Obsessive–compulsive disorder
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Comprehensive Psychiatry 55 (2014) 489–496 www.elsevier.com/locate/comppsych
Mediators and moderators of functional impairment in adults with obsessive–compulsive disorder
Eric A. Storcha,b,⁎, Monica S. Wua,c, Brent J. Smalld, Erika A. Crawforda, Adam B. Lewina,b, Betty Hornga, Tanya K. Murphya,b
aDepartment of Pediatrics, University of South Florida, St. Petersburg, FL 33701, USA bDepartment of Psychiatry and Behavioral Neurosciences, University of South Florida, St. Petersburg, FL 33701, USA
cDepartment of Psychology, University of South Florida, St. Petersburg, FL 33701, USA dSchool of Aging Studies, University of South Florida, St. Petersburg, FL 33701, USA
The current study examined correlates, moderators, and mediators of functional impairment in 98 treatment-seeking adults with obsessive–compulsive disorder (OCD). Participants completed or were administered measures assessing obsessive–compulsive symptom severity, functional impairment, resistance against symptoms, interference due to obsessive–compulsive symptoms, depressive symptoms, insight, and anxiety sensitivity. Results indicated that all factors, except insight into symptoms, were significantly correlated with functional impairment. The relationship between obsessive–compulsive symptom severity and functional impairment was not moderated by patient insight, resistance against obsessive–compulsive symptoms, or anxiety sensitivity. Mediational analyses indicated that obsessive–compulsive symptom severity mediated the relationship between anxiety sensitivity and obsessive–compulsive related impairment. Indeed, anxiety sensitivity may play an important contributory role in exacerbating impairment through increases in obsessive–compulsive symptom severity. Depressive symptoms mediated the relationship between obsessive–compulsive symptom severity and obsessive–compulsive related impairment. Implications for assessment and treatment are discussed. © 2014 Elsevier Inc. All rights reserved.
Obsessive–compulsive disorder (OCD) is a debilitating neuropsychiatric condition characterized by obsessions (i.e., recurrent and distressing thoughts, images, or impulses) and/ or compulsions (i.e., repetitive behaviors or mental acts performed to reduce distress) [1]. Although the severity of obsessive–compulsive symptoms is directly associated with the degree of functional impairment experienced [2–5], this relationship is not absolute; there are other variables that contribute to understanding who is at greater risk of compounded impairment and which mechanisms operate in influencing impairment. Accordingly, this study extends the literature by examining factors believed to be theoretically relevant in understanding impairment among treatment- seeking adults with OCD. Obsessive–compulsive disorder
⁎ Corresponding author at: Department of Pediatrics, University of South Florida, 880 6th St. South, Box 460, St. Petersburg, FL 33701, USA. Tel.: +1 727 767 8230.
E-mail address: estorch@health.usf.edu (E.A. Storch).
0010-440X/$ – see front matter © 2014 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.comppsych.2013.10.014
To date, several studies have examined clinical charac- teristics associated with functional impairment. In addition to obsessive–compulsive symptom severity, ability to resist and control obsessive–compulsive symptoms [2–4,6] and co-occurring depressive and anxiety symptoms [5–8] have been associated with functional impairment. Among children and adolescents with OCD, insight predicted parent- and child-rated functional impairment above and beyond obses- sive–compulsive symptom severity [19]. In an effort to understand potential mechanisms of impairment, one recent study of adults with OCD found that depressive symptoms and obsessive–compulsive symptom resistance/control me- diated the relationship between obsessive–compulsive symptom severity and functional impairment [6]. Although informative, other variables may be relevant in understand- ing why some individuals experience compounded impair- ment beyond that which is conferred by the degree of obsessive–compulsive symptom severity.
Anxiety sensitivity has emerged as an important variable in understanding the development and maintenance of various
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490 E.A. Storch et al. / Comprehensive Psychiatry 55 (2014) 489–496
anxiety disorders [9]. Defined as a fear of arousal- or anxiety- related sensations which are misinterpreted by the individual as harmful or dangerous [10], elevated anxiety sensitivity is associated with difficulty experiencing and tolerating anxiety- related sensations [9]. Conceptually, anxiety sensitivity may relate to impairment by virtue of how someone with OCD experiences his or her symptoms and associated distress. An individual with high anxiety sensitivity may experience the distress associated with his or her obsessive–compulsive symptoms as unbearable and be more likely to engage in rituals or active avoidance of anxiogenic triggers, thus compounding impairment. Problematically, such behaviors contribute to the increased potential for illness chronicity through negative reinforcement (i.e., distress reduction) of obsessive–compulsive symptoms.
