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. Author manuscript; available in PMC: 2026 Jul 23.
Published in final edited form as: Behav Ther. 2023 May 24;55(1):80–92. doi: 10.1016/j.beth.2023.05.008

Reciprocal and indirect effects among intervention, perceived social support, and anxiety sensitivity within a randomized controlled trial for anxiety disorders

Allison V Metts a, Peter Roy-Byrne b, Murray B Stein c, Cathy D Sherbourne d, Alexander Bystritsky e, Michelle G Craske a,e
PMCID: PMC13390608  NIHMSID: NIHMS2192314  PMID: 38216239

Abstract

Social support may facilitate adaptive reappraisal of stressors, including somatic symptoms. Anxiety sensitivity refers to negative beliefs about somatic symptoms of anxiety, which may influence one’s perception of social support. Evidence-based treatment may impact these associations. The current longitudinal study evaluated reciprocal relationships between perceived social support and anxiety sensitivity, and explored indirect intervention effects, in a randomized controlled trial for anxiety disorders that compared cognitive behavioral therapy with or without medications (CALM) to usual care. Data collected over 18 months from 940 primary care patients were examined in random intercept cross-lagged panel models. There were significant reciprocal associations between perceived social support increases and anxiety sensitivity decreases over time. There were significant indirect effects from intervention to perceived social support increases through anxiety sensitivity decreases and from intervention to anxiety sensitivity decreases through social support increases. These data suggest that, relative to usual care, CALM predicted changes in one construct, which predicted subsequent changes in the other. Secondary analyses revealed an influence of anxiety and depressive symptoms on reciprocal associations and indirect effects. Findings suggest that future treatments could specifically address perceived social support to enhance reappraisal of somatic symptoms, and vice versa.

Keywords: cognitive behavioral therapy, social support, anxiety sensitivity, anxiety, depression

Introduction

Cognitive behavioral therapy (CBT) and pharmacotherapy effectively treat anxiety disorders (Bandelow et al., 2017; Norton & Price, 2007; Roy-Byrne & Cowley, 2007), but almost half of patients who receive these treatments fail to achieve full remission (Springer et al., 2018; Stein & Craske, 2017). Most prior work on treatment response has focused on how certain treatments lead to changes to symptomology. However, there is also value in examining associations among mechanisms affected by treatment, which can ultimately enhance treatment efficacy. Two constructs relevant to anxiety treatment are perceived social support and anxiety sensitivity (Birkeland et al., 2020; Price et al., 2018; Smits et al., 2008). The present secondary analysis aims to examine reciprocal associations between perceived social support and anxiety sensitivity within the context of a randomized controlled trial (RCT) for anxiety disorders, and whether cognitive behavioral therapy with pharmacological augmentation indirectly leads to change in anxiety sensitivity through perceived social support, or vice versa, to gain more knowledge about mechanistic change during and following treatment.

Social Support

Perceived social support refers to global impressions of the availability of support for assisting with responses to challenges (i.e., informational support), providing warmth or comfort (i.e., emotional support), providing tangible assistance (i.e., instrumental support), and making oneself available for companionship (i.e., companionate support) (Thoits, 2011). Higher social support has been linked to reduced risk for depression and anxiety (Auerbach et al., 2011; Metts et al., 2021; Zimmermann et al., 2020) and more positive treatment outcomes for depression and anxiety (Bosworth et al., 2008; Jakubovski & Bloch, 2016; Oxman & Hull, 2001; Saghafi et al., 2007; Sherbourne et al., 2004). Separately, perceived social support has been found to increase with cognitive behavioral therapy (CBT) in trauma-exposed youth (Birkeland et al., 2020) and prolonged exposure in veterans (Price et al., 2018), serving as evidence of malleability of perceived social support in evidence-based behavioral treatments.

Anxiety Sensitivity

Anxiety sensitivity refers to beliefs that anxiety-related sensations are harmful (Reiss et al., 1986) by leading to physical harm, social embarrassment, or mental incapacitation (Smits et al., 2008). These negative reappraisals of somatic symptoms are implicated in the etiology and maintenance of anxiety and mood disorders (Schmidt et al., 2006). Meta-analytic research has shown that CBT effectively reduces anxiety sensitivity (Smits et al., 2008). Moreover, anxiety sensitivity has been demonstrated to mediate the effects of CBT (Asnaani et al., 2020; Meuret et al., 2010). As such, anxiety sensitivity may both be changed and lead to change within evidence-based treatment for anxiety disorders.

Theory Linking Social Support and Anxiety Sensitivity

Recent efforts have moved beyond psychosocial pathways through which social support confers benefits to examine other mechanisms of social support. One such line of mechanistic work focuses on reappraisal assistance. Stressors can weaken coping-style reappraisals (Cohen & McKay, 1984) and individuals under stress often turn to others for assistance in coping (Zaki & Williams, 2013). During such ‘interpersonal emotion regulation,’ others may facilitate reappraisal of a situation or one’s capacity to manage the situation. Consequently, higher levels of social support are posited to strengthen coping reappraisals of stressful situations relative to lower levels of social support.

