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Anxiety sensitivity within the anxiety disorders: Disorder-specific sensitivities and depression comorbidity
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Anxiety sensitivity within the anxiety disorders: Disorder-specific sensitivities and depression comorbidity Neil A. Rectora,b,, Kate Szacun-Shimizua, Michelle Leybmana a
Centre for Addiction and Mental Health, Canada Mood and Anxiety Program, Centre for Addiction and Mental Health, University of Toronto, 250 College Street, Clarke Site, Toronto, Ont., Canada M5T 1R8
b
Received 11 July 2005; received in revised form 31 March 2006; accepted 26 September 2006
Abstract The tendency to perceive anxious states as aversive and harmful is hypothesized to confer vulnerability to the development of anxiety disorders. The most commonly used measure of anxiety sensitivity, the Anxiety Sensitivity Index [ASI; Reiss, S., Peterson, R.A., Gursky, D.M., & McNally R.J. (1986). Anxiety sensitivity, anxiety frequency, and the prediction of fearfulness. Behavior Research and Therapy, 24, 1–8], is composed of multiple lower-order factors, assessing fear of physical symptoms, fear of publicly observable anxious symptoms, and fear of cognitive dyscontrol. This study examined the convergent validity of the lower-order anxiety sensitivity dimensions in DSM-IV diagnosed anxiety disorders. Participants with primary diagnoses of panic disorder with agoraphobia, social phobia, and generalized anxiety disorder (GAD) completed the ASI and measures of anxiety and depression severity. Support was found for the convergent validity of all ASI dimensions in reference to thematically related anxiety disorders and in the identification of patients presenting with and without secondary major depressive disorder (MDD). The ASI-fear of cognitive dyscontrol dimension displayed strong and nonredundant associations with GAD, dimensional depression scores, and secondary diagnoses of MDD. The conceptual implications of the shared importance of fear of cognitive dyscontrol in GAD and MDD are discussed. r 2006 Elsevier Ltd. All rights reserved. Keywords: Anxiety sensitivity; Anxiety disorders; Cognitive; Vulnerability; Co-morbidity
Introduction Anxiety sensitivity refers to the fear of anxiety symptoms as a result of beliefs about their perceived harmful physical, social or psychological consequences (Reiss, 1987; Reiss & McNally, 1985; Reiss, Peterson, Gursky, & McNally, 1986). The initial conceptualization (Reiss & McNally, 1985) and operationalization of the anxiety sensitivity construct with the 16-item Anxiety Sensitivity Index (ASI; Reiss, Peterson, Gursky, & McNally, 1986), promoted a unitary view of vulnerability for the development and maintenance of anxiety and panic. Early studies demonstrated that ASI scores distinguish between Corresponding author. Tel.: +1 416 535 8501; fax: +1 416 979 8653.
E-mail address: [email protected] (N.A. Rector). 0005-7967/$ - see front matter r 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.brat.2006.09.017
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individuals with and without a lifetime history of panic attacks (for review, see Norton, Cox, & Malan, 1992), and between individuals experiencing panic attacks versus those with bona fide panic disorder (Cox, Endler, & Swinson, 1991). Further, patients with panic disorder were found to have higher ASI scores than all other anxiety disorder groups except post-traumatic stress disorder (PTSD) (Taylor, Koch, McNally, & Crockett, 1992). As such, there is considerable empirical support for the importance of anxiety sensitivity in the pathogenesis of panic disorder (for review, see Taylor, 1999). The current research aimed to provide further tests of the role of anxiety sensitivity in anxiety disorders presenting with and without depression comorbidity. The unitary view of anxiety sensitivity was supported by early psychometric examinations of the ASI that found a uni-dimensional factor structure (e.g., Reiss, Peterson, Gursky, & McNally, 1986). Subsequently more extensive examinations of the ASI have resulted in an emerging consensus that the ASI, and the anxiety sensitivity construct, is composed of a unifactorial structure at the higher-order level and a multifactorial structure at the lower-order level. While factorial studies of the 16-item ASI have extracted between two and four second-order factors, the modal solution converges on three (See Taylor, 1999 for review). While there is some variability in the factor names, the three replicable factors reflect: (1) fear of physical symptoms (ASIPhysical), (2) fear of publicly observable anxiety symptoms (ASI-Social) and (3) fear of cognitive dyscontrol (ASI-Cognitive), respectively. To date, there has been only minimal research examining the convergent validity of the lower-order ASI dimensions within patient groups with anxiety disorders. Zinbarg, Brown, and Barlow (1997) demonstrated that patients with DSM-III-R diagnosed panic disorder with/without agoraphobia (PD/A) had comparatively greater score elevations on ASI-Physical compared to patients with generalized anxiety disorder (GAD), social phobia (SP), obsessive-compulsive disorder (OCD), simple phobia and nonaffected controls. Further, ASI-Social scores were highest in the SP group and were also significantly higher than in the PD (but not PD/A), GAD, OCD, simple phobia and nonaffected control groups. No hypotheses were established regarding the possible convergent validity of the ASI-Cognitive scale and no differences were observed between patients with PD/A, GAD, or OCD, although all three groups had higher scores than patients with SP and simple phobia, as well as nonaffected controls. Despite different factor loadings, Blais et al., 2001 obtained similar findings regarding the convergent validity between ASI-Physical scores and PD and between ASI-Social scores and SP, although groups did not differ on the ASI-Cognitive dimension. Rodriguez and colleagues (Rodriguez, Bruce, Pagano, Spencer, & Keller, 2004) employed a series of multiple regression analyses to determine whether DSM-III-R diagnosed anxiety disorders were predictive of the different ASI dimensional scores. The PD/A diagnosis uniquely predicted ASI-Physical scores, the SP diagnosis predicted ASI-Social scores (as did GAD and MDD diagnoses), and the GAD diagnosis predicted ASI-Cognitive scores (as did SP and MDD diagnoses). With respect to the latter, whereas Zinbarg, Brown, and Barlow (1997) found ASI-Cognitive scores to be higher in patients with GAD than SP and simple phobia, Rodriguez, Bruce, Pagano, Spencer, & Keller, 2004 found that ASI-Cognitive scores were most strongly associated with GAD. The cognitive dyscontrol items of the ASI-Cognitive dimension, such as ‘‘When I cannot keep my mind on a task, I worry that I might be going crazy’’ or ‘‘When I am nervous, I worry that I am mentally ill,’’ appear consistent with the commonly reported cognitive appraisals of worry in GAD (Wells, 1997, p.202) and the empirically demonstrated spontaneous automatic thoughts of ‘‘mental catastrophe’’ typical of patients with GAD during anxious arousal (Breitholtz, Westling, & O¨st, 1998). Moreover, the item content of the ASI-Cognitive dimension overlaps considerably with the content of measures assessing anticipated danger associated with perceived uncontrollable cognitive processes, or negative meta-beliefs about worry (Wells, 2005). Negative meta-beliefs about worry have, in turn, been found to discriminate between nonanxious, nonworried-anxious, and GAD participants (80% correct classification) (Davis & Valentiner, 2000) and between high worriers with and without GAD (Ruscio & Borkovec, 2004). Negative meta-beliefs (i.e., perceived uncontrollability) about thought processes have also been found to be associated with depression (Papageorgiou & Wells, 2003). Interestingly, there is an even greater extant literature linking ASI-Cognitive scores to dimensional depression scores in anxious (Schmidt, Lerew, & Joiner, 1998; Taylor, Koch, Woody, & McLean, 1996; Zinbarg, Brown, Barlow, & Rapee, 2001) and depressed (Cox, Enns, Murray, Freeman, & Walker, 2001) clinical samples as well as nonclinical samples
