Journal of Anxiety Disorders 23 (2009) 420–428
Contents lists available at ScienceDirect
Journal of Anxiety Disorders
Anxiety sensitivity and CO2 challenge anxiety during recovery: Differential correspondence of arousal and perceived control Bunmi O. Olatunji a,*, Kate B. Wolitzky-Taylor b, Kimberly A. Babson c, Matthew T. Feldner c a
Department of Psychology, Vanderbilt University, 301 Wilson Hall, 111 21st Avenue South, Nashville, TN 37203, United States University of Texas-Austin, United States c University of Arkansas, United States b
A R T I C L E I N F O
A B S T R A C T
Article history: Received 5 June 2008 Received in revised form 15 August 2008 Accepted 20 August 2008
The relations between changes in arousal and perceived control with changes in anxiety-related distress during a 10-min recovery period after exposure to 10% CO2-enriched air was examined among community participants (N = 47) high (n = 23) and low (n = 24) in anxiety sensitivity (AS). Rate of decline in arousal was significantly positively associated with rate of decline in anxiety among high and low AS participants when controlling for valence. Rate of increase in perceived control was significantly negatively related to rate of decline in anxiety in the high AS group but not in the low AS group when controlling for valence. These findings suggest that associations between arousal, perceived control, and anxiety-related recovery from a panic-relevant episode of abrupt increases in bodily arousal differ as a function of pre-existing fears of anxiety-related symptoms (i.e., AS). Implications of these findings for disorders associated with elevated AS are discussed. ß 2008 Elsevier Ltd. All rights reserved.
Keywords: Anxiety sensitivity Anxiety Habituation Valence Arousal Control
Anxiety sensitivity (AS) is defined as the fear of anxiety-related bodily sensations based on beliefs that these symptoms have harmful physical, psychological, or social consequences (Reiss & McNally, 1985). AS is proposed to arise from the combination of genetic predispositions (Stein, Jang, & Livesley, 1999) and learning experiences that result in the acquisition of beliefs about potentially harmful effects of autonomic arousal (e.g., Stewart et al., 2001). An extensive literature suggests that relatively elevated AS may amplify fearful reactions to various events (e.g., abrupt increases in bodily arousal), thereby placing individuals at risk for the development of anxiety-related conditions, especially panic disorder (e.g., Reiss, 1991; Taylor, 1999). Accordingly, studies have consistently demonstrated a strong, positive relation between AS and panic symptoms (e.g., Apfledorf, Shear, Leon, & Portera, 1994; McNally & Lorenz, 1987). In addition, AS has been shown to predict fearful responding to panic-related events, such as abrupt increases in bodily arousal (Rapee, Brown, Antony, & Barlow, 1992), and AS prospectively predicts the development of panic attacks (Schmidt, Lerew, & Jackson, 1997). Despite ongoing research on AS, there remains a paucity of research identifying individual difference variables and processes that may influence the association between AS and the development of anxiety. The available literature suggests that periods of high
* Corresponding author. E-mail address:
[email protected] (B.O. Olatunji). 0887-6185/$ – see front matter ß 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.janxdis.2008.08.006
arousal are particularly distressing for individuals high in AS. High AS individuals are theorized to perceive physical sensations marked with autonomic arousal as danger signals and, as a result, to experience elevated levels of anxiety during periods of arousal (Schmidt & Zvolensky, 2007). Biological challenge laboratory studies that evaluate fear responding to a wide range of procedures that elicit bodily arousal offer direct evidence for the association between AS and anxious reactivity to arousal (see Zvolensky & Eifert, 2000 for review). For example, laboratory studies indicate that AS is a significant predictor of fear responses to inhalation of carbon dioxide-enriched air (CO2; Zvolensky et al., 2002) independent of trait anxiety among adults (Zinbarg, Brown, Barlow, & Rapee, 2001; Zvolensky, Feldner, Eifert, & Stewart, 2001) and youth (Leen-Feldner, Feldner, Bernstein, McCormick, & Zvolensky, 2005). In addition to the likely interaction between arousal and AS, perceived control also likely interacts with AS to influence anxious responsivity. A large collection of laboratory-based experiments with animals and humans, has found uncontrollable aversive events to have a substantial impact on anxiety (Chorpita & Barlow, 1998; Mineka & Zinbarg, 2006). Accordingly, perceived control may influence association between AS and symptoms of anxiety. In a longitudinal study on military participants undergoing basic training, Schmidt and Lerew (2002) found that high perceived control regarding basic training was protective against the development of panic disorder at 5 months for high AS individuals. A more recent study also found that lower perceived control was associated with a stronger relation between AS and agoraphobia (White,