In the case of anxiety disorders, negative appraisals of somatic symptoms (i.e., anxiety sensitivity) render somatic symptoms a source of stress. As such, the current study extends prior work on interpersonal emotion regulation to stressors in the form of somatic symptoms. Specifically, anxious individuals with stronger social support may become less stressed by their somatic sensations than anxious individuals without such social support because support figures facilitate adaptive reappraisal of their somatic sensations. For example, social support figures could provide cognitive support, such as lending more helpful ways to think about symptoms, or assist with attention reallocation and help individuals shift their attention to more positive or neutral stimuli (Marroquín, 2011). Notably, adaptive reappraisal assistance contrasts with maladaptive interpersonal emotion regulation wherein social support contributes to anxiety and depression, such as ‘partner accommodation’ when partners alter their behaviors to prevent or decrease distress in ways that inadvertently reinforce anxiety or avoidance (Baucom et al., 2019; Hofmann, 2014). Adaptive reappraisal is measurable through reductions in anxiety sensitivity.

There are several reasons to believe that anxiety sensitivity in turn impacts perceived social support. Anxiety sensitivity includes fear of social evaluative consequences from somatic symptoms (Smits et al., 2008), and extends to sensitivity to negative evaluation in social interactions (Casale et al., 2014). There is some evidence, albeit limited, for negative correlations between fear of negative evaluation and perceived social support (Casale et al., 2014). Therefore, individuals with high anxiety sensitivity, who appraise their sensations as harmful, may be more likely to interpret their social interactions as less supported. Conversely, individuals with low anxiety sensitivity, who do not view their sensations as harmful, may perceive their social interactions as more supportive. In line with this proposed relationship, there is some evidence, albeit limited, for negative correlations between perceived social support and anxiety sensitivity (Latifi et al., 2019; Latifi & Kiani, 2021; Molero Jurado et al., 2021).

Potential Impact of Treatment upon Anxiety Sensitivity and Perceived Support

Reappraisal skills are central to cognitive restructuring and behavioral hypothesis testing exercises within CBT (Clark & Beck, 2010), including CBT for anxious beliefs that somatic symptoms are harmful (i.e., anxiety sensitivity) (Smits et al., 2008). Given that (1) CBT has been found to increase social support, even when not directly targeted (Birkeland et al., 2020; Price et al., 2018), (2) social support can facilitate reappraisal of stressful situations (Zaki & Williams, 2013), and (3) anxiety sensitivity functions as appraisal of a somatic-related stressor, then CBT may lead to decreases in anxiety sensitivity indirectly through the effects of social support. Alternatively, given that (1) reappraisal of anxiety-related sensations is central to CBT which in turn effectively reduces anxiety sensitivity (Smits et al., 2008), (2) anxiety sensitivity includes fears of negative evaluation and extends to more general social evaluative concerns (Casale et al., 2014), and (3) fears of negative evaluation influence perceived social support (Casale et al., 2014), then CBT may lead to increases in perceived social support indirectly through the effects of reducing anxiety sensitivity.

The Present Study

The current study seeks to examine the reciprocal relationships between perceived social support and anxiety sensitivity throughout treatment for anxiety disorders. We extend prior work on social support in relation to life stressors by testing the relationship between perceived social support and appraisals of anxiety symptoms. Additionally, we explore whether changes in anxiety sensitivity lead to subsequent changes in perceived social support. Further, we examine whether CBT combined with pharmacological augmentation leads to changes in anxiety sensitivity or perceived social support indirectly through the other construct during or following intervention. Our examination of two potential treatment mechanisms simultaneously can lead to more informed and targeted approaches for interventions. Specifically, from this approach we examine dynamic relationships among constructs affected by treatment, and how one specific intervention may lead to changes in another construct not directly targeted by the intervention. These questions were addressed in a secondary analysis of 940 primary care patients with anxiety disorders who were randomized to CBT with or without pharmacotherapy (Coordinated Anxiety Learning and Management; CALM) or usual care (UC) for anxiety disorder treatment (Roy-Byrne et al., 2010).

Prior published findings demonstrate greater effects from CALM upon 12- and 18-month anxiety and depression symptoms compared to UC (Craske et al., 2011; Roy-Byrne et al., 2010). One study previously examined perceived social support as a mediator of anxiety and depression symptom change using path analysis in this sample (Dour et al., 2014). Results indicated that perceived social support mediated depression and anxiety symptom change over 18 months, with effects being stronger in CALM compared to UC. However, this analytic approach did not decompose within- and between-person variance, making it unclear whether observed associations were due to stable, between-person differences or dynamic, within-person changes. Within-person changes are particularly important to consider when examining whether intervention produces changes over time beyond influencing average construct levels. The present study builds upon prior work by examining whether within-person changes in anxiety sensitivity relate to within-person changes in perceived social support, and by examining whether these within-person associations are influenced by the CALM intervention.