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(Deacon, Abramowitz, Woods, & Tolin, 2003). These findings have led investigators to conclude that fear of mental dyscontrol represents a ‘‘depression-specific form of anxiety sensitivity’’ (Cox, Enns, & Taylor, 2001; Taylor, Koch, Woody, & McLean, 1996). A central problem in establishing the convergent validity of the ASI dimensions in patient participants with anxiety disorders is that approximately 50–55% of patients with a principal anxiety disorder have at least one additional anxiety or depressive disorder at the time of assessment (Brown & Barlow, 1992; Barlow, 2002). This problem may be especially pertinent for the examination of the convergent validity of the ASI-Cognitive dimension since among patients with GAD, approximately 65% present with comorbid conditions, with the most common additional diagnoses being SP (22%) and major depression (20%) (Barlow, 2002, p. 310). An alternative approach would include the examination of the ASI dimensions in clinical samples based on the patient’s principal diagnosis, irrespective of the presence of secondary diagnoses, while also controlling for general depression and anxiety severity. Given the strong association between ASI-Cognitive scores and depression, this approach would offer an especially rigorous test of whether ASI-Cognitive scores are associated with GAD while controlling for the shared variance with depression severity. Moreover, it would be of special significance if ASI-Cognitive scores were found to be associated with GAD and MDD given that ASI-Cognitive items do not overlap with any of the diagnostic criterion of these disorders (APA, 2000). It was hypothesized that the ASI dimensions would be associated with thematically related anxiety disorders: ASI-Physical would be higher in patients with PD/A compared to other disorders, ASI-Social would be higher in patients with SP than in the other disorders, and ASI-Cognitive would be higher in patients with GAD than in the other anxiety disorders, when controlling for nonspecific symptoms of depression and anxiety severity. It was also hypothesized that ASI-Cognitive would be uniquely associated with depression severity scores and distinguish patients with and without secondary major depressive disorder. Method Participants and procedure One hundred and twenty six (N ¼ 126) participants meeting DSM-IV-TR (APA, 2000) criteria for primary panic disorder with agoraphobia (PDA) (n ¼ 48), SP (n ¼ 50), and GAD (n ¼ 28) based on the Structured Clinical Interview for Axis 1 Disorders (SCID-1/P version 2.0) were recruited for the present study. Participants were continuous referrals to a large anxiety disorders specialty clinic. Participant mean age was 35.41 years (SD ¼ 9.78), 56% were female, and the majority had at least some university education (73.8%). Further, the sample was predominately Caucasian (88.6%), single (58.7%) with a modal family income between $20,000–$39,999. There were no significant differences between diagnostic groups on any of the demographic variables (p’sX.12). For participants on psychotropic medications (65.6%), all were on stable medications, as defined by no change in medication type or dose during 6 weeks prior to assessment. There were equivalent rates of medication use between patient groups. All participants provided informed consent. The SCID-I interviews were administered by research staff whom had received extensive formal training in the administration and scoring of the interview protocol with anxiety disordered patient populations, and who had completed a rigorous inter-rater reliability training program prior to administration. Additionally, the SCID-I assessors attended weekly clinical case conference meetings with senior psychologists who specialize in the assessment and treatment of anxiety disorders, to establish consensus principal and secondary psychiatric diagnoses. A diagnosis was considered a principal diagnosis if it was the patient’s primary source of distress and if it was the disorder for which they were seeking treatment.1 1 A formal aspect of the SCID-I clinical ratings is the application of a clinical severity rating from 0 ‘absent’ to 8 ‘very severe’ for all disorders diagnosed. Ordinarily, the diagnosis with the highest clinical severity rating would be the patient’s principal diagnosis. However, the SCID-I allows for the presence of co-principal diagnoses (i.e., two disorders with equal severity ratings). For this reason, our assessment interview includes the administration of the SCID-I as well as a semi-structured clinical interview to determine the patient’s sole principal diagnosis for treatment planning purposes (Rector & Cox, 1999). In the current study, the principal diagnosis was assigned a higher or equivalent clinical severity rating to the secondary disorder(s) in every case but two. A principal diagnosis was assigned to the disorder with a lower clinical severity rating in these cases based on the determination of treatment needs.
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For the PDA group, the following comorbid diagnoses were established: SP (14.6%), GAD (10.4%), specific phobia (14.6%), OCD (4.2%), other mood disorder NOS (2.1%), and substance abuse/dependence (2.1%). In the SP group, the following secondary diagnoses were observed: GAD (10.0%), specific phobia (8.0%), OCD (4.0%), PD/A (4%), dysthymic disorder (6.0%), bipolar disorder (2.0%), somatoform disorder (2.0%), eating disorder (2.0%), and substance abuse/dependence (2.0%). Finally, in the GAD group, the diagnostic comorbidities included: PD/A (10.7%), SP (35.7%), specific phobia (7.1%), and PTSD (3.6%). 8.3% of the PDA group, 20% of the SP group, and 42.9% of the GAD group were in the midst of a depressive episode at the time of assessment. Measures Anxiety Sensitivity Index (ASI) The ASI (Reiss, Peterson, Gursky, & McNally, 1986) consists of 16 items scored from 0 to 4, measuring fear of negative consequences of anxiety. The scale was constructed in order to measure individual differences in anxiety sensitivity. It has been demonstrated to have adequate reliability and validity (Reiss, Peterson, Gursky, & McNally, 1986; for review, see Peterson & Plehn, 1999). The coefficient a for the ASI scale in the current study was .85. Beck Depression Inventory (BDI-II) The BDI-II is a 21-item measure that assesses the severity of depressive symptoms (Beck & Steer, 1987). Respondents are asked to choose one of four statements for each of the 21 items, on a 0–3 scale, which best describes how they have been feeling in the past 2 weeks. There is considerable validity and reliability data on this measure across various populations (for review, see Beck, Steer, & Garbin, 1988). Beck Anxiety Inventory (BAI) The BAI is a 21-item self-report measure of anxiety symptoms (Beck & Steer 1990). Respondents are asked to report how much they have been bothered by several symptoms in the previous week on a four-point scale ranging from ‘not at all’ to ‘severely.’ Internal consistency estimates have been found to be .92 in general psychiatric samples (Beck, Epstein, Brown, & Steer, 1988) and .85 to .93 in anxiety disorder patients (Beck & Steer, 1993). Results Principal components analysis of the ASI The ASI was examined using principal components analysis with oblimin rotation. Using scree plot analysis plus eigenvalueX1 and factor varianceX5% criteria, all concurred on a three-component solution accounted for 55.6% of the variance: fear of physical symptoms (ASI-Physical: eigenvalue ¼ 5.20, variance ¼ 32.5%), fear of cognitive dyscontrol (ASI-Cognitive: eigenvalue ¼ 2.42, Variance ¼ 15.1%), and fear of publicly observable anxious symptoms (ASI-Social: eigenvalue ¼ 1.28, Variance ¼ 8.0%).2 The extracted components replicate those previously reported in anxious samples by Zinbarg, Brown, and Barlow (1997) and Rodriguez, Bruce, Pagano, Spencer, & Keller (2004) with nearly identical loadings except that item #3, ‘‘It scares me when I feel ‘shaky’ (trembling)’’ double-loaded on the ASI-Physical and ASI-Cognitive components in our study whereas in Rodriguez, Bruce, Pagano, Spencer, & Keller, 2004 study, this item double-loaded on the ASI-Physical and ASI-Social components. Using the regression method, dimension scores were calculated for the ASI dimensions. 2
Principal axis factor with Oblimin rotation resulted in an identical three-factor solution accounting for 55.59% of the variance, with identical factor loadings with the exception that ASI item #7 loaded on the ASI-Social dimension at .12 whereas it previously loaded at .40.