B.O. Olatunji et al. / Journal of Anxiety Disorders 23 (2009) 420–428
Brown, Somers, & Barlow, 2006). Biological challenge studies have also yielded similar findings. For example, Telch, Silverman, and Schmidt (1996) found that high AS participants in a no-perceived control condition experienced significantly more distress during a caffeine administration challenge than high AS participants in a perceived control condition, whereas no differences in distress were observed between conditions for low AS participants. Laboratory studies employing inhalation of CO2-enriched air have also examined the role of perceived control in anxious responding. For example, patients with panic disorder given the ‘‘illusion’’ they could stop presentation of CO2-enriched air have been shown to report less anxiety compared to persons without the perception of control (Sanderson, Rapee, & Barlow, 1989). Zvolensky and colleagues also have examined the impact of control over the repeated presentation of CO2-enriched air on anxious responding among high AS individuals (Zvolensky, Lejuez, & Eifert, 1998; Zvolensky, Eifert, Lejuez, & McNeil, 1999). This line of research has shown that participants without control report significantly more anxiety and more intense panic experiences compared to those with control. The anxiety-related effect of a lack of control also appears to persist in future situations where a control option is available. Taken together, the available literature suggests that autonomic arousal exerts a significant effect on anxiety-related distress for individuals high in AS. Moreover, for those high in AS, low perceived control results in greater anxiety-related distress compared to higher perceived control. Unfortunately, the question of how the impact of arousal and control on anxiety may differentially relate to AS has been largely investigated in the context of reactivity to various laboratory provocations with very little research examining the effects of these processes on recovery from laboratory provocations.1 The importance of examining less commonly studied facets of emotional responding such as recovery has been previously emphasized (Davidson, 2000; Davidson, Jackson, & Kalin, 2000). However, there is a noticeable absence of systematic research along these lines, which has direct implications for better understanding the role of AS in anxietyrelated phenomena (cf., Feldner, Zvolensky, Stickle, Bonn-Miller, & Leen-Feldner, 2006; Zvolensky et al., 2004). Broadening assessment to recovery periods after a biological challenge may advance our knowledge of how the impact of arousal and perceived control on anxiety-related distress differentially relate to AS across time. As a result of panic-related sensations (e.g., racing heart, lightheadedness, sweating), individuals low in perceived control may begin to experience anxiety about having future panic attacks. Indeed, laboratory studies have shown that perceived control buffers panic-relevant reactivity to biological challenges (Sanderson et al., 1989; Zvolensky, Eifert, & Lejuez, 2001). Comparably, theoretical models also posit that reductions of autonomic arousal may lead to reduced estimates of danger and promote general changes in anxiety (Foa & Kozak, 1986). Together, this work suggests that reductions in anxiety symptoms following a panic-like episode (recovery) may be dependent upon increases in perceived control and decreases in arousal, particularly among high AS individuals. This postulation is in line with existing evidence suggesting that high AS individuals show less habituation to CO2 presentations relative to low AS individuals (Beck, Shipherd, & Zebb, 1996), panic symptoms elicited by biological challenges differ as a function of pre-experimental AS levels (Forsyth, Palav, & Duff, 1999),
1 It should be noted that operational definitions of recovery may vary. For the purpose of the present study, recovery refers to simple habituation of response to an aversive event. Further theoretical and empirical development is needed to determine if strategic processing and evaluation of an aversive event is a necessary condition for recovery.