Our primary hypothesis was that perceived social support changes would negatively predict subsequent anxiety sensitivity changes over an 18-month period, and that CALM (compared to UC) would have indirect effects on decreases in anxiety sensitivity through perceived social support. Our secondary hypothesis was that anxiety sensitivity changes would negatively predict subsequent perceived social support changes over an 18-month period, and that CALM (compared to UC) would have indirect effects on increases in perceived social support through anxiety sensitivity. As a secondary analysis, we explored whether reciprocal associations and indirect effects of CALM on perceived social support increases and anxiety sensitivity decreases would remain when accounting for symptoms of anxiety and depression.

Material and methods

Participants

Participants were 940 adults with diagnoses of panic disorder, generalized anxiety, social anxiety, or posttraumatic stress disorder (Craske et al., 2011; Roy-Byrne et al., 2010). They were referred by primary care physicians, clinic nursing staff, and providers, recruited via advertisements and distribution of promotional materials, or found via brief screenings available over a two-year period with providers in 17 clinics, across four sites: Little Rock, Los Angeles, San Diego, and Seattle. Eligibility criteria were between age of 18–75 years, met diagnostic criteria for at least one of the aforementioned anxiety disorders, and scored ≥ 8 on the Overall Anxiety Severity and Impairment Scale (OASIS) (Norman et al., 2006). Exclusion criteria were ongoing CBT or psychotropic medication, limited fluency in English or Spanish, unstable medical conditions, marked cognitive impairment, active suicidal ideation (intent or plan), psychosis, bipolar I disorder, or substance abuse/dependence other than alcohol or marijuana abuse. See full details in the primary outcomes paper for this randomized clinical trial (RCT) (Roy-Byrne et al., 2010).

Sixteen hundred and twenty individuals consented to be screened for eligibility, of whom 1,062 met criteria and 1,036 gave written informed consent. Because of communication difficulties and dropout, only 1,004 of those individuals were randomized. Given our hypotheses pertaining to the effects of CBT compared to usual care, 43 patients in the CALM arm who received medication only and 21 patients in the CALM arm who did not complete any intervention sessions were excluded from analyses. The resulting sample was 940 patients (CALM n = 439; UC n = 501). Participants were 57.4% White and 70.7% female with an average age of 43.50 (SD = 13.56) years. Participants presented with a variety of anxiety disorder diagnoses (many of which were comorbid), including 74.7% with generalized anxiety disorder, 47.6% with panic disorder, 40.2% with social anxiety disorder, and 17.8% with post-traumatic stress disorder. There was also substantial mood disorder comorbidity in the sample, with 63.3% meeting criteria for major depressive disorder. The majority had received at least 12 years of education and had private insurance. The CALM intervention and usual care groups did not differ in age, gender, race, education, insurance status, or diagnosis (ps ≥ .13). All participants provided written informed consent prior to intervention and assessment onset.

Design

Data were collected within the context of an RCT comparing two treatments (CALM and UC) delivered in a primary care setting. Study procedures complied with all participating institutional review boards. Participants who were referred to the study underwent eligibility screening conducted by specially trained clinicians and anxiety clinical specialists (ACS). ACSs were master-level or recent doctoral-level individuals who had little to no prior CBT experience prior to their roles as behavioral health specialists (Roy-Byrne et al., 2005). After screening, participants were randomized to CALM or UC. Randomization was conducted using an automatic computer program at RAND and stratified by clinic and by presentation of major depressive disorder comorbidity (Roy-Byrne et al., 2010). Participants were assessed at four timepoints, 6-months apart: baseline, 6, 12, and 18 months.

CALM.

In CALM, participants received CBT or CBT and medication management for up to 12 months, although the average number of CBT sessions was 7.47 (SD = 3.60, range: 1–21) over an average of 3.61 months. A total of 43% of participants completed treatment within 3 months and 87% of participants completed treatment within 6 months. The resulting distribution of treatments was: 34% CBT only, 9% medication management only (excluded from the present study), and 57% CBT and medication management (Roy-Byrne et al., 2010). CBT consisted of the following modules: (1) self-monitoring, (2) psychoeducation, (3) fear hierarchy, (4) breathing retraining, (6) cognitive restructuring, (7) exposure and (8) relapse prevention. Some modules were tailored to the most distressing and disabling anxiety disorder (e.g., exposure) and some were generic (e.g., breathing retraining). The ACSs guided participants through CBT with the aid of a computer program and implemented motivational interviewing for engagement or additional cognitive restructuring and behavioral activation for depressed mood when necessary (Craske et al., 2009). PCPs, within whom ACSs had regular contact, prescribed medication, with study psychiatrists providing consultation as deemed appropriate. Initial use of selective serotonin reuptake inhibitors or serotonin and norepinephrine reuptake inhibitors was emphasized. If the patient presented with minimal or no improvement, another antidepressant was prescribed in addition to or instead of the originally prescribed medication in most cases. ACSs provided medication adherence monitoring and counseling in avoidance of caffeine or alcohol, sleep hygiene, and behavioral activities by phone or in person.