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0.6
PDA SP GAD
0.4 ASI Factor Scores
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0.2 0 -0.2 -0.4 -0.6 ASI-Physical
ASI-Social ASI Dimensions
ASI-Cognitive
Fig. 1. ASI dimension scores for diagnostic groups.
Comparison of ASI dimensional scores between diagnostic groups The ASI dimension scores were compared between the diagnostic groups using a repeated measures multivariate analysis of variance (MANOVA). The between-subject factor was diagnostic group (PDA, SP, and GAD) and the within-group factor was ASI scores (ASI-Physical, ASI-Social, and ASI-Cognitive), and BAI and BDI-II scores served as the covariates. Neither the ASI scores by BAI nor the ASI scores by BDI-II multivariate effects were significant. However, an ASI scores by diagnostic group two-way multivariate interaction was observed, Wilks’ l ¼ .69, F(4,242) ¼ 12.31, po.001.3 Three separate ANOVA’s with post-hoc comparisons (LSD) were computed for each of the three ASI dimensions, while retaining BAI and BDI-II scores as covariates. To correct for potential Type I error, a Bonferroni correction was applied for the determination of significance for the univariate analyses (a ¼ .05/3 tests ¼ .02). The results of the between-group comparisons can be seen in Fig. 1. There was a significant main effect for diagnostic group on the ASI-Physical score, F(4,126) ¼ 15.29, pp.001). Post-hoc comparisons revealed that patients with PDA scored significantly higher than patients with SP (mean difference ¼ .95, pp.001, d ¼ 1.33) and GAD (mean difference ¼ .73, pp.001, d ¼ .78). A significant main effect for diagnostic group was also observed for ASI-Social scores, F(4,126) ¼ 5.20, pp.007. Post-hoc comparisons revealed that patients with SP had significantly higher scores than patients with PDA (mean difference ¼ .56, pp.006, d ¼ .38) and GAD (mean difference ¼ .61, pp.008, d ¼ .40). Finally, a significant main effect was observed for ASI-Cognitive scores, F(4,126) ¼ 5.21, pp.007. Patients with GAD scored significantly higher than patients with SP (mean difference ¼ .62, pp.003, d ¼ .92) but not PDA (mean difference ¼ .19, pX.35, d ¼ .34).4,5 3 To determine whether medication use could have differentially affected the ASI scores across diagnostic groups, we conducted a repeated measures MANOVA with medication use (dummy coded ‘1’ for present and ‘2’ for absent) and diagnostic group as the betweengroup variables and ASI scores as the repeated measure. The ASI scores by medication use multivariate effect was not significant, Wilks’ l ¼ .99, F(2,118) ¼ .85, p ¼ .43 nor was the ASI by medication use by diagnostic group multivariate effect, Wilks’ l ¼ .98, F(4,236) ¼ .62, p ¼ .65. 4 The analyses were repeated again with the cross-loading ASI item #3 removed and the results remained unchanged, with the PDA and GAD groups remaining equivalent. 5 Because diagnostic groups were found to differ on the BAI, F(2,126) ¼ 5.76, po.005, these analyses were repeated without BAI as a covariate. All results remained as before although the multivariate effect for ASI-Social scores was reduced to a strong trend, F(2,126) ¼ 2.94, p ¼ .057. However, the multiple contrasts demonstrated that the SP group still scored significantly higher on the ASISocial dimension than the PDA (mean difference ¼ .38, pp.05) and GAD (mean difference ¼ .50, pp.05) groups.
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Association between ASI dimensions, anxiety severity and depression severity To test the hypothesis that ASI-Cognitive scores would be more strongly associated with dimensional depression scores than either ASI-Physical or ASI-Social scores, zero-order Pearson correlations were computed between the ASI factor scores and measures of anxiety and depression. The ASI-Physical (r ¼ .38, pp.01), ASI-Social (r ¼ .25, pp.05), and ASI-Cognitive (r ¼ .46, pp.01) scores were all positively and significantly associated with BAI total scores. Whereas the ASI-Physical scores were not significantly associated with BDI-II scores (r ¼ .15 ns), both the ASI-Social (r ¼ .18, pp.05) and ASI-Cognitive (r ¼ .42, pp.01) scores were positively and significantly correlated with BDI-II scores. To determine whether the magnitude of the correlations differed, Fisher’s r-to-z transformations were computed following the steps outlined by Meng, Rosenthal and Rubin (1992). The results indicated that the correlation between ASI-Cognitive and BDI-II scores was greater than the correlation between the ASI-Physical and BDI-II scores (z ¼ 2.34, pp.01) and the ASI-Social and BDI-II scores (z ¼ 2.32, pp.01).
ASI dimensional scores between patients with and without secondary major depression To test whether the ASI dimensions differed between patients with and without secondary major depression, a repeated measures MANOVA was conducted with one between-group factor, secondary depression (dummy coded for present or absent), and ASI dimensions as the within-subject factor. The results indicated a two-way multivariate interaction, Wilks’ l ¼ .82, F(2,123) ¼ 9.03, po.001 between ASI dimensions and secondary depression status. Three separate ANOVA’s were conducted for each of the ASI dimensions with secondary major depression status as the between-group variable. Again, a Bonferroni correction was applied for the determination of significance for the univariate analyses (a ¼ .05/3, tests ¼ .02). The results can be seen in Fig. 2. No significant differences were noted for ASI-Physical scores, F(1,125) ¼ 4.15, p4.05, d ¼ .43 and no between-group differences were observed for ASI-Social scores, F(1,125) ¼ .23, p4.60, d ¼ .09. However, a main effect for ASI-Cognitive scores was observed, F(1,125) ¼ 8.65, pp.01, d ¼ .65 with patients with comorbid MDD (M ¼ .49, SD ¼ .98) scoring higher than patients without secondary MDD (M ¼ .13, SD ¼ 0.97).
0.5 0.4
No Comorbid MDD Comorbid MDD
ASI Factor Scores
0.3 0.2 0.1 0 -0.1 -0.2 -0.3 -0.4 ASI-Physical
ASI-Social ASI-Cognitive ASI Dimensions
Fig. 2. ASI dimension scores by secondary MDD status.
