical clinic (Buffalo, NY) as part of a National Institutes of Health (NIH) funded multisite study of 2 psychological IBS treatments. Inclusionary criteria required a Rome II IBS diagnosis (29) confirmed by a board-certified gastroenterologist who conducted a medical examination comprising a medical history, a physical examination, and, where appropriate, laboratory tests (negative lactose tolerance test and/or sigmoidoscopy) to exclude organic gastrointestinal (GI) disease. Patients were excluded from participation if they had inflammatory bowel disease (ulcerative colitis, Crohn’s disease or ileitis, or proctitis), lactose malabsorption syndrome, or had a history of current or past psychotic disorders. Subjects were included if they were either not taking IBS medications or their dosage was stabilized for at least 3 months before trial entry. Ethnicity was represented by 95.5% (N = 233) white, whereas 3.7% (N = 9) were minorities and 0.8% (N = 2) did not identify a racial category. The mean age of participants was 47 years (SD = 14). The average duration of GI symptoms was 16 years. Patients were classified on the basis of their predominant bowel habit: 45.1% were mixed, 39.7% diarrhea-predominant, and 15.2% constipation-predominant. The severity of IBS symptoms was assessed by the study gastroenterologist, who rated the overall severity of IBS symptoms as mild, moderate, severe, or very severe (1 = mild, 4 = very severe) in a manner comparable with prior IBS research (9). Three percent were classified as mild, 34% as moderate, 53% as severe, and 10% as very severe. Self-reported comorbid medical problems within 12 months before evaluation were identified with the IASP Comorbid Medical Problem Checklist (30). The most frequently endorsed complaints were hypertension (19%), bladder dysfunction (19%), skin rash (19%), chronic fatigue (23%), arthritis (32%), musculoskeletal pain (43%), and headache (53%).

Procedure
Subjects underwent a brief telephone interview conducted by either the research coordinator or an advanced graduate student. If deemed eligible, subjects were scheduled for psychological and medical assessments. During psychological assessment, patients completed the Coping Strategies Questionnaire, State Trait Anxiety Inventory (STAI), Beck Depression Inventory (BDI), Dysfunctional Attitudes Scale (DAS), and the Short Form-36 Health Survey (SF-36). The testing battery and the experimental procedures of the study were approved by the Health Sciences IRB of the University at Buffalo. Informed consent was obtained from all subjects before participation.

Instruments
Catastrophizing
Catastrophizing was measured using the Catastrophizing subscale of the Coping Strategies Questionnaire (31). The 6 items of the subscale ask patients to rate the frequency with which they, during an episode of pain, engage in various beliefs thought to index catastrophizing (eg,"When I am in pain, I feel I can’t stand it anymore," "it’s awful and I feel it overwhelms me"). Respondents rate how characteristic each item is of them using a 6-point Likert scale ranging from 0 (never do) to 6 (always do).

Pain Severity
The severity of pain experience was measured using the Bodily Pain (BP) subscale of the SF-36 Health Survey (32). The BP subscale is a weighted combination of 2 items measuring (1) the intensity of pain using a 6-point verbal rating scale (1 = none, 6 = very severe) and (2) the effect of pain on normal activities (0 = not at all, 5 = extremely). These items yield an empirically validated (33) composite index of the severity of pain and its effects. Subjects were explicitly instructed to respond to the pain items in light of the intensity and effects of abdominal pain alone. The BP scale is scored so that a higher score indicates no pain/limitations due to pain and lower scores indicate very intense/extremely limiting pain. The BP scale has been used by previous researchers to measure pain severity of patients with IBS (34–37) and other painful medical disorders (38–41). Psychometric studies indicate that SF-36 subscales satisfy rigorous criteria for validity and internal consistency for a variety of medically ill patients, including those with painful GI disease (42). Recent research with pain patients with musculoskeletal indicates that the SF-36 BP scale has psychometric advantages over condition specific pain measures (43), although this pattern of results has not been replicated with patients with IBS.