Usual Care.

PCPs provided the usual care that would be given to patients with anxiety disorders. This practice included no intervention, medication, counseling, or referral to a mental health specialist.

Measures

All measures were completed at baseline (T1), and 6 months (T2), 12 months (T3), and 18 months (T4) during telephone assessments conducted by interviewers at the RAND Corporation who were blind to treatment condition and timing of assessment.

MOS Social Support survey (MOS; Sherbourne & Stewart, 1991).

This 4-item self-report measure assesses how often each kind of support—companionate, instrumental, informational, emotional—is available to participants if support is needed. Items are rated on a 5-point Likert scale ranging from 1 (none of the time) to 5 (all of the time). The original version was developed to be easily administered to medical care patients. The abbreviated version demonstrates good fit with the original version and good psychometric properties (Gjesfjeld et al., 2008). Of note, the measure used in the present study uses the item “someone to get together with for relaxation” whereas the original version (Gjesfjeld et al., 2008) instead used the item “someone to do something enjoyable with.” High interitem reliability was observed in our sample at baseline (α = .80).

Anxiety Sensitivity Index (ASI; Reiss et al., 1986).

The ASI is a 16-item1 self-report measure that assesses threatening beliefs regarding the social, mental, and physical consequences of anxiety symptoms (Reiss & McNally, 1985). Items are rated on a 0 (very little) to 4 (very much) Likert scale. Examples of cognitive symptoms on this measure include fears of feeling nervous and feeling faint. The ASI has demonstrated good reliability (Peterson & Heilbronner, 1987). High interitem reliability was observed in our sample at baseline (α = .88).

Brief Symptom Index (BSI-18).

The BSI-18 is a self-report measure that assesses psychological symptoms, such as restlessness and spells of panic (Derogatis, 1993). The current study used 12 items comprising the anxiety and somatic subscales but excluded the depression subscale. Items are rated from 0 (not at all) to 4 (extremely). This measure has demonstrated good psychometric properties (Meijer et al., 2011) and good test-retest reliability (Derogatis, 1993). High interitem reliability was observed in our sample at baseline (α = .87).

Patient Health Questionnaire (PHQ-8).

The PHQ-8 is an 8-item self-report scale assesses depressive symptom severity from 0 (not at all) to 3 (nearly every day) (Kroenke et al., 2001). The suicidality item was excluded from the current analyses.2 The PHQ-8 demonstrated high validity in a primary care setting (Kroenke et al., 2007) with excellent test-retest reliability (Löwe et al., 2004). High interitem reliability was observed in our sample at baseline (α = .85).

Data Analysis

We tested cross-lagged paths between perceived social support and anxiety sensitivity as well as indirect paths of intervention on these constructs as part of a single random-intercept cross-lagged panel model (RI-CLPM) (Hamaker et al., 2015). This approach decomposes longitudinal panel data into stable, between-person differences and dynamic, within-person differences, which controls for reverse causality and for between- and within- third variable confounds. For our study, this approach was chosen because (1) cross-lagged models control for previous levels of the predicted variables in the time-lagged effects, (2) it enables modelling of within- and between-person variance in anxiety sensitivity and social support, and (4) allows for flexibility with modeling the effect of intervention on the intraindividual change components and within-person cross-lagged associations.

The primary RI-CLPM of interest (Figure 1) was estimated in Mplus Version 8 (Muthén & Muthén, 1998–2017). Analyses included intervention (CALM = 1, UC = 0) as a between-level predictor, perceived social support (stable between-person levels; dynamic, within-person differences), and anxiety sensitivity (stable between-person levels; dynamic, within-person differences). Variances of observed variables were constrained to zero, allowing all variance to be captured by the within-person latent factors and between-person latent factors. Trait-like, between-person differences in perceived social support and anxiety sensitivity were captured by random intercepts, which were created by loading observed variables at all four timepoints onto the latent factor. These loadings were constrained to one. Age, gender, and ethnicity were modeled as between-person covariates. Correlations among random intercepts were included. To model within-person change in social support and anxiety sensitivity (i.e., intraindividual change), each observed construct was loaded onto its own latent factor.3 These loading factors were also constrained to one. These latent factors (modeling time-specific deviations from an individual’s expected means; Hamaker et al., 2015) were used to model within-time correlations across domains, autoregressive stability over time, and cross-lagged paths. The indirect paths of interest were (1) intervention to T2 perceived social support to T3 perceived social support to T4 anxiety sensitivity, (2) intervention to T2 perceived social support to T3 anxiety sensitivity to T4 anxiety sensitivity, (3) intervention to T2 anxiety sensitivity to T3 anxiety sensitivity to T4 perceived social support and (4) intervention to T2 anxiety sensitivity to T3 perceived social support to T4 perceived social support. The bootstrapped method (1,000 iterations) was employed (Cheung & Lau, 2008). See Supplementary Material for more information on paths modeled and model fit per established cutoffs (Hooper et al., 2008).