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Discussion This study aimed to examine the convergent validity of the ASI dimensions in patients with DSM-IV anxiety disorders. Consistent with past research (Blais et al., 2001; Rodriguez, Bruce, Pagano, Spencer, & Keller, 2004; Zinbarg, Brown, and Barlow (1997)), ASI-Physical scores were found to be most strongly associated with PD/A, whereas ASI-Social scores were most strongly associated with SP. Patients with GAD scored highest on the ASI-Cognitive dimension. While the GAD group had a mean ASI-Cognitive score that was nearly twice that of the PDA group, these differences did not reach conventional levels of statistical significance. These results replicate the findings reported by Zinbarg, Brown, and Barlow (1997) that also observed non-significant differences between PD/A and GAD diagnostic groups on the ASI-Cognitive dimension. One possible explanation is that ASI-Cognitive scores are associated with PDA to the extent that patients present with cognitive symptoms of panic, such as fears of ‘‘going crazy’’ and ‘‘losing control,’’ a previously demonstrated subgroup of panic patients (Cox, Swinson, Endler, & Norton, 1994). Consistent with past research in clinical samples with primary anxiety disorders (Schmidt et al., 1998; Taylor, Koch, Woody, & McLean, 1996; Zinbarg, Brown, Barlow, & Rapee, 2001), the ASI-Cognitive scores were associated with dimensional depression scores (BDI-II) to a greater extent than were the ASI-Physical and ASI-Social dimensions. Moreover, ASI-Cognitive scores discriminated anxious patient groups with and without secondary MDD. While previous research demonstrated the convergent validity of the ASI-Cognitive dimension in relation to PD/A patients with and without comorbid depression (Taylor, Koch, Woody, & McLean, 1996), our results extend this pattern to patients with and without secondary MDD across PDA, GAD, and SP groups. The results from this study suggest that the ASI-Cognitive dimension is strongly associated with GAD and depression (both dimensional depression scores and a bona fide MDD diagnosis). One possible explanation for these associations is that ASI-Cognitive scores are associated with both GAD and MDD because patients fear symptoms that are similar to both disorders such as difficulties concentrating, sleep disturbance, restlessness, and fatigue (APA, 2000). A second possibility is that fear of cognitive dyscontrol is related to the diagnoses of GAD and MDD to the extent that it is associated with the cognitive processes that are characteristic of the disorders. The hallmark feature of GAD is the presence of excessive and uncontrollable worry (APA, 2000, p.472). Borkovec (1994) has defined worry as ‘‘a predominately verbal-linguistic attempt to avoid future aversive events’’ (Borkovec, 1994, p.7). While characteristic of GAD, worry is common to many psychiatric conditions, including depression (Chelminski & Zimmerman, 2003). Further, repetitive or ruminative thinking in depression has been hypothesized to confer vulnerability to the experience of more severe and protracted episodes of major depressive disorder (Nolen-Hoeksema, 1991). While worry (Borkovec, Ray, & Stober, 1998) and rumination (Nolen-Hoeksema, 1991) have emerged as distinct cognitive constructs to assess recurrent negative thinking in GAD and depression, respectively, more recent research has suggested that these cognitive processes represent manifest variables as part of a latent variable titled repetitive thought, the latter showing equivalent associations with anxiety and depression measures (Sergerstrom, Tsao, Alden, & Craske, 2000). Preliminary research demonstrates an association between ASICognitive scores and cognitive rumination in clinically depressed patients (Cox, Enns, & Taylor, 2001). Finally, a third possible explanation for the overlapping role of fears of cognitive dyscontrol in GAD and MDD is that the ASI-Cognitive items tap meta-cognitive constructs that are specific to GAD and MDD. Wells and Matthews (1994) have theorized that the cognitive processes of worry in GAD and rumination in MDD are driven by meta-cognitive beliefs pertaining to the perception that repetitive thought is uncontrollable and dangerous, tantamount to mental catastrophe (Wells, 2005). Items of the ASI-Cognitive component, such as ‘‘When I cannot keep my mind on a task, I worry that I might be going crazy’’ appear to similarly tap anticipated danger associated with perceived uncontrollable cognitive processes. Despite the potential overlap between the ASI-fear of cognitive dyscontrol component and previously operationalized meta-cognitive variables, we are unaware of any published study that has examined the convergent and divergent validity of these constructs and so additional research is required. The cross-sectional design of the current study does not allow for the determination of whether say ASI-Social scores represent vulnerability for the development of SP, or alternatively, whether the onset of clinical SP leads to the exacerbation of ASI-Social concerns. The directionality issue becomes even more
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salient when considering that the ASI-Cognitive dimension has been explicitly conceptualized as both a preexisting vulnerability to and a psychological ‘scar’ resulting from depressive states (e.g., Cox, Enns, & Taylor, 2001). Prospective examination with the ASI-Cognitive dimension in relation to related disorders would help address the directionality question as would the determination of whether ASI-Cognitive can predict depressive relapse (and periods of exacerbation in GAD). Further, treatment studies are needed to establish whether ASI-Cognitive scores can be significantly reduced in psychological interventions for depression and GAD and the extent to which these reductions mediate successful treatment outcomes. Finally, significant advancements in the psychometric refinement of the ASI scale have been made, including expansion of the number of items that comprise the ASI-Cognitive dimension (Taylor & Cox, 1998). For instance, the Anxiety Sensitivity Profile (ASP; Taylor & Cox, 1998) added more items to the fear of cognitive dyscontrol factor, so that it assessed a greater breadth of cognitive symptoms (e.g., derealization, depersonalization, etc.). While one study examined the original ASI-Cognitive factor with the new expanded content of the ASP-Cognitive Dyscontrol and found the latter to offer no increase in predictive validity than the ASI factor in relation to depressive symptoms (Cox, Taylor & Enns, 1999), future research may focus on the discriminant validity of more broadly operationalized anxiety sensitivity constructs within the anxiety disorder spectrum. Acknowledgments The authors would like to thank Drs. Nancy Kocovski and Marla Engelberg for their comments on an earlier draft of this manuscript.
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Davis, R. N., & Valentiner, D. P. (2000). Does meta-cognitive theory enhance our understanding of pathological worry of anxiety? Personality and Individual Differences, 29, 513–526. Deacon, B. J., Abramowitz, J. S., Woods, C. M., & Tolin, D. F. (2003). The Anxiety Sensitivity Index-revised: Psychometric properties and factor structure in two nonclinical samples. Behavior Research and Therapy, 41, 1427–1449. Meng, X. L., Rosenthal, R., & Rubin, D. B. (1992). Comparing correlated correlation coefficients. Psychological Bulletin, 111, 172–175. Nolen-Hoeksema, S. (1991). Response to depression and their effects on the duration of depressive episodes. Journal of Abnormal Psychology, 100, 569–582. Norton, G. R., Cox, B. J., & Malan, J. (1992). Nonclinical panicers: A critical review. Clinical Psychology Review, 12, 121–139. Papageorgiou, C., & Wells, A. (2003). An empirical test of a clinical metacognitive model of rumination and depression. Cognitive Therapy and Research, 27, 261–273. Peterson, R. A., & Plehn, K. (1999). Measuring anxiety sensitivity. In S. Taylor (Ed.), Anxiety sensitivity: Theory, research, and treatment of the fear of anxiety (pp. 61–81). Mahwah, NJ: Lawrence