421
and reductions in arousal correspond to reductions in AS (Schmidt, Trakowski, & Staab, 1997). A better understanding of how arousal and perceived control relate to anxiety-related recovery as a function of AS may prove to be especially informative in the development of panic prevention programs, as such efforts necessitate an understanding of malleable processes that impact individual differences in recovery from acute panic-relevant experiences (Feldner, Zvolensky, & Schmidt, 2004; Feldner, Zvolensky, Babson, Leen-Feldner, & Schmidt, 2008; Schmidt et al., 2007; Zvolensky, Schmidt, Bernstein, & Keough, 2006). Despite considerable research documenting the deleterious effects of high arousal and low perceived control on emotional responding among high AS individuals, surprisingly few published studies have been devoted to improving the understanding of the relationship between these processes during recovery from a theoretically relevant stressor. It was predicted in the present investigation that significant reductions would be observed in anxiety, arousal (self-reported and physiological), uncontrollability, and negative valence during recovery after a CO2 challenge among high and low AS individuals. It was also predicted that reductions in anxiety during recovery would be accelerated by corresponding decreases in arousal and increases in perceived control among high, but not low, AS individuals. Perceived valence (negative–positive) has been proposed to explain significant variance in the emotional meaning of a negative event (Osgood, Suci, & Tannenbaum, 1957). Furthermore, research has shown that negative perceived valence of a CO2 challenge is predicted by anxiety-related variables (Zvolensky, Eifert et al., 2001; Zvolensky, Feldner et al., 2001). Given that reductions in anxiety-related distress during habituation may then be confounded by changes in the perceived valence of the feared context (Foa & Kozak, 1986), the influence of arousal and control on anxiety as a function of AS was examined after controlling for valence ratings. Controlling for the potential confounding effects of changes in valence allows for a relatively stringent test of the specific contributions of changes in arousal and control on anxiety-related distress during habituation. 1. Method 1.1. Participants One hundred and two (44 females) adults (Mage = 23.19 years, SD = 8.2) were recruited via fliers and announcements within a relatively large southern community (i.e., northwestern Arkansas; population of approximately 350,000). Of this sample, 4.9% completed high school, 86.3% partial 4-year college programs, 2.0% a 2-year college program, 2.0% a 4-year college program, 3.9% partial graduate school, and 1.0% completed graduate school. In terms of ethnicity, 95% were Caucasian, 2.5% African-American, and 2.5% Asian. In order to be eligible for this study, participants must have been at least 18 years of age. Participants were excluded based on evidence of: (1) a lifetime history of Axis I psychopathology, including panic attacks or psychotropic medication use; (2) history of significant medical illness, such as cardiovascular, endocrine, pulmonary (including asthma), and gastrointestinal illness; (3) limited mental competency and the inability to give informed, voluntary, written consent to participate; (4) pregnancy; and (5) suicidality. Participants reporting current Axis I psychopathology or suicidality were given referral information when appropriate. The Structured Clinical Interview-Non-Patient Version for the Diagnostic and Statistical Manual (DSM)-Fourth Edition (SCID-IV; First, Spitzer, Gibbon, & Williams, 1995) was used to assess for histories of Axis I psychopathology, suicidality, and medication
422
B.O. Olatunji et al. / Journal of Anxiety Disorders 23 (2009) 420–428