Figure 1. Focal RI-CLPM.

Figure 1

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Note. SS = Social Support, observed variable; AS = Anxiety Sensitivity, observed variable; cSS = within-person social support; cAS = within-person anxiety sensitivity; RIss = random intercept for social support; RIAS = random intercept for anxiety sensitivity. The four direct paths from perceived social support at Time T to perceived social support at Time T + 2 and those from anxiety sensitivity at Time T to anxiety sensitivity at Time T + 2 are not depicted to reduce complexity of the figure diagram.

For our secondary analysis, we included symptoms of anxiety and depression in a single model to examine whether reciprocal and indirect associations held when accounting for symptomology.4 This analysis used the primary analysis model as the base and added a random intercept and latent within-person symptom changes for a composite score of anxiety and depression symptoms. Intervention effects on symptoms, autoregressive stability paths within symptoms, and cross-lagged paths including symptoms were accounted for in the model.

Full information maximum likelihood addressed missing data (0% at baseline, 12.2% at 6 months, 18.2% at 12 months, 19.5% at 18 months). The level of statistical significance was p < .05 for cross-lagged paths (two-tailed). Cross-lagged effect sizes were determined per Orth et al. (2022)’s benchmarks: .03 (small), .07 (medium), and .12 (large). To describe effect sizes for indirect intervention effects, ratios of indirect effects over the total effect of intervention to the 18-month outcome of interest were calculated.

Results

Descriptive Statistics

Descriptive statistics by condition are displayed in Table 1 and bivariate correlations for the full sample are displayed in Supplementary Table 1. Social support was significantly higher in CALM than UC at T2, T3, and T4 (all ps < .004), but there were no significant differences in social support levels at T1 (p = .71). Anxiety sensitivity, anxiety symptoms, and depression symptoms were significantly lower in CALM than UC at T2, T3, and T4 (all ps < .001), but there were no significant differences in these constructs at baseline (all ps > .63). Perceived social support demonstrated significant weak negative correlations with anxiety sensitivity as well as significant weak to moderate correlations with anxiety symptoms and depression symptoms across timepoints. Anxiety sensitivity demonstrated significant strong positive correlations with anxiety symptoms and depression symptoms across timepoints.

Table 1.

Descriptive statistics by Condition

CALM Usual Care
Measure M SD M SD
T1 (N = 940)
Social Support 3.16 1.06 3.19 1.08
Anxiety Sensitivity 29.40 13.76 29.89 13.89
Anxiety 16.21 8.93 16.25 8.94
Depression 12.28 6.27 12.47 5.86
T2 (N = 826)
Social Support 3.55 1.06 3.33 1.08
Anxiety Sensitivity 28.66 13.03 23.70 14.60
Anxiety 8.55 7.94 11.53 8.54
Depression 7.00 5.72 9.01 6.21
T3 (N = 769)
Social Support 3.67 1.02 3.40 1.08
Anxiety Sensitivity 16.17 13.04 22.00 14.27
Anxiety 7.60 7.78 10.69 8.55
Depression 7.60 7.78 8.77 6.38
T4 Up (N = 760)
Social Support 3.65 1.09 3.42 1.10
Anxiety Sensitivity 15.78 12.88 20.00 14.21
Anxiety 7.56 8.09 9.69 8.23
Depression 6.07 5.77 7.82 6.07
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Note.

*

p < .001 (pairwise deletion).

Within-Person Cross-Lagged Effects

Table 2 reports statistics for cross-lagged paths and indirect effects estimated in the primary model (Supplementary Table 2 contains autoregressive path, between person effect, and direct intervention effect estimates). Results supported some reciprocal within-person relations between perceived social support and anxiety sensitivity as evidenced by significance and confidence intervals not containing zero. Specifically, there was a large effect of perceived social support increases at T1 predicting anxiety sensitivity decreases at T3 and a large effect perceived social support increases at T2 to anxiety sensitivity decreases at T3.5 There was also evidence of anxiety sensitivity decreases significantly predicting perceived social support increases across time. Specifically, there was a large effect of anxiety sensitivity decreases at T2 predicting perceived social support increases at T3 and a large effect of anxiety sensitivity decreases at T3 predicting perceived social support increases at T4.

Table 2.