A modest literature exists examining anxiety sensitivity among adults with OCD. Anxiety sensitivity levels were elevated in adults with OCD relative to non-clinical controls [11–13], and were at comparable levels to adults with non- OCD anxiety disorders [11]. There are a limited number of examinations into the association between anxiety sensitivity and obsessive–compulsive symptom severity. In 280 adults with OCD, Calamari et al. [14] found that anxiety sensitivity and obsessive–compulsive symptom severity were signifi- cantly related. Wheaton et al. [15] demonstrated modest associations between anxiety sensitivity and dimensional ratings of obsessive–compulsive symptoms in a large non- clinical sample of university students. Collectively, these studies suggest that OCD caseness is linked to elevated anxiety sensitivity relative to non-clinical samples, and may be directly linked with obsessive–compulsive symptom severity. However, these studies do not address the manner in which anxiety sensitivity may contribute to functional impairment, which has potential implications for the conceptualization and care of individuals with OCD. First, anxiety sensitivity may be one method through which obsessive–compulsive symptom severity is exacerbated and/or maintained. As stated, high anxiety severity may be linked to greater ritualizing/avoidance and less symptom resistance, contributing to impairment and sustained symp- tomology. Second, anxiety sensitivity may be linked to a more chronic symptom course. Individuals with high anxiety sensitivity may be less likely to exhibit decreases in symptom severity relative to those with lower anxiety sensitivity [16], perhaps explaining, in part, the chronic nature of OCD in the absence of treatment.
Beyond anxiety sensitivity, other variables may hold relevance in understanding which individuals may experi- ence compounded impairment. Insight into the degree to which obsessive–compulsive symptoms are recognized by the person as absurd, excessive, and senseless has been linked to obsessive–compulsive symptom severity and functional impairment in past studies of adults [17] and children with OCD [18,19]. Additionally, individuals with poor insight into their OCD symptomology have exhibited more complicated clinical presentations and poorer treatment
response when compared to individuals with higher insight [17,20]. It is reasonable to consider that insight may moderate the relationship between obsessive–compulsive symptom severity and impairment such that those with poor insight may be more clinically complex and be less able to function effectively or actively challenge symptoms. Simi- larly, symptom resistance is also hypothesized to be relevant in understanding who is at risk for greater impairment in that those who actively try to challenge their symptoms would be less likely to experience OCD-related impairment. Indeed, the lower levels of resistance against obsessive–compulsive symptoms have been linked with increased obsessive– compulsive symptom severity [21], as well as decreased functioning and higher impairment [6,22].
In the present study, we examine correlates, moderators, and mediators of functional impairment in adults with OCD. Our specific study questions and hypotheses were as follows. First, what are the relations among domains of functional impairment and obsessive–compulsive symptom severity, symptom resistance, interference due to obsessive– compulsive symptoms, anxiety sensitivity, depressive symptoms, and insight? We expected that the varied domains of functional impairment would be directly associated with obsessive–compulsive symptom severity, interference due to obsessive–compulsive symptoms, anx- iety sensitivity, and depressive symptoms, and inversely related to symptom resistance and insight. Second, we examined the extent to which insight, resistance against obsessive–compulsive symptoms, and anxiety sensitivity moderated the relationship between obsessive–compulsive symptom severity and OCD-related impairment. We expected that each variable would moderate this association such that the relationship between obsessive–compulsive symptom severity and OCD-related impairment would be more robust for those with lower insight and symptom resistance, and higher anxiety sensitivity. Third, would the relationship between anxiety sensitivity and OCD-related functional impairment be mediated by obsessive–compul- sive symptom severity? We predicted that as anxiety sensitivity increased, obsessive–compulsive symptom se- verity would increase, which would be positively associated with functional impairment. Finally, in an effort to replicate Storch et al. (2009), would the relationship between obsessive–compulsive symptom severity and OCD-related functional impairment be mediated by depressive symp- toms? We expected that as obsessive–compulsive symptom severity increased, depressive symptoms would increase, which would be directly associated with augmented functional impairment.