use. A structured interview medical screening was conducted to assess current and/or past physical health conditions including asthma, cardiac problems, and pregnancy. This medical screening has been successfully used in past research using biological challenge paradigms (e.g., Feldner, Zvolensky, Eifert, & Spira, 2003; Feldner et al., 2006). Of interested persons, 13 were excluded due to histories of a medical condition and 54 were excluded on the basis of meeting at least one other exclusionary criterion. A subset of the entire sample was included in the present investigation. Participants were classified into two mutually exclusive groups based on their scores on the Anxiety Sensitivity Index (ASI; Reiss, Peterson, Gursky, & McNally, 1986). The high AS group consisted of those whose scores on the ASI fell in the top 25% of the sample (n = 23) and the low AS group consisted of those whose scores on the ASI fell in the bottom 25% of the sample (n = 24).2 1.2. Pre-challenge measures 1.2.1. Medical Health Screening (MHS) Interview The MHS is a structured clinical interview used to assess current and lifetime medical conditions. This measure has been used successfully in past biological challenge studies (e.g., Feldner et al., 2003, 2006). The interview consisted of 15 two-part openended questions. During part 1, participants are asked whether a ‘‘physician had ever diagnosed them with specific medical conditions’’ (e.g., respiratory, cardiac, gastrointestinal problems). In part 2, participants were asked ‘‘whether they had any reason to believe they had any of these medical conditions even though they had not received a diagnosis by a doctor.’’ Endorsement of any medical condition diagnosed by a doctor, or reason to believe they had a medical condition, resulted in exclusion from the study. Furthermore, any response that included uncertainty (e.g., ‘‘I’m not sure’’) was conservatively managed and resulted in exclusion from the study. 1.2.2. Structured Clinical Interview for DSM-IV (SCID-IV) Lifetime and current Axis I psychopathology (i.e., panic disorder), suicidality, and psychotropic medication use were assessed using the SCID-IV (First et al., 1995). The SCID-NP (non-patient) version was used because subjects were identified as nonclinical and it administered to all participants by a trained advanced graduate student. Adequate reliability of the SCID has been demonstrated (Spitzer, Williams, Gibbon, & First, 1989). 1.2.3. ASI The ASI (Reiss et al., 1986) is a 16-item measure on which respondents indicate on a five-point Likert-type scale (0 = ‘‘very little’’ to 4 = ‘‘very much’’) the degree to which they are concerned about possible negative consequences of anxiety symptoms. The ASI has high levels of internal consistency (average alpha coefficient: 0.84) and good test–retest reliability (r = .70 for 3 years; Peterson & Reiss, 1992). The ASI is unique from, and demonstrates incremental validity to, trait anxiety (McNally, 1996; Rapee & Medoro, 1994). The mean ASI score for individuals with panic disorder is 44.20 (SD = 9.21). The means for nonclinical male and female college students are 15.40 (SD = 8.10) and 20.50 (SD = 10.20), respectively (Reiss et al., 1986). As the sample was screened for current psychopathology, the mean ASI scores for those high in AS (M = 22.30, SD = 9.21) are comparable to nonclinical student sample norms. 2
Although this approach of grouping high/low groups has some limitations, it is consistent with the anxiety sensitivity literature. Furthermore, a grouping of high/ low may better reflect the underlying latent structure of anxiety sensitivity as indicated by preliminary taxometric findings.
1.3. Measures of challenge response 1.3.1. Subjective Units of Distress Scale (SUDS) The SUDS (Wolpe, 1958) was used to measure self-reported anxiety pre- and post-CO2 challenge. Ratings were made on an eight-point Likert-type scale (0 = ‘‘no anxiety’’ to 8 = ‘‘extreme anxiety’’). This measure is well established in biological challenge studies (e.g., Feldner et al., 2003, 2006; Forsyth, Eifert, & Canna, 2000). 1.3.2. Self-Assessment Manikin (SAM) The SAM (Lang, 1980) is a self-report measure used to measure core aspects of affect. Factor analytic research suggests the SAM assesses three dimensions of affective responding: valence (scale 1), arousal (scale 2), and control (scale 3; Lang, 1984). Participants rank each factor on a scale of five human-like figures. Participants rate (current) levels of valence, arousal, and control/dominance by pressing a button below any single computer-presented figure or between any two figures, yielding a possible range of 0–9. Of note, the control scale is reverse scored such that higher scores indicate less control, while low scores indicate relatively greater control. The SAM is a well-established measure with good psychometric properties (Bradley & Lang, 1994) that has been successfully employed in prior laboratory-based biological