Focal RI-CLPM Results

Parameter b Beta SE b/SE p 95% CI Ratios
Cross-Lagged Effects
SS1 → AS2 −2.35 −.16 1.21 −1.94 .052 −4.72, .02 --
SS1 → AS3 −2.59 −.18 .79 −3.29 .001 −4.14, −1.05 --
AS1 → SS2 −.01 −.11 .01 −1.58 .12 −.02, .002 --
AS1 → SS3 −.001 −.01 .004 −.23 .82 −.01, .01 --
SS2 → AS3 −2.47 −.18 .84 −2.94 .003 −4.12, −.82 --
SS2 → AS4 −.41 −.03 .62 −.66 .51 −1.61, .80 --
AS2 → SS3 −.01 −.16 .01 −2.07 .038 −.01, .01 --
AS2 → SS4 −.002 −.03 .01 −.41 .69 −.01, .01 --
SS3 → AS4 .37 .03 .61 .62 .54 −.81, 1.56 --
AS3 → SS4 −.02 −.33 .006 −3.93 .000 −.04, −.01 --
Specific Indirect Effects
Int→ SS2 → ASI3 → ASI4 −.23 −.01 .10 −2.34 .019 −.42, −.04 5.45%
Int→ SS2 → SS3 → ASI4 .02 .001 .04 .61 .54 −.05, .10 −.05%
Int → ASI2 → SS3 → SS4 .01 .003 .01 .85 .39 −.01, .02 1.97%
Int → ASI2 → ASI3 → SS4 .05 .03 .02 3.26 .001 .02, .08 19.29%
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Note. SS = Social support; AS = Anxiety Sensitivity; “Int” = Intervention; Covariates were gender, ethnicity, and age. “RI” = Random Intercept.

Intervention to Within-Person Indirect Effects

There was a significant indirect effect was from intervention to T2 perceived social support increases, to T3 anxiety sensitivity decreases, to T4 anxiety sensitivity decreases. This indirect effect accounted for 5.45% of the effect of intervention on anxiety sensitivity decreases. This indirect effect indicates that, relative to UC, the CALM intervention predicted increases in perceived social support, that in turn predicted decreases in anxiety sensitivity. In addition, there was a significant indirect effect was from intervention to T2 anxiety sensitivity decreases, to T3 anxiety sensitivity decreases, to T4 perceived social support increases. The indirect effect accounted for 19.29% of the effect of intervention on perceived social support increases. This indirect effect indicates that, relative to UC, the CALM intervention predicted decreases in anxiety sensitivity, that in turn predicted increases in perceived social support.

Secondary Analysis

Results from the analysis that included anxiety and depression symptoms in the primary model are reported in Supplementary Table 3. Some reciprocal associations remained significant and were unaffected substantially in magnitude (i.e., remained large cross-lagged effects). However, the path from T2 anxiety sensitivity decreases to T3 perceived social support increases reduced to non-significance and the magnitude of the effect changed from a large cross-lagged effect to a medium cross-lagged effect. Regarding intervention effects, the indirect effect of intervention on T4 anxiety sensitivity changes (b = −.17, 95% CI[-.34, .002], p = .053) reduced to non-significance and accounted for 3.99% of the total effect of intervention on anxiety sensitivity decreases at T4. In addition, the indirect effect of intervention on T4 perceived social support changes reduced to non-significance (b = .03, 95% CI[.00, .05], p = .057) and accounted for 10.76% of the total effect of intervention on perceived social support increases at T4.

Discussion

In this study, we examined reciprocal associations between changes in perceived social support and changes in anxiety sensitivity, as well as indirect effects of intervention on such changes, within the context of a randomized controlled trial for anxiety disorders over 18 months. Within-person results provided some evidence of bidirectional relationships between increases in perceived social support and decreases in anxiety sensitivity over time. Significant indirect effects suggest that increases in perceived social support mediate subsequent anxiety sensitivity decreases, and that decreases in anxiety sensitivity mediate increases in subsequent perceived social support, 12 to 18 months following baseline of evidence-based treatment for anxiety. These effects were not the result of following any treatment given that these effects were stronger in CALM compared to usual care. Secondary analysis results also suggest that reciprocal associations between perceived social support and anxiety sensitivity, as well as the indirect effect on anxiety sensitivity decreases through perceived social support increases, seem to be explained in part by anxiety and depression symptoms.

Within-person effects suggest that changes in these variables, over and above average levels, are significantly associated with one another. These associations are in line with previous research demonstrating significant negative correlations between perceived social support and anxiety sensitivity (e.g., Molero Jurado et al., 2021). However, we add to existing work by demonstrating predictive within-person associations over time. Further, these results are consistent with the idea that perceived social support enhances adaptive reappraisal of symptoms, resulting in decreased anxiety sensitivity. This finding aligns with the notion of interpersonal emotion regulation (Zaki & Williams, 2013) whereby social support assists with stressor reappraisal. Our results extend previous work by applying this framework to stressors of anxiety-related symptoms. Reciprocal association results also support the idea that a decrease in harmful appraisals of anxiety-related sensations may result in more positive perceptions of social support. Future work specifically testing the impact of perceived social support on anxiety sensitivity, and vice versa, is needed to lend more confidence to support these theories.