1. Method
1.1. Participants and procedures
Participants included 98 adults with a primary diagnosis of OCD that presented to an OCD specialty center to initiate
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cognitive–behavioral treatment (Table 1). Diagnoses were established using best estimate diagnostic procedures in which consensus between two experienced clinicians (one of whom interviewed the participant in an unstructured assessment) was required on the primary diagnosis and the presence of comorbid diagnoses. Clinicians used all available information to ascertain an accurate diagnostic profile by including clinical information gleaned from an unstructured clinical interview, reviewing participants’ completed measures as part of this study, and examining past clinical records. Participants were excluded in the absence of 100% agreement for the primary or comorbid diagnoses, or if diagnosed with psychosis, mental retarda- tion, or bipolar disorder. The participants were between 18 and 72 years of age (M = 33.1, SD = 13.53) and were 57% female. The sample was 84% Caucasian, 10% Hispanic, 2% African American, 2% Asian, and 2% classified as ‘other.’ Common comorbid diagnoses included depression (57%), generalized anxiety disorder (30%), impulse control disorder-not otherwise specified (12%), and social phobia (10%). Seventy-nine participants (81%) reported currently taking psychotropic medication.
All study procedures were approved by the local institutional review board. Following a regularly scheduled clinic visit, patients appropriate for the study were approached by a member of the research team who was otherwise uninvolved in the individual’s care to review the study; interested participants provided their written consent. Participants then were administered the Yale–Brown Obsessive Compulsive Scale (Y-BOCS) [23,24] by a trained rater and thereafter completed self-report measures. Based on the Y-BOCS interview, the clinician rated the National Institutes of Mental Health Global Obsessive Compulsive
Table 1 Demographic characteristics of the study sample (n = 98).
Variable
Gender (Male/Female) 41 Males (42%)/57 Females (58%) Age (Years) M = 33.10, SD = 13.53
Range = 18 to 72 years Race/Ethnicity Caucasian n = 82 (84%) Hispanic n = 10 (10%) African–American n = 2 (2%) Asian n = 2 (2%) Other n = 2 (2%) Comorbid Diagnosesa
Depressive disordersb n = 56 (57%) Generalized anxiety disorder n = 29 (30%) Impulse control disorder not otherwise specified
n = 12 (12%)
Social phobia n = 10 (10%) Taking Psychotropic Medication n = 79 (81%)
a The four most common comorbidities are listed in the table. Comorbid diagnoses occurring with less frequency are not reported.
b Depressive disorders included those diagnosed with major depression, dysthymia, and depressive disorder not otherwise specified.
Scale (NIMH-GOCS) [25]. All independent evaluators underwent extensive training with the first author in the administration of Y-BOCS and NIMH-GOCS.
1.2. Measures
1.2.1. Yale–Brown Obsessive Compulsive Scale (Y-BOCS) [23,24]
The Y-BOCS is a clinician-administered semi-struc- tured interview that assesses the presence and severity of obsessive–compulsive symptoms. Insight into obsessive– compulsive symptoms (item #11 on the Y-BOCS; possible score ranges from 0 to 4), interference due to obsessive–compulsive symptoms (sum of items #1, 2, 3, 6, 7, and 8; possible scores ranging from 0 to 24), resistance against obsessive–compulsive symptoms (sum of items #4, 5, 9, and 10; possible scores ranging from 0 to 16), and Severity Scale total score (possible scores ranging from 0 to 40) were all gathered through this measure. Higher scores on insight indicate poorer insight, higher scores on interference indicate higher interference, and higher scores on resistance indicate greater difficulty with resistance. The Y-BOCS has demonstrated excellent psychometric properties with regard to reliability and validity [26–28].