Erlbaum Associates. Rector, N. A., & Cox, B. C. (1999). Patient suitability for cognitive behaviour therapy for anxiety disorders. Presented at the annual meeting of the association for the advancement of behaviour therapy, Toronto, Canada. Reiss, S. (1987). Theoretical perspectives on the fear of anxiety. Clinical Psychology Review, 7, 585–596. Reiss, S., & McNally, R. J. (1985). The expectancy model of fear. In S. Reiss, & R. R. Bootzin (Eds.), Theoretical issues in behavior therapy (pp. 107–121). New York: Academic Press. Reiss, S., Peterson, R. A., Gursky, D. M., & McNally, R. J. (1986). Anxiety sensitivity, anxiety frequency, and the prediction of fearfulness. Behavior Research and Therapy, 24, 1–8. Rodriguez, B. F., Bruce, S. E., Pagano, M. E., Spencer, M. A., & Keller, M. B. (2004). Factor structure and stability of the anxiety sensitivity index in a longitudinal study of anxiety disorder patients. Behavior Research and Therapy, 42, 79–91. Ruscio, A. M., & Borkovec, T. D. (2004). Experience and appraisal of worry among high worriers with and without generalized anxiety disorder. Behavior Research and Therapy, 42, 1469–1482. Schmidt, N. B., Lerew, D. R., & Joiner, T. E. (1998). Anxiety sensitivity and the pathogenesis of anxiety and depression: Evidence for symptom specificity. Behavior Research and Therapy, 36, 165–177. Sergerstrom, S. C., Tsao, J. C. I., Alden, L. E., & Craske, M. G. (2000). Worry and rumination: Repetitive thoughts as a concomitant and predictor of negative mood. Cognitive Therapy and Research, 24, 671–688. Taylor, S. (1999). Anxiety sensitivity: Theory, research, and treatment of the fear of anxiety. The LEA series in personality and clinical psychology. Mahwah, NJ, USA: Lawrence Erlbaum Associates, Publishers. Taylor, S., & Cox, B. J. (1998). An expanded anxiety sensitivity index: Evidence for a hierarchic structure in a clinical sample. Journal of Anxiety Disorders, 12, 463–483. Taylor, S., Koch, W. J., McNally, R. J., & Crockett, D. J. (1992). Conceptualizations of anxiety sensitivity. Psychological Assessment, 4, 245–250. Taylor, S., Koch, W. J., Woody, S., & McLean, P. (1996). Anxiety sensitivity and depression: How are they related? Journal of Abnormal Psychology, 105, 474–479. Wells, A. (1997). Cognitive therapy of anxiety disorders: A practice manual and conceptual guide. New York: Wiley. Wells, A. (2005). The metacognitive model of GAD: Assessment of meta-worry and relationship with DSM-IV generalized anxiety disorder. Cognitive Therapy and Research, 29, 107–121. Wells, A., & Matthews, G. (1994). Self-consciousness and cognitive failures as predictors of coping in stressful episodes. Cognition and Emotion, 8, 279–295. Zinbarg, R. E., Barlow, D. H., & Brown, T. A. (1997). Hierarchical structure and general factor saturation of the Anxiety Sensitivity Index: Evidence and implications. Psychological Assessment, 9, 277–284. Zinbarg, R. E., Brown, T. A., Barlow, D. H., & Rapee, R. M. (2001). Anxiety sensitivity, panic, and depressed mood: A reanalysis teasing apart the contributions of the two levels in the hierarchical structure of the anxiety sensitivity index. Journal of Abnormal Psychology, 110, 372–377.
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Shorter communication
Anxiety sensitivity within the anxiety disorders: Disorder-specific sensitivities and depression comorbidity Neil A. Rectora,b,, Kate Szacun-Shimizua, Michelle Leybmana a
Centre for Addiction and Mental Health, Canada Mood and Anxiety Program, Centre for Addiction and Mental Health, University of Toronto, 250 College Street, Clarke Site, Toronto, Ont., Canada M5T 1R8
b
Received 11 July 2005; received in revised form 31 March 2006; accepted 26 September 2006
Abstract The tendency to perceive anxious states as aversive and harmful is hypothesized to confer vulnerability to the development of anxiety disorders. The most commonly used measure of anxiety sensitivity, the Anxiety Sensitivity Index [ASI; Reiss, S., Peterson, R.A., Gursky, D.M., & McNally R.J. (1986). Anxiety sensitivity, anxiety frequency, and the prediction of fearfulness. Behavior Research and Therapy, 24, 1–8], is composed of multiple lower-order factors, assessing fear of physical symptoms, fear of publicly observable anxious symptoms, and fear of cognitive dyscontrol. This study examined the convergent validity of the lower-order anxiety sensitivity dimensions in DSM-IV diagnosed anxiety disorders. Participants with primary diagnoses of panic disorder with agoraphobia, social phobia, and generalized anxiety disorder (GAD) completed the ASI and measures of anxiety and depression severity. Support was found for the convergent validity of all ASI dimensions in reference to thematically related anxiety disorders and in the identification of patients presenting with and without secondary major depressive disorder (MDD). The ASI-fear of cognitive dyscontrol dimension displayed strong and nonredundant associations with GAD, dimensional depression scores, and secondary diagnoses of MDD. The conceptual implications of the shared importance of fear of cognitive dyscontrol in GAD and MDD are discussed. r 2006 Elsevier Ltd. All rights reserved. Keywords: Anxiety sensitivity; Anxiety disorders; Cognitive; Vulnerability; Co-morbidity
Introduction Anxiety sensitivity refers to the fear of anxiety symptoms as a result of beliefs about their perceived harmful physical, social or psychological consequences (Reiss, 1987; Reiss & McNally, 1985; Reiss, Peterson, Gursky, & McNally, 1986). The initial conceptualization (Reiss & McNally, 1985) and operationalization of the anxiety sensitivity construct with the 16-item Anxiety Sensitivity Index (ASI; Reiss, Peterson, Gursky, & McNally, 1986), promoted a unitary view of vulnerability for the development and maintenance of anxiety and panic. Early studies demonstrated that ASI scores distinguish between Corresponding author. Tel.: +1 416 535 8501; fax: +1 416 979 8653.
E-mail address: [email protected] (N.A. Rector). 0005-7967/$ - see front matter r 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.brat.2006.09.017
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individuals with and without a lifetime history of panic attacks (for review, see Norton, Cox, & Malan, 1992), and between individuals experiencing panic attacks versus those with bona fide panic disorder (Cox, Endler, & Swinson, 1991). Further, patients with panic disorder were found to have higher ASI scores than all other anxiety disorder groups except post-traumatic stress disorder (PTSD) (Taylor, Koch, McNally, & Crockett, 1992). As such, there is considerable empirical support for the importance of anxiety sensitivity in the pathogenesis of panic disorder (for review, see Taylor, 1999). The current research aimed to provide further tests of the role of anxiety sensitivity in anxiety disorders presenting with and without depression comorbidity. The unitary view of anxiety sensitivity was supported by early psychometric examinations of the ASI that found a uni-dimensional factor structure (e.g., Reiss, Peterson, Gursky, & McNally, 1986). Subsequently more extensive examinations of the ASI have resulted in an emerging consensus that the ASI, and the anxiety sensitivity construct, is composed of a unifactorial structure at the higher-order level and a multifactorial structure at the lower-order level. While factorial studies of the 16-item ASI have extracted between two and four second-order factors, the modal solution converges on three (See Taylor, 1999 for review). While there is some variability in the factor names, the three replicable factors reflect: (1) fear of physical symptoms (ASIPhysical), (2) fear of publicly observable anxiety symptoms (ASI-Social) and (3) fear of cognitive dyscontrol (ASI-Cognitive), respectively. To date, there has been only minimal research examining the convergent validity of the lower-order ASI dimensions within patient groups with anxiety disorders. Zinbarg, Brown, and Barlow (1997) demonstrated that patients with DSM-III-R diagnosed panic disorder with/without agoraphobia (PD/A) had comparatively greater score elevations on ASI-Physical