Depression
Depression was measured using the BDI (44), a 21-item measure that evaluates the presence and severity of depressive symptoms. Items are rated on a 4-point scale of intensity. The BDI is the most widely used self-report measure of depression and has sound psychometric properties (45).

Dysfunctional Attitudes
The DAS (46) is a 40-item self-report measure designed to assess the extent to which an individual endorses general attitudes, beliefs, and underlying assumptions characteristics of a general cognitive bias toward negative thinking. The DAS includes a series of adaptive ("One can get pleasure from an activity regardless of the end result") or maladaptive ("People will think less of me if I make a mistake") attitude statements rated on a 7-point Likert scale, ranging from Totally Agree to Totally Disagree. Scores range from 40 to 280, with higher scores indicating a greater propensity for negative thinking. Lackner et al. (20) found that DAS scores for patients with IBS are elevated relative to normative means.

Trait Anxiety
Trait anxiety was measured using the Trait subscale of the STAI (47). In responding to the 20 items of the T-Anxiety scale, subjects indicate how they generally feel by rating the frequency of their feelings of anxiety on a 4-point scale ranging from 1 (almost never) to 4 (almost always). The trait scale of the STAI has sound psychometric properties (eg, internal consistency, stability, validity) (47).

	RESULTS

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We first examined the zero-order correlations between all the predictors and the criterion measure of pain severity (Table 1). As can be seen, depression was significantly related to DAS, catastrophizing, and pain severity. Catastrophizing was significantly related to pain severity. This pattern of correlations is suggestive of a possibly more complex relationship among the variables and is suggestive that the hypothesized mediation of the relationship between depression and pain by catastrophizing may exist. In order to examine this possible mediation effect, the series of multiple regression analyses suggested by Baron and Kenny (48) for testing mediation were conducted. In these analyses, DAS, age, gender (0 = female; 1 = male), race (0 = minority, 1 = European American), trait anxiety, and global IBS symptom severity were used as covariates because prior research indicates that these variables are either associated with increased risk for IBS (eg, age, gender, trait anxiety) or are theoretically or methodologically relevant (eg, dysfunctional attitudes, IBS symptom severity).

To examine possible mediation by a variable on the relationship between 2 other variables, the indirect effect of the predictor (depression) on the outcome (pain severity) via the mediator (depression) should be tested by using the test devised by Sobel (49). The Sobel test measures the extent to which the mediator carries the influence of an independent variable to dependent variables and distributed as a Z-statistic. A statistically significant effect indicates that the indirect effect of the predictor (depression) on the outcome (pain severity) works through the effects of the mediator (catastrophizing) on the outcome.

Test for Mediation
The first step necessary to identify a mediating variable is to establish a direct effect that may be mediated by an intervening variable. Univariate correlations (Table 1) indicate that there is a relationship between current depression and pain severity. In order to examine whether this relationship holds when control variables were held constant, pain severity was regressed on age, race, gender, IBS symptom severity, trait anxiety, DAS, and depression. In the first regression equation (Equation 1) pain severity was significantly predicted by symptom intensity and depression, R² = 0.15, F(7, 175) = 5.12, p < .001 (Table 2). These variables accounted for 14% of the variance in pain severity, R² = 0.14.

In order to test for the possible mediation of the relationship between depression and pain by catastrophizing, catastrophizing was added as a predictor to Equation 1. When catastrophizing was entered (Equation 3), it was a significant predictor, F(8, 174) = 7.07, p < .001. The beta weight for depression decreased in magnitude to nonsignificance, indicating a possible mediation effect (Table 2). To substantiate the apparent mediation effect, the indirect effect of depression on pain severity was tested using the procedures described by Sobel (49). The results indicated a significant indirect effect, Z = –2.17, p < .05, substantiating the partial mediation of catastrophizing on the relationship between depression and pain severity. The addition of the mediating variable of catastrophizing increased the variance accounted for in pain severity to 21%, R² = 0.21.