1.2.2. Sheehan Disability Scale (SDS) [29] The SDS is a 3-item self-report questionnaire that
assesses the level of impairment experienced due to obsessive–compulsive symptoms in social, occupational, and family life. The impairment scores for each domain (possible scores range from 0 to 10) and the total score were used (possible scores range from 0 to 30), and higher scores indicate higher impairment. The SDS has shown good psychometric properties with regard to internal consistency and validity [30,31].
1.2.3. National Institutes of Mental Health Global Obsessive Compulsive Scale (NIMH-GOCS) [25]
The NIMH-GOCS is a one-item clinician-administered measure that assesses the severity of obsessive–compulsive symptoms on a scale from 1 to 15, with higher scores indicating more severe obsessive–compulsive symptoms.
1.2.4. Beck Depression Inventory-Second Edition (BDI-II) [32] The BDI-II is a 21-item self-report questionnaire that
assesses the presence and severity of depressive symptoms in the past week. The total score was used (possible scores range from 0 to 63), and higher scores on the BDI-II indicate more depressive symptoms. The BDI-II has demonstrated adequate validity and reliability, including discriminant and construct validity, internal consistency, and test-retest reliability [32,33].
1.2.5. Anxiety Sensitivity Index-Revised (ASI-R) [34] The ASI-R is a 36-item self-report questionnaire that
assesses the respondent’s fear of anxiety and its respective sensations, due to the perceived negative consequences of
Table 2 Correlation coefficients, means, standard deviations, and ranges for all study measures (n = 98).
1 2 3 4 5 6 7 8 9 10 11
1. SDS Total Score 0.79⁎⁎⁎ 0.88⁎⁎⁎ 0.83⁎⁎⁎ 0.65⁎⁎⁎ 0.17 0.76⁎⁎⁎ 0.31⁎⁎ 0.70⁎⁎⁎ 0.72⁎⁎⁎ 0.26⁎
2. SDS Work 0.55⁎⁎⁎ 0.45⁎⁎⁎ 0.57⁎⁎⁎ 0.11 0.65⁎⁎⁎ 0.22⁎ 0.58⁎⁎⁎ 0.54⁎⁎⁎ 0.14 3. SDS Social 0.65⁎⁎⁎ 0.56⁎⁎⁎ 0.19 0.64⁎⁎⁎ 0.33⁎⁎ 0.62⁎⁎⁎ 0.68⁎⁎⁎ 0.30⁎⁎
4. SDS Family/Home 0.51⁎⁎⁎ 0.13 0.62⁎⁎⁎ 0.23⁎ 0.56⁎⁎⁎ 0.58⁎⁎⁎ 0.20⁎
5. NIMH GOCSa 0.21⁎ 0.86⁎⁎⁎ 0.47⁎⁎⁎ 0.84⁎⁎⁎ 0.51⁎⁎⁎ 0.26⁎
6. Y-BOCS Insight 0.17 0.31⁎⁎ 0.27⁎⁎ 0.22⁎ 0.08 7. Y-BOCS Interference 0.38⁎⁎⁎ 0.90⁎⁎⁎ 0.59⁎⁎⁎ 0.30⁎⁎
8. Y-BOCS Resistance 0.74⁎⁎⁎ 0.30⁎⁎ 0.18 9. Y-BOCS Total Score 0.57⁎⁎⁎ 0.30⁎⁎
10. BDI-II Total Scorea 0.37⁎⁎⁎
11. ASI-R Total Scorea
Mean 19.26 6.27 6.36 6.63 9.26 0.62 15.00 9.44 24.44 21.93 47.45 SD 7.16 2.79 3.01 2.76 2.10 0.86 3.73 2.35 5.10 11.31 28.91 Range 0–30 0–10 0–10 0–10 5–13 0–3 7–24 4–16 13–36 0–49 0–122
⁎ p b 0.05. ⁎⁎ p b 0.01. ⁎⁎⁎ p b 0.001. a Indicates sporadic missing data. NIMH GOCS (n = 95), BDI-II (n = 97), ASI-R (n = 97).