compared to patients with generalized anxiety disorder (GAD), social phobia (SP), obsessive-compulsive disorder (OCD), simple phobia and nonaffected controls. Further, ASI-Social scores were highest in the SP group and were also significantly higher than in the PD (but not PD/A), GAD, OCD, simple phobia and nonaffected control groups. No hypotheses were established regarding the possible convergent validity of the ASI-Cognitive scale and no differences were observed between patients with PD/A, GAD, or OCD, although all three groups had higher scores than patients with SP and simple phobia, as well as nonaffected controls. Despite different factor loadings, Blais et al., 2001 obtained similar findings regarding the convergent validity between ASI-Physical scores and PD and between ASI-Social scores and SP, although groups did not differ on the ASI-Cognitive dimension. Rodriguez and colleagues (Rodriguez, Bruce, Pagano, Spencer, & Keller, 2004) employed a series of multiple regression analyses to determine whether DSM-III-R diagnosed anxiety disorders were predictive of the different ASI dimensional scores. The PD/A diagnosis uniquely predicted ASI-Physical scores, the SP diagnosis predicted ASI-Social scores (as did GAD and MDD diagnoses), and the GAD diagnosis predicted ASI-Cognitive scores (as did SP and MDD diagnoses). With respect to the latter, whereas Zinbarg, Brown, and Barlow (1997) found ASI-Cognitive scores to be higher in patients with GAD than SP and simple phobia, Rodriguez, Bruce, Pagano, Spencer, & Keller, 2004 found that ASI-Cognitive scores were most strongly associated with GAD. The cognitive dyscontrol items of the ASI-Cognitive dimension, such as ‘‘When I cannot keep my mind on a task, I worry that I might be going crazy’’ or ‘‘When I am nervous, I worry that I am mentally ill,’’ appear consistent with the commonly reported cognitive appraisals of worry in GAD (Wells, 1997, p.202) and the empirically demonstrated spontaneous automatic thoughts of ‘‘mental catastrophe’’ typical of patients with GAD during anxious arousal (Breitholtz, Westling, & O¨st, 1998). Moreover, the item content of the ASI-Cognitive dimension overlaps considerably with the content of measures assessing anticipated danger associated with perceived uncontrollable cognitive processes, or negative meta-beliefs about worry (Wells, 2005). Negative meta-beliefs about worry have, in turn, been found to discriminate between nonanxious, nonworried-anxious, and GAD participants (80% correct classification) (Davis & Valentiner, 2000) and between high worriers with and without GAD (Ruscio & Borkovec, 2004). Negative meta-beliefs (i.e., perceived uncontrollability) about thought processes have also been found to be associated with depression (Papageorgiou & Wells, 2003). Interestingly, there is an even greater extant literature linking ASI-Cognitive scores to dimensional depression scores in anxious (Schmidt, Lerew, & Joiner, 1998; Taylor, Koch, Woody, & McLean, 1996; Zinbarg, Brown, Barlow, & Rapee, 2001) and depressed (Cox, Enns, Murray, Freeman, & Walker, 2001) clinical samples as well as nonclinical samples
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(Deacon, Abramowitz, Woods, & Tolin, 2003). These findings have led investigators to conclude that fear of mental dyscontrol represents a ‘‘depression-specific form of anxiety sensitivity’’ (Cox, Enns, & Taylor, 2001; Taylor, Koch, Woody, & McLean, 1996). A central problem in establishing the convergent validity of the ASI dimensions in patient participants with anxiety disorders is that approximately 50–55% of patients with a principal anxiety disorder have at least one additional anxiety or depressive disorder at the time of assessment (Brown & Barlow, 1992; Barlow, 2002). This problem may be especially pertinent for the examination of the convergent validity of the ASI-Cognitive dimension since among patients with GAD, approximately 65% present with comorbid conditions, with the most common additional diagnoses being SP (22%) and major depression (20%) (Barlow, 2002, p. 310). An alternative approach would include the examination of the ASI dimensions in clinical samples based on the patient’s principal diagnosis, irrespective of the presence of secondary diagnoses, while also controlling for general depression and anxiety severity. Given the strong association between ASI-Cognitive scores and depression, this approach would offer an especially rigorous test of whether ASI-Cognitive scores are associated with GAD while controlling for the shared variance with depression severity. Moreover, it would be of special significance if ASI-Cognitive scores were found to be associated with GAD and MDD given that ASI-Cognitive items do not overlap with any of the diagnostic criterion of these disorders (APA, 2000). It was hypothesized that the ASI dimensions would be associated with thematically related anxiety disorders: ASI-Physical would be higher in patients with PD/A compared to other disorders, ASI-Social would be higher in patients with SP than in the other disorders, and ASI-Cognitive would be higher in patients with GAD than in the other anxiety disorders, when controlling for nonspecific symptoms of depression and anxiety severity. It was also hypothesized that ASI-Cognitive would be uniquely associated with depression severity scores and distinguish patients with and without secondary major depressive disorder. Method Participants and procedure One hundred and twenty six (N ¼ 126) participants meeting DSM-IV-TR (APA, 2000) criteria for primary panic disorder with agoraphobia (PDA) (n ¼ 48), SP (n ¼ 50), and GAD (n ¼ 28) based on the Structured Clinical Interview for Axis 1 Disorders (SCID-1/P version 2.0) were recruited for the present study. Participants were continuous referrals to a large anxiety disorders specialty clinic. Participant mean age was 35.41 years (SD ¼ 9.78), 56% were female, and the majority had at least some university education (73.8%). Further, the sample was predominately Caucasian (88.6%), single (58.7%) with a modal family income between $20,000–$39,999. There were no significant differences between diagnostic groups on any of the demographic variables (p’sX.12). For participants on psychotropic medications (65.6%), all were on stable medications, as defined by no change in medication type or dose during 6 weeks prior to assessment. There were equivalent rates of medication use between patient groups. All participants provided informed consent. The SCID-I interviews were administered by research staff whom had received extensive formal training in the administration and scoring of the interview protocol with anxiety disordered patient populations, and who had completed a rigorous inter-rater reliability training program prior to administration. Additionally, the SCID-I assessors attended weekly clinical case conference meetings with senior psychologists who specialize in the assessment and treatment of anxiety disorders, to establish consensus principal and secondary psychiatric diagnoses. A diagnosis was considered a principal diagnosis if it was the patient’s primary source of distress and if it was the disorder for which they were seeking treatment.1 1 A formal aspect of the SCID-I clinical ratings is the application of a clinical severity rating from 0 ‘absent’ to 8 ‘very severe’ for all disorders diagnosed. Ordinarily, the diagnosis with the highest clinical severity rating would be the patient’s principal diagnosis. However, the SCID-I allows for the presence of co-principal diagnoses (i.e., two disorders with equal severity ratings). For this reason, our assessment interview includes the administration of the SCID-I as well as a semi-structured clinical interview to determine the patient’s sole principal diagnosis for treatment planning purposes (Rector & Cox, 1999). In the current study, the principal diagnosis was assigned a higher or equivalent clinical severity rating to the secondary disorder(s) in every case but two. A principal diagnosis was assigned to the disorder with a lower clinical severity rating in these cases based on the determination of treatment needs.