The indirect effect from intervention at the between-person level to within-person anxiety sensitivity decreases at 18 months suggest that within-person increases in perceived social support throughout or following the CALM intervention may contribute to anxiety sensitivity reduction. Our results demonstrate that CBT with or without pharmacotherapy strengthens the impact of perceived social support upon reappraisal as measured by decreases in anxiety sensitivity. These results add to previous work demonstrating perceived social support as a mediator of symptom outcomes from CALM between-person and within-person (i.e., combined effect) in this sample (Dour et al., 2014) and suggest that perceived social support has a positive benefit on not only symptoms, but also target processes within CBT.

The indirect effect from intervention to perceived social support increases at 18 months suggests that decreases in anxiety sensitivity might lead to subsequent increases in perceived social support, indicating that anxiety sensitivity may function as a mediator of improvement in perceived social support during or following CBT with or without pharmacotherapy for anxiety disorders. Interestingly, the magnitude of the indirect effect of intervention on social support increases (19.29%) seems to be more robust than that on anxiety sensitivity through social support (5.45%), suggesting some specificity in terms of directionality and potency of effects. Previous work has demonstrated that anxiety sensitivity is implicated in the etiology and maintenance of anxiety disorders (Schmidt et al., 2006) and predicts treatment outcomes (Blakey et al., 2017). These results extend previous work by demonstrating that anxiety sensitivity impacts perceived social support, a factor that positively impacts psychopathology and treatment response (e.g., Auerbach et al., 2011; Metts et al., 2021; Zimmermann et al., 2020).

Secondary analysis results suggest that reciprocal effects between perceived social support and anxiety sensitivity as well as indirect effects of intervention were influenced by depression symptoms and anxiety symptoms, indicating a role of psychological distress in these associations. Specifically, intervention effects on reduced anxiety sensitivity and increased perceived social support seem to be in part due to reduced depression and anxiety symptoms. The influence of symptoms on reciprocal associations was less robust compared to symptom influence on indirect effects of intervention. In addition, the influence of symptoms on the indirect effect of intervention on perceived social support appears stronger than that on the indirect effect of intervention on anxiety sensitivity. In line with this influence of symptoms on the effect of intervention on perceived social support, previous research in this sample has demonstrated how changes in perceived social support over time are associated with changes in depression and anxiety following evidence-based intervention (Dour et al., 2014). Nevertheless, our results suggest that there is still some variance to be explained in reciprocal associations and indirect effects of intervention apart from that shared with depression and anxiety symptoms.

The current findings are consistent with prior evidence for CBT to lead to increases in social support (Birkeland et al., 2020; Price et al., 2018) and decreases in anxiety sensitivity (Asnaani et al., 2020; Meuret et al., 2010; Smits et al., 2008). This is the first study to demonstrate that perceived social support may increase through changes in anxiety sensitivity and, conversely, that anxiety sensitivity may decrease through changes in perceived social support. Most prior studies have examined social support independent of anxiety sensitivity (e.g., Cowan et al., 2008; Dour et al., 2014).

Treatment implications from the present findings include specifically targeting social support in cognitive and behavioral intervention strategies in order to bolster reappraisal of anxiety-related sensations. Strategies could include thorough assessment of social support, psychoeducation on the utility of social support for reappraising harmful beliefs about symptoms, challenging perceptions of social support through cognitive restructuring (i.e., looking for evidence to come to more realistic conclusions about support availability), and environmental changes to increase access to adequate support. Findings also speak to the potential value of including a support person in therapy for reappraisal assistance. Studies have explored involving partners in interventions including anxiety disorder treatment to address partner accommodation (e.g., Cerny et al., 1987; Craske et al., 1989) and in post-traumatic stress disorder treatment to decrease symptom severity, enhance relationship functioning, and reduce exposure dropout (Acierno, 2019; Monson & Fredman, 2012) as well as parents assisting with cognitive restructuring techniques in child therapy approaches (Cardy et al., 2020). In addition, there is a growing body of research on the inclusion of peer coaching by community members and volunteers to deliver evidence-based treatment strategies (e.g., Rosenberg et al., 2022). Future RCTs specifically examining interventions targeting social support and anxiety sensitivity are needed to test the proposed benefits on these constructs.

Despite notable strengths, including a large outpatient sample, examining changes in constructs over time, and examining between- and within-person reciprocal and indirect effects, the present study is not without limitations. First, our measure of social support does not indicate the source of support (e.g., partner, friend, therapist) and may not capture the complexity of social support given its rudimentary nature (i.e., indicators of felt closeness, network size, and availability of support). In addition, our measure was subjective and assesses one’s perception of social support. Perceived social support is distinct from enacted social support (Cohen et al., 2000). Future work should include more comprehensive and objective measures of social support, such as an interview conducted by an independent rater that assesses multiple support indicators within interpersonal relationships (Hammen et al., 1987). Our measure of anxiety sensitivity is also limited in that the number of items that compose the subscales is not balanced, which skews the total scores to favor a specific domain depending on how subscales are scored (Taylor et al., 1996; Zinbarg et al., 1997). Given that most patients completed treatment within six months, we lack repeated assessment during active treatment. As such, the timing of assessments makes it more difficult to conclude that changes in social support or anxiety sensitivity happened during, as opposed to during or following, treatment. In addition, despite the strength of comparing the CALM intervention to heterogenous control group, we cannot be certain how the indirect effects of CALM on construct changes compare to the effects of a specific service offered as part of Usual Care. All measures were also self-report questionnaires and common method variance may inflate these associations as a result (Klein et al., 2011). Separately, mechanisms that may account for the observed associations in this study, including adaptive reappraisal, are not directly measured. Further, study results may be limited in terms of generalizability as the sample did not include patients with current suicidality, bipolar disorder, psychosis, and substance abuse or dependence. Anxiety sensitivity has also been found to associate positively with suicidal ideation and suicide risk (Stanley et al., 2018). As such, our exclusion of patients with active suicidal ideation is a limitation and the strength of effects of anxiety sensitivity may have been impacted by excluding actively suicidal patients.