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the feelings. The total score was used (possible scores range from 0 to 144), with higher scores indicating greater anxiety sensitivity. The ASI-R has been shown to be psychometri- cally sound as demonstrated through high internal consis- tency and reliability [35]. The ASI-R also contains six factorially derived subscales, investigating: (1) fear of cardiovascular symptoms, (2) fear of respiratory symptoms, (3) fear of gastrointestinal symptoms, (4) fear of publicly observable anxiety reactions, (5) fear of dissociative and neurological symptoms, and (6) fear of cognitive dyscontrol.
1.3. Statistical analyses
Prior to analysis, variables were evaluated for the presence of outliers and multicollinearity, and distributional properties were examined. For the moderation effects in regression, analyses were conducted using the MODPROBE macro through SPSS as described by Hayes and Matthes [36]. The mediation analyses were computed in Mplus [37] with bootstrapped standard errors for the direct and indirect effects. This method provides the same basic information as the classic Baron and Kenny [38] approach, but provides a specific test for the mediated effect and increases statistical power through the bootstrapped resampling [39]. For the correlations, there were sporadic missing values and the pairwise sample sizes are reported. For the moderation and mediation analyses, multiple imputation using SAS Proc MI [40,41] and maximum likelihood estimates using Mplus were employed, respectively.
2. Results
2.1. Descriptive statistics and correlations
Descriptive statistics (i.e., mean, standard deviation, and range) were calculated for all study variables (see
Table 2). Pearson correlation coefficients were calculated for all study variables and statistical significance was adjusted for multiple comparisons using the Holm- Bonferroni correction [42]. Regardless of examining corrected or non-corrected correlations, all variables remained significantly correlated with the SDS total score (OCD-related impairment), except for insight into obses- sive–compulsive symptoms. Specifically, the SDS total score demonstrated a strong positive correlation with obsessive–compulsive symptom severity (NIMH GOCS, Y-BOCS Total score), interference (Y- BOCS Interfer- ence), and depressive symptoms (BDI-II), a moderate positive correlation with resistance against obsessive– compulsive symptoms (Y-BOCS Resistance), and a weak positive correlation with anxiety sensitivity (ASI-R). Impairment in work possessed a strong positive correlation with obsessive–compulsive symptom severity, interference, and depressive symptoms, and a weak positive correlation with resistance against obsessive–compulsive symptoms and anxiety sensitivity. Social impairment exhibited a strong positive correlation with obsessive–compulsive symptom severity, interference, and depressive symptoms, and a moderate positive correlation with resistance against obsessive–compulsive symptoms and anxiety sensitivity. Lastly, impairment in family life or home responsibilities demonstrated a strong positive correlation with obsessive–compulsive symptom severity, interference, and depressive symptoms, and a weak positive correlation with resistance against obsessive–compulsive symptoms and anxiety sensitivity. No impairment domain possessed a statistically significant correlation with insight into obsessive–compulsive symptoms.
To explore potentially differential relationships between specific components of anxiety sensitivity and obsessive– compulsive symptom severity, Pearson correlation coeffi- cients were also run to examine the relationship between
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each subscale on the ASI-R and the Y-BOCS Total score (Table 3).1 Fear of cardiovascular symptoms (subscale 1) and fear of gastrointestinal symptoms (subscale 3) did not demonstrate statistically significant correlations with obsessive–compulsive symptom severity. Fear of respiratory symptoms (subscale 2), fear of publicly observable anxiety reactions (subscale 4), fear of dissociative and neurological symptoms (subscale 5), and fear of cognitive dyscontrol (subscale 6) all shared weak to moderate relationships with obsessive–compulsive symptom severity.
2.2. Moderation analyses
Insight into obsessive–compulsive symptoms, resistance against obsessive–compulsive symptoms, and anxiety sen- sitivity were not significant moderators of the relationship between obsessive–compulsive symptom severity and OCD-related impairment. In testing insight, resistance, and anxiety sensitivity as potential moderators, NIMH GOCS was a significant predictor of OCD-related impairment (β = 2.04, p b 0.0001; β = 2.05, p b 0.0001; β = 1.89, p b 0.0001), respectively. However, insight was not a significant predictor of OCD-related impairment (β = 0.60, p = 0.40), and neither was the interaction term for NIMH GOCS and insight (β = −0.31, p = 0.41). Additionally, neither resistance (β = 0.05, p = 0.87) nor the interaction term between NIMH GOCS and resistance was a significant predictor for OCD-related impairment (β = −0.20, p = 0.09). Lastly, anxiety sensitivity was not a significant predictor of OCD-related impairment (β = 0.04, p = 0.09), nor was the interaction term between NIMH GOCS and anxiety sensitivity (β = −0.01, p = 0.17).