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For the PDA group, the following comorbid diagnoses were established: SP (14.6%), GAD (10.4%), specific phobia (14.6%), OCD (4.2%), other mood disorder NOS (2.1%), and substance abuse/dependence (2.1%). In the SP group, the following secondary diagnoses were observed: GAD (10.0%), specific phobia (8.0%), OCD (4.0%), PD/A (4%), dysthymic disorder (6.0%), bipolar disorder (2.0%), somatoform disorder (2.0%), eating disorder (2.0%), and substance abuse/dependence (2.0%). Finally, in the GAD group, the diagnostic comorbidities included: PD/A (10.7%), SP (35.7%), specific phobia (7.1%), and PTSD (3.6%). 8.3% of the PDA group, 20% of the SP group, and 42.9% of the GAD group were in the midst of a depressive episode at the time of assessment. Measures Anxiety Sensitivity Index (ASI) The ASI (Reiss, Peterson, Gursky, & McNally, 1986) consists of 16 items scored from 0 to 4, measuring fear of negative consequences of anxiety. The scale was constructed in order to measure individual differences in anxiety sensitivity. It has been demonstrated to have adequate reliability and validity (Reiss, Peterson, Gursky, & McNally, 1986; for review, see Peterson & Plehn, 1999). The coefficient a for the ASI scale in the current study was .85. Beck Depression Inventory (BDI-II) The BDI-II is a 21-item measure that assesses the severity of depressive symptoms (Beck & Steer, 1987). Respondents are asked to choose one of four statements for each of the 21 items, on a 0–3 scale, which best describes how they have been feeling in the past 2 weeks. There is considerable validity and reliability data on this measure across various populations (for review, see Beck, Steer, & Garbin, 1988). Beck Anxiety Inventory (BAI) The BAI is a 21-item self-report measure of anxiety symptoms (Beck & Steer 1990). Respondents are asked to report how much they have been bothered by several symptoms in the previous week on a four-point scale ranging from ‘not at all’ to ‘severely.’ Internal consistency estimates have been found to be .92 in general psychiatric samples (Beck, Epstein, Brown, & Steer, 1988) and .85 to .93 in anxiety disorder patients (Beck & Steer, 1993). Results Principal components analysis of the ASI The ASI was examined using principal components analysis with oblimin rotation. Using scree plot analysis plus eigenvalueX1 and factor varianceX5% criteria, all concurred on a three-component solution accounted for 55.6% of the variance: fear of physical symptoms (ASI-Physical: eigenvalue ¼ 5.20, variance ¼ 32.5%), fear of cognitive dyscontrol (ASI-Cognitive: eigenvalue ¼ 2.42, Variance ¼ 15.1%), and fear of publicly observable anxious symptoms (ASI-Social: eigenvalue ¼ 1.28, Variance ¼ 8.0%).2 The extracted components replicate those previously reported in anxious samples by Zinbarg, Brown, and Barlow (1997) and Rodriguez, Bruce, Pagano, Spencer, & Keller (2004) with nearly identical loadings except that item #3, ‘‘It scares me when I feel ‘shaky’ (trembling)’’ double-loaded on the ASI-Physical and ASI-Cognitive components in our study whereas in Rodriguez, Bruce, Pagano, Spencer, & Keller, 2004 study, this item double-loaded on the ASI-Physical and ASI-Social components. Using the regression method, dimension scores were calculated for the ASI dimensions. 2
Principal axis factor with Oblimin rotation resulted in an identical three-factor solution accounting for 55.59% of the variance, with identical factor loadings with the exception that ASI item #7 loaded on the ASI-Social dimension at .12 whereas it previously loaded at .40.
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0.6
PDA SP GAD
0.4 ASI Factor Scores
1971
0.2 0 -0.2 -0.4 -0.6 ASI-Physical
ASI-Social ASI Dimensions
ASI-Cognitive
Fig. 1. ASI dimension scores for diagnostic groups.
Comparison of ASI dimensional scores between diagnostic groups The ASI dimension scores were compared between the diagnostic groups using a repeated measures multivariate analysis of variance (MANOVA). The between-subject factor was diagnostic group (PDA, SP, and GAD) and the within-group factor was ASI scores (ASI-Physical, ASI-Social, and ASI-Cognitive), and BAI and BDI-II scores served as the covariates. Neither the ASI scores by BAI nor the ASI scores by BDI-II multivariate effects were significant. However, an ASI scores by diagnostic group two-way multivariate interaction was observed, Wilks’ l ¼ .69, F(4,242) ¼ 12.31, po.001.3 Three separate ANOVA’s with post-hoc comparisons (LSD) were computed for each of the three ASI dimensions, while retaining BAI and BDI-II scores as covariates. To correct for potential Type I error, a Bonferroni correction was applied for the determination of significance for the univariate analyses (a ¼ .05/3 tests ¼ .02). The results of the between-group comparisons can be seen in Fig. 1. There was a significant main effect for diagnostic group on the ASI-Physical score, F(4,126) ¼ 15.29, pp.001). Post-hoc comparisons revealed that patients with PDA scored significantly higher than patients with SP (mean difference ¼ .95, pp.001, d ¼ 1.33) and GAD (mean difference ¼ .73, pp.001, d ¼ .78). A significant main effect for diagnostic group was also observed for ASI-Social scores, F(4,126) ¼ 5.20, pp.007. Post-hoc comparisons revealed that patients with SP had significantly higher scores than patients with PDA (mean difference ¼ .56, pp.006, d ¼ .38) and GAD (mean difference ¼ .61, pp.008, d ¼ .40). Finally, a significant main effect was observed for ASI-Cognitive scores, F(4,126) ¼ 5.21, pp.007. Patients with GAD scored significantly higher than patients with SP (mean difference ¼ .62, pp.003, d ¼ .92) but not PDA (mean difference ¼ .19, pX.35, d ¼ .34).4,5 3 To determine whether medication use could have differentially affected the ASI scores across diagnostic groups, we conducted a repeated measures MANOVA with medication use (dummy coded ‘1’ for present and ‘2’ for absent) and diagnostic group as the betweengroup variables and ASI scores as the repeated measure. The ASI scores by medication use multivariate effect was not significant, Wilks’ l ¼ .99, F(2,118) ¼ .85, p ¼ .43 nor was the ASI by medication use by diagnostic group multivariate effect, Wilks’ l ¼ .98, F(4,236) ¼ .62, p ¼ .65. 4 The analyses were repeated again with the cross-loading ASI item #3 removed and the results remained unchanged, with the PDA and GAD groups remaining equivalent. 5 Because diagnostic groups were found to differ on the BAI, F(2,126) ¼ 5.76, po.005, these analyses were repeated without BAI as a covariate. All results remained as before although the multivariate effect for ASI-Social scores was reduced to a strong trend, F(2,126) ¼ 2.94, p ¼ .057. However, the multiple contrasts demonstrated that the SP group still scored significantly higher on the ASISocial dimension than the PDA (mean difference ¼ .38, pp.05) and GAD (mean difference ¼ .50, pp.05) groups.
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Association between ASI dimensions, anxiety severity and depression severity To test the hypothesis that ASI-Cognitive scores would be more strongly associated with dimensional depression scores than either ASI-Physical or ASI-Social scores, zero-order Pearson correlations were computed between the ASI factor scores and measures of anxiety and depression. The ASI-Physical (r ¼ .38, pp.01), ASI-Social (r ¼ .25, pp.05), and ASI-Cognitive (r ¼ .46, pp.01) scores were all positively and significantly associated with BAI total scores. Whereas the ASI-Physical scores were not significantly associated with BDI-II scores (r ¼ .15 ns), both the ASI-Social (r ¼ .18, pp.05) and ASI-Cognitive (r ¼ .42, pp.01) scores were positively and significantly correlated with BDI-II scores. To determine whether the magnitude of the correlations differed, Fisher’s r-to-z transformations were computed following the steps outlined by Meng, Rosenthal and Rubin (1992). The results indicated that the correlation between ASI-Cognitive and BDI-II scores was greater than the correlation between the ASI-Physical and BDI-II scores (z ¼ 2.34, pp.01) and the ASI-Social and BDI-II scores (z ¼ 2.32, pp.01).