	DISCUSSION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION ACKNOWLEDGMENTS REFERENCES

 
The purpose of this study was to test the mediational role of catastrophizing in the link between depression and pain severity in a large sample of patients diagnosed with IBS. Results from a series of regression analyses, as specified by Baron and Kenney (48), indicate that catastrophizing partly mediates the effect between depression and pain. These data indicate that the effects of depression on the experience of pain in severely affected patients with IBS partly work through their beliefs regarding pain (ie, catastrophizing). In other words, catastrophizing accounts for part of the relationship between depression and pain. Patients with IBS who experience higher levels of depression engage in more catastrophic thinking, and partly through this thinking style experience more intense pain and greater activity limitations due to pain (ie, pain severity). Our data challenge traditional single-factor views that IBS pain is strictly a somatic manifestation of an underlying psychiatric condition (50,51) or a product of a relatively stable propensity toward negative thinking. What emerges from our data is a more complex picture whereby the association between depression and pain severity owes its strength in part to patients’ beliefs regarding their pain. While Geisser et al. (19) found that catastrophizing mediates the relationship between depression and the emotional unpleasantness of pain (ie, pain affect) in a sample of patients with persistent painful medical disorders, few (4 of 85) subjects had abdominal pain (none of whom were diagnosed with IBS), limiting the results’ generalizability to patients with IBS. Our findings add to the literature by studying the intensity and effects of abdominal pain in a large sample of patients whose IBS status was confirmed through medical diagnosis. Our data suggest that the mediational role of catastrophizing is not strictly limited to the depression–pain affect relation established by Geisser et al. but underlies the association between depression and pain severity (ie, pain intensity and its effect on function) as well.

At a general level, our data add to a growing list of findings that highlight the importance of cognitive processes in IBS. Previous research indicates that cognitive factors such as patients’ beliefs, expectations, and interpretations influence IBS through 2 major pathways (52). One pathway is directly through biological systems that mediate gut sensation and function (43,44); a second pathway is through the adoption of illness behaviors that can exacerbate IBS symptoms, complicate illness trajectory, obscure symptom profile, and compromise function. The prospective study by Drossman (8) of the influence of patient beliefs on health outcomes speaks to the impact of cognitive process on illness behaviors. Interestingly, there is surprisingly little research linking cognitive processes to the cardinal symptom of IBS: pain. Part of the problem is that IBS research exploring the pain–depression link has been largely based on between-group comparisons of patients with IBS against various reference groups (eg, healthy controls, organic GI patients, non–treatment-seeking patients with IBS) or within-group studies examining prospective changes in depression of patients with IBS undergoing a clinical trial. These 2 lines of research have expanded our understanding of the general psychosocial features of IBS but shed little light on the precise nature of the relationship between psychosocial factors (eg, depression, catastrophizing) and IBS symptoms. More "fine grained" research flushing out the nature of relationships between psychosocial factors and IBS symptoms is urgently needed.

This study adds to the knowledge base of IBS by using relatively advanced regression procedures to investigate the relationship of depression and pain as they relate to catastrophizing. The biomedical research audience has to some extent been leery of "methodological" studies whose findings are driven by statistical procedures and not explicitly gleaned though the experimental manipulation or design per se. We share this skepticism when statistical methods are used to prop up studies with weak theoretical foundations. That said, to the extent that IBS is best conceptualized from a biopsychosocial model (53), understanding the complex interplay of physiological, behavioral, and psychological factors requires sufficiently sophisticated statistical methods capable of disentangling relationships that are multivariate in nature. The pattern of our data would not have been discernible had our data analysis strategy isolated specific relations (depression and pain) using univariate statistical methods used previously (54). A shift from a strict disease model to a biopsychosocial model of IBS calls not only for a conceptual shift in thinking (53) but also a methodological shift in statistical practice to maximize the explanatory power of the biopsychosocial model for IBS. The regression analytic procedures and mediational model used here are particularly appropriate to IBS research because the biopsychosocial model is to our way of thinking an inherently mediational model of illness.