2.3. Mediation analyses2
Obsessive–compulsive symptom severity (NIMH GOCS) was tested as a potential mediator between anxiety sensitivity (ASI-R) and OCD-related impairment (SDS). The indirect effect was statistically significant (β = 0.03, SE = 0.01, p b 0.05) suggesting that the relationship between anxiety sensitivity and OCD-related impairment was explained by symptom severity, with higher anxiety sensitivity scores associated with higher obsessive– compulsive symptom severity scores (β = 0.02, SE = 0.01, p b 0.05), and higher obsessive–compulsive symptom severity scores associated with higher OCD-related impair- ment (β = 2.11, SE = 0.26, p b 0.001). Finally, the direct effect between anxiety sensitivity and OCD-related impair-
1 Correlations with each ASI-R subscale remained statistically significant with highly comparable strengths when the correlations were re-run with NIMH GOCS as the measure of OCD symptom severity.
2 All mediating effects remained the same when the mediation analyses were re-run with Y-BOCS Total score as the measure of OCD symptom severity. As such, NIMH GOCS was utilized as the metric for OCD symptom severity throughout the moderation and mediation analyses to maintain consistency.
ment was no longer statistically significant after the mediator was added to the model (β = 0.03, SE = 0.02, p = 0.17).
Depressive symptoms were tested as a potential mediator between obsessive–compulsive symptom severity (NIMH GOCS) and OCD-related impairment (SDS). The results demonstrated that depressive symptoms were a statistically significant mediator, with an indirect effect of 0.94 (SE = 0.19, p b 0.001) suggesting that the relationship between symptom severity and OCD-related impairment was explained by depressive symptoms, with higher scores on obsessive–compulsive symptom severity associated with higher depressive symptoms (β = 2.81, SE = 0.43, p b 0.001), and higher scores on depressive symptoms being associated with higher OCD-related impairment (β = 0.33, SE = 0.05, p b 0.001). Although the indirect effect was statistically significant, the direct effect of obsessive– compulsive symptom severity and OCD-related impairment was also statistically significant (β = 1.26, SE = 0.27, p b 0.001).
3. Discussion
We report on correlates, moderators, and mediators of functional impairment in adults with OCD. As expected, domains of impairment were strongly related to obsessive– compulsive symptom severity and interference, and mod- estly associated with symptom resistance and depressive symptoms. Relations of this magnitude are reflective of the impairing and distressing nature associated with obsessive– compulsive symptom severity. Indeed, OCD distinguishes itself from other anxiety disorders in terms of the degree of impairment [43], which contributes to it being listed as a leading cause of disability [44,45]. Weak associations were found between impairment and anxiety sensitivity and insight, which suggest that OCD caseness confers greater risk for impairment regardless of insight or anxiety sensitivity, such that more severe presentations are not necessarily linked with limited insight. It may also be that those with poor insight have similarly limited awareness into their own impairment. Additionally, only certain subscales on the assay of anxiety sensitivity were significantly correlated with obsessive–compulsive symptom severity, which may suggest that fear of cardiovascular and gastrointestinal symptoms may be less related to obses- sive–compulsive symptom severity when compared to other domains of anxiety sensitivity. Furthermore, the strength of the statistically significant correlations with obsessive– compulsive symptom severity was highly comparable not only across the ASI-R subscales, but also with the ASI-R total score. As such, it appears that the fears of respiratory symptoms, publicly observable anxiety reactions, dissocia- tive and neurological symptoms, and cognitive dyscontrol do not seem to show differential associations with obsessive– compulsive symptom severity when compared to one another, nor when compared to anxiety sensitivity as a
Table 3 Correlation coefficients, means, standard deviations, and ranges for ASI-R subscales and OCD symptom severity (n = 98).