Conclusions

This study found reciprocal effects between perceived social support increases and anxiety sensitivity decreases as well as indirect intervention effects on these constructs over time in patients who underwent evidence-based treatment for anxiety disorders. Results suggest that CBT for anxiety may be enhanced by increasing social support to strengthen adaptive reappraisals during or following treatment and coping with anxiety-related symptoms and that perceptions of support may increase during or after evidence-based treatment because of improved appraisals of somatic symptoms.

Supplementary Material

Supplement: Model Information
Supplement: Table 1
Supplement: Table 2
Supplement: Table 3

Acknowledgements

We thank Dr. Greer Sullivan for her involvement on the CALM clinical trial. We thank Dr. Andy Lin, Dr. Amanda Montoya, and Dr. Craig Enders for statistical consultation. This work was supported by the National Institute of Mental Health [grant numbers U01 MH070018 (Dr. Sherbourne), U01 MH058915 (Dr. Craske), U01 MH057835 (Dr. Stein), U01 MH057858 (Dr. Roy-Byrne), U01 MH070022 (Dr. Greer Sullivan), K24 MH64122 (Dr. Stein), K24 MH065324 (Dr. Roy-Byrne)].

Declaration of Interest Statement

Dr. Roy-Byrne has editorial positions and received royalties from UpToDate and Journal Watch. Dr. Stein has in the past 3 years received consulting income from Acadia Pharmaceuticals, Aptinyx, atai Life Sciences, Boehringer Ingelheim, Bionomics, BioXcel Therapeutics, Clexio, Eisai, EmpowerPharm, Engrail Therapeutics, Janssen, Jazz Pharmaceuticals, and Roche/Genentech. Dr. Stein has stock options in Oxeia Biopharmaceuticals and EpiVario. He is paid for his editorial work on Depression and Anxiety (Editor-in-Chief), Biological Psychiatry (Deputy Editor), and UpToDate (Co-Editor-in-Chief for Psychiatry). He has also received research support from NIH, Department of Veterans Affairs, and the Department of Defense. He is on the scientific advisory board for the Brain and Behavior Research Foundation and the Anxiety and Depression Association of America. Dr. Craske has editorial positions and receives royalties from Behaviour Research and Therapy (Editor-in-Chief) and for UpToDate (Author). She has also received research support from NIMH. All other authors (Brystritsky, Metts, Sherbourne) have no conflicts of interest to disclose.

Footnotes

1

Subsequent versions of the ASI have more items (i.e., the ASI-R contains 36 items and the ASI-3 contains 18 items). The ASI used here is an older version of the gold-standard ASI-3 (Taylor et al., 2007) and has an unbalanced item count across subscales (Zinbarg et al., 1997 scoring: 4 items social concerns, 8 items physical concerns, 4 items mental concerns; Taylor, 1996 scoring: 7 items social concerns, 6 items physical concerns, 3 items mental concerns) skewing the total score more towards specific domains (e.g., physical, social) than the balanced ASI-3 (6 items per subscale).

2

The suicidality item was excluded, as is often done in large studies (Kroenke et al., 2009), given lack of feasibility of immediate risk management and lack of adequate intervention by phone during assessments in the trial.

3

Despite modeling within-person change, the model does not account for individual differences in rate of change during the trial period. Given that the RCT compares an intervention that affects perceived social support and anxiety sensitivity to a control group, detrending variables or accounting for time may distort the nature of the RCT and prevent observing effects of interest (within-person and between person; Wang & Maxwell, 2015).

4

We did not examine social anxiety symptoms as a covariate because it was not a main outcome in the CALM trial and only collected for a subsample of participants.

5

There was also a large effect of T1 perceived social support increases predicting T2 anxiety sensitivity decreases. However, this effect was not statistically significant (p = .052, 95% CI: −4.72, .02).

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Supplementary Materials

Supplement: Model Information
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Supplement: Table 1
NIHMS2192314-supplement-Supplement__Table_1.docx (23.7KB, docx)
Supplement: Table 2
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Supplement: Table 3
NIHMS2192314-supplement-Supplement__Table_3.docx (25.9KB, docx)

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