These data should be interpreted in light of a number of study limitations. Because our data are cross sectional and correlational, we do not intend to suggest that the findings demonstrate causal relationships among pain, depression, and catastrophizing. At best, our data can be construed as suggestive of a possible causal relationship that could be confirmed through longitudinal methodology. Although the direct effect between depression and pain decreased significantly when catastrophizing was added to the final regression equation, the magnitude of effect was modest and not necessarily clinically significant. It is possible that a sample of more severely depressed patients with IBS would have yielded more dramatic results. Furthermore, our data reflected a subset of treatment-seeking individuals who were willing to enroll in a randomized controlled trial of 2 psychological treatments. Therefore, our findings may not necessarily generalize to primary care settings or community populations (ie, nonconsulters) representative of the majority of individuals with symptoms compatible with IBS. Although patients were explicitly instructed to respond to the SF-36 Bodily Pain questions based on their abdominal pain alone, it is difficult to know whether any comorbid extraintestinal symptoms (eg, muscle pain (55) figured in patient responding and are reflected in the data. Because we used a composite index of pain severity that integrates self-reported intensity of pain and its effects on functional activities, our results do not necessarily generalize to other important aspects of pain experience (eg, pain affect). It is also unclear whether the pattern of data would have been found using a conventional measure of pain intensity. As noted above, research indicates that for studies of patients with other painful medical disorders (eg, low back pain), the bodily pain measure of the SF-36 is a sufficient pain measure that does not require a condition-specific instrument. Whether this pattern of data applies to patients with IBS is an important research question. Although our findings support the hypothesis that patients’ beliefs partially mediate the link between depression and pain, the data do not rule out the alternative notion that the relationship among study variables might be explained by a higher order biobehavioral process (eg, somatization) whose focus was beyond the scope of the present study.

In spite of its limitations, the study has a number of strengths. To our knowledge, this is the first study of either psychosocial or biological orientation that has formally established cognitive processes as a mediator linking depression to the hallmark feature of IBS (pain). Our data also lend empirical validation to the notion drawn from the biopsychosocial model that the relationship between psychosocial factors and pain is not simply a linear one, as conceptualized by psychogenic models that see somatic symptoms as physical manifestations of an underlying mental disorder. Instead, the effect of psychosocial factors on IBS pain is partly indirect via the mediational role of patients’ pain-related beliefs. The data are also consistent with recent imaging research showing that visceral stimulation of patients with IBS is associated with activation of brain regions that govern cognitive processing (eg, encoding) and modulation of afferent input. In this respect, our findings suggest that cognitive variables such as catastrophizing could enrich imaging research that, with few exceptions, has focused on more distal psychological variables (eg, history of abuse, psychopathology) as they relate to activations in brain function during visceral distension. Our results may provide a clue as to why depression severity has been found to moderate treatment response in a subset of patients with IBS who undergo cognitive behavioral therapy (9). Negative mood associated with severe depression may "short circuit" information processing (56) (ie, increased catastrophic thoughts) in a way that both inhibits CNS down-regulating mechanisms for modulating noxious stimuli and aggravates pain beyond what can be adequately resolved solely through psychological treatments structured around IBS symptoms per se (57). Future prospective research that identifies possible mechanisms by which drug and nondrug therapies control abdominal pain might not only enhance the structure and efficiency of existing treatments but also might advance our understanding of the nature of IBS.

	ACKNOWLEDGMENTS

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Supported in part by a research grant from the NIDDK of the National Institutes of Health (RO1-DK54211).

Received for publication July 28, 2003.

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TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION ACKNOWLEDGMENTS REFERENCES

 

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