1 2 3 4 5 6 7
1. Y-BOCS Total Score 0.13 0.29⁎⁎ 0.12 0.29⁎⁎ 0.27⁎⁎ 0.28⁎⁎
2. ASI-R S1: Fear of Cardiovascular Symptomsa 0.59⁎⁎⁎ 0.59⁎⁎⁎ 0.45⁎⁎⁎ 0.69⁎⁎⁎ 0.36⁎⁎⁎
3. ASI-R S2: Fear of Respiratory Symptoms 0.43⁎⁎⁎ 0.53⁎⁎⁎ 0.75⁎⁎⁎ 0.46⁎⁎⁎
4. ASI-R S3: Fear of Gastrointestinal Symptomsa 0.43⁎⁎⁎ 0.64⁎⁎⁎ 0.20⁎
5. ASI-R S4: Fear of Publicly Observable Anxiety Symptoms 0.64⁎⁎⁎ 0.48⁎⁎⁎
6. ASI-R S5: Fear of Dissociative and Neurological Symptomsa 0.65⁎⁎⁎
7. ASI-R S6: Fear of Cognitive Dyscontrola
Mean 24.44 6.57 9.10 3.32 14.40 7.89 6.32 SD 5.10 6.18 7.77 4.19 7.28 5.58 5.94 Range 13–36 0–23 0–28 0–16 0–32 0–23 0–20
⁎ p b 0.05. ⁎⁎ p b 0.01. ⁎⁎⁎ p b 0.001. a Indicates sporadic missing data. ASI-R Subscales 1, 3, 5, and 6 (n = 97).
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construct in general. These results suggest that relatively equal consideration should be given to the respective components of anxiety sensitivity when considering their relationship with OCD symptom severity.
One of the primary findings of interest was that obsessive–compulsive symptom severity mediated the relationship between anxiety sensitivity and OCD-related impairment. Stated differently, as anxiety sensitivity in- creased, obsessive–compulsive symptom severity increased, which was directly associated with augmented functional impairment. This is consistent with past findings implicating the role of anxiety sensitivity and symptom severity [14,16], and provides a potential mechanism through which anxiety sensitivity exacerbates symptom severity and ultimately functional impairment. Among individuals presenting with elevated anxiety sensitivity, this may trigger more severe clinical presentations characterized by extreme distress, decreased distress tolerance, and difficulty resisting/control- ling obsessive–compulsive symptoms, which translate into greater functional impairment relative to those with lower levels of anxiety sensitivity. Speculatively, anxiety sensitiv- ity may be one variable associated with attenuated homework compliance in exposure and response prevention treatment. That is, individuals with high anxiety sensitivity may be less likely to independently engage in homework tasks as they may find the experience too distressing. Problematically, homework compliance is a key element of psychotherapeutic treatment in which poor compliance is associated with reduced response [46,47].
Similar to past findings [6], the relationship between obsessive–compulsive symptom severity and OCD-related functional impairment was mediated by depressive symp- toms, such that as obsessive–compulsive symptom severity increased, depressive symptoms correspondingly increased, contributing to greater functional impairment. Studies document the temporal association between obsessive– compulsive symptom onset and a corresponding increase in depressive symptoms [48], which is believed to be secondary to the distressing and time intensive nature of
obsessive–compulsive symptoms. The contribution of depressive symptoms to the clinical picture of OCD may increase risk for impairment by virtue of additional psychiatric morbidity or the interactional nature of having two impairing problems. Correspondingly, there is evidence that reducing obsessive–compulsive symptoms through evidence-based OCD interventions translates into improve- ments in depressive symptomology [49,50]. Thus, treating obsessive–compulsive symptoms may be one method of improving comorbid depressive symptoms that are function- ally related to OCD. However, this approach may not translate to all patients; modular interventions that are personalized to individual patient characteristics such as comorbid depression would be well-suited for this cohort.