ASI dimensional scores between patients with and without secondary major depression To test whether the ASI dimensions differed between patients with and without secondary major depression, a repeated measures MANOVA was conducted with one between-group factor, secondary depression (dummy coded for present or absent), and ASI dimensions as the within-subject factor. The results indicated a two-way multivariate interaction, Wilks’ l ¼ .82, F(2,123) ¼ 9.03, po.001 between ASI dimensions and secondary depression status. Three separate ANOVA’s were conducted for each of the ASI dimensions with secondary major depression status as the between-group variable. Again, a Bonferroni correction was applied for the determination of significance for the univariate analyses (a ¼ .05/3, tests ¼ .02). The results can be seen in Fig. 2. No significant differences were noted for ASI-Physical scores, F(1,125) ¼ 4.15, p4.05, d ¼ .43 and no between-group differences were observed for ASI-Social scores, F(1,125) ¼ .23, p4.60, d ¼ .09. However, a main effect for ASI-Cognitive scores was observed, F(1,125) ¼ 8.65, pp.01, d ¼ .65 with patients with comorbid MDD (M ¼ .49, SD ¼ .98) scoring higher than patients without secondary MDD (M ¼ .13, SD ¼ 0.97).
0.5 0.4
No Comorbid MDD Comorbid MDD
ASI Factor Scores
0.3 0.2 0.1 0 -0.1 -0.2 -0.3 -0.4 ASI-Physical
ASI-Social ASI-Cognitive ASI Dimensions
Fig. 2. ASI dimension scores by secondary MDD status.
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Discussion This study aimed to examine the convergent validity of the ASI dimensions in patients with DSM-IV anxiety disorders. Consistent with past research (Blais et al., 2001; Rodriguez, Bruce, Pagano, Spencer, & Keller, 2004; Zinbarg, Brown, and Barlow (1997)), ASI-Physical scores were found to be most strongly associated with PD/A, whereas ASI-Social scores were most strongly associated with SP. Patients with GAD scored highest on the ASI-Cognitive dimension. While the GAD group had a mean ASI-Cognitive score that was nearly twice that of the PDA group, these differences did not reach conventional levels of statistical significance. These results replicate the findings reported by Zinbarg, Brown, and Barlow (1997) that also observed non-significant differences between PD/A and GAD diagnostic groups on the ASI-Cognitive dimension. One possible explanation is that ASI-Cognitive scores are associated with PDA to the extent that patients present with cognitive symptoms of panic, such as fears of ‘‘going crazy’’ and ‘‘losing control,’’ a previously demonstrated subgroup of panic patients (Cox, Swinson, Endler, & Norton, 1994). Consistent with past research in clinical samples with primary anxiety disorders (Schmidt et al., 1998; Taylor, Koch, Woody, & McLean, 1996; Zinbarg, Brown, Barlow, & Rapee, 2001), the ASI-Cognitive scores were associated with dimensional depression scores (BDI-II) to a greater extent than were the ASI-Physical and ASI-Social dimensions. Moreover, ASI-Cognitive scores discriminated anxious patient groups with and without secondary MDD. While previous research demonstrated the convergent validity of the ASI-Cognitive dimension in relation to PD/A patients with and without comorbid depression (Taylor, Koch, Woody, & McLean, 1996), our results extend this pattern to patients with and without secondary MDD across PDA, GAD, and SP groups. The results from this study suggest that the ASI-Cognitive dimension is strongly associated with GAD and depression (both dimensional depression scores and a bona fide MDD diagnosis). One possible explanation for these associations is that ASI-Cognitive scores are associated with both GAD and MDD because patients fear symptoms that are similar to both disorders such as difficulties concentrating, sleep disturbance, restlessness, and fatigue (APA, 2000). A second possibility is that fear of cognitive dyscontrol is related to the diagnoses of GAD and MDD to the extent that it is associated with the cognitive processes that are characteristic of the disorders. The hallmark feature of GAD is the presence of excessive and uncontrollable worry (APA, 2000, p.472). Borkovec (1994) has defined worry as ‘‘a predominately verbal-linguistic attempt to avoid future aversive events’’ (Borkovec, 1994, p.7). While characteristic of GAD, worry is common to many psychiatric conditions, including depression (Chelminski & Zimmerman, 2003). Further, repetitive or ruminative thinking in depression has been hypothesized to confer vulnerability to the experience of more severe and protracted episodes of major depressive disorder (Nolen-Hoeksema, 1991). While worry (Borkovec, Ray, & Stober, 1998) and rumination (Nolen-Hoeksema, 1991) have emerged as distinct cognitive constructs to assess recurrent negative thinking in GAD and depression, respectively, more recent research has suggested that these cognitive processes represent manifest variables as part of a latent variable titled repetitive thought, the latter showing equivalent associations with anxiety and depression measures (Sergerstrom, Tsao, Alden, & Craske, 2000). Preliminary research demonstrates an association between ASICognitive scores and cognitive rumination in clinically depressed patients (Cox, Enns, & Taylor, 2001). Finally, a third possible explanation for the overlapping role of fears of cognitive dyscontrol in GAD and MDD is that the ASI-Cognitive items tap meta-cognitive constructs that are specific to GAD and MDD. Wells and Matthews (1994) have theorized that the cognitive processes of worry in GAD and rumination in MDD are driven by meta-cognitive beliefs pertaining to the perception that repetitive thought is uncontrollable and dangerous, tantamount to mental catastrophe (Wells, 2005). Items of the ASI-Cognitive component, such as ‘‘When I cannot keep my mind on a task, I worry that I might be going crazy’’ appear to similarly tap anticipated danger associated with perceived uncontrollable cognitive processes. Despite the potential overlap between the ASI-fear of cognitive dyscontrol component and previously operationalized meta-cognitive variables, we are unaware of any published study that has examined the convergent and divergent validity of these constructs and so additional research is required. The cross-sectional design of the current study does not allow for the determination of whether say ASI-Social scores represent vulnerability for the development of SP, or alternatively, whether the onset of clinical SP leads to the exacerbation of ASI-Social concerns. The directionality issue becomes even more
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salient when considering that the ASI-Cognitive dimension has been explicitly conceptualized as both a preexisting vulnerability to and a psychological ‘scar’ resulting from depressive states (e.g., Cox, Enns, & Taylor, 2001). Prospective examination with the ASI-Cognitive dimension in relation to related disorders would help address the directionality question as would the determination of whether ASI-Cognitive can predict depressive relapse (and periods of exacerbation in GAD). Further, treatment studies are needed to establish whether ASI-Cognitive scores can be significantly reduced in psychological interventions for depression and GAD and the extent to which these reductions mediate successful treatment outcomes. Finally, significant advancements in the psychometric refinement of the ASI scale have been made, including expansion of the number of items that comprise the ASI-Cognitive dimension (Taylor & Cox, 1998). For instance, the Anxiety Sensitivity Profile (ASP; Taylor & Cox, 1998) added more items to the fear of cognitive dyscontrol factor, so that it assessed a greater breadth of cognitive symptoms (e.g., derealization, depersonalization, etc.). While one study examined the original ASI-Cognitive factor with the new expanded content of the ASP-Cognitive Dyscontrol and found the latter to offer no increase in predictive validity than the ASI factor in relation to depressive symptoms (Cox, Taylor & Enns, 1999), future research may focus on the discriminant validity of more broadly operationalized anxiety sensitivity constructs within the anxiety disorder spectrum. Acknowledgments The authors would like to thank Drs. Nancy Kocovski and Marla Engelberg for their comments on an earlier draft of this manuscript.
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