Interestingly, insight into obsessive–compulsive symp- toms, resistance against obsessive–compulsive symptoms, and anxiety sensitivity did not significantly moderate the relationship between obsessive–compulsive symptom se- verity and OCD-related functional impairment. Regarding insight, past studies, including this one, have found relatively weak associations between symptom insight and obsessive– compulsive symptom severity [51–53]. This suggests that insight may not be the driving force in understanding why some people are more impaired than others. It may be that people with very limited insight are not aware of the degree to which they are impacted by their symptoms; alternatively, they may have family members who are providing significant accommodation with the goal of reducing functional impairment. However, the finding that insight was not a significant mediator may also be attributed to a range restriction problem with the variable; upon examina- tion of the mean and standard deviation for the insight variable within this sample, a truncated range was indeed observed and could have been the source of precluding support for the hypothesis. It is somewhat surprising that resistance against obsessive–compulsive symptoms did not moderate the association between symptom severity and impairment, as it was expected that those who resist less would be more likely to experience impairment as their
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symptoms increased. Although there are clearly merits of resisting symptoms, it may be that symptom resistance yields differential effects across people; that is, some people may experience some cathartic benefits associated with reduced impairment, while others may not experience the same benefits through the emotional and tangible efforts required for successful resistance. It may be that anxiety sensitivity does not function as a moderator but rather exerts its effect through mediation by contributing to obsessive–compulsive severity, which in turn compounds functional impairment.
Several limitations to this study should be noted. First, the generalizability of the results may be restricted due to demographics of the study sample, as participants were primarily Caucasian and seeking treatment for their OCD. Second, the study was cross-sectional, limiting the ability to establish causality. Third, our assessment of insight relied on one clinician administered item and may not be as sensitive and/or comprehensive as using a tailored measure of insight (e.g., BrownAssessment ofBeliefs) or other related constructs, such as overvalued ideas (e.g., Overvalued Ideas Scale). Lastly, other variables not examined in the present study (e.g., cognitive variables) may be relevant in understanding the relationship between obsessive–compulsive symptoms and OCD-related impairment.
Within these limitations, this study has important implica- tions for the care of individuals with OCD. First, these data speak to the importance of assessing anxiety sensitivity in addition to more traditional constructs (e.g., comorbidity, insight, etc.). Given that anxiety sensitivity is linked to elevated obsessive–compulsive symptom severity, which in turn is associated with increased functional impairment, evaluating the patient’s level of anxiety sensitivity may help identify potential risk factors for OCD-related impairment. Addressing heightened anxiety sensitivity in treatment may also help with improved tolerability and quicker habituation to anxiety- producing situations, aiding in the process of exposure and response prevention. However, it remains unclear if anxiety sensitivity improves through standard therapies (e.g., cognitive behavioral therapy, antidepressant medications) or requires alternative, adjunctive approaches (e.g., interoceptive expo- sure) [54]. Second, depressive symptoms should correspond- ingly be assessed; these symptoms may serve as an underlying mechanism that is influenced by obsessive–compulsive symptom severity, ultimately contributing to functional impairment. As such, it is important to monitor the severity of depressive symptoms as treatment progresses, examining any changes (or lack thereof) secondary to the alleviation of obsessive–compulsive symptoms. Given the influence of depressive symptomology on functional impairment, any substantial symptoms remaining after OCD treatment may warrant more targeted interventions for the depression. Collectively, it is important to consider variables that contribute to OCD-related disability, as it allows clinicians to better predict risk factors and utilize targeted interventions to decrease functional impairment. Given the association with decreased functioning and poorer treatment response [55],
prudent identification and interventions for these constructs are hoped to help improve the prognosis of individuals with OCD.
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- Mediators and moderators of functional impairment in adults with obsessive–compulsive disorder
- 1. Method
- 1.1. Participants and procedures
- 1.2. Measures
- 1.2.1. Yale–Brown Obsessive Compulsive Scale �(Y-BOCS) [23,24]
- 1.2.2. Sheehan Disability Scale (SDS) [29]
- 1.2.3. National Institutes of Mental Health Global �Obsessive Compulsive Scale (NIMH-GOCS) [25]
- 1.2.4. Beck Depression Inventory-Second Edition (BDI-II) [32]
- 1.2.5. Anxiety Sensitivity Index-Revised (ASI-R) [34]
- 1.3. Statistical analyses
- 2. Results
- 2.1. Descriptive statistics and correlations
- 2.2. Moderation analyses
- Mediation analyses2
- 3. Discussion
- References
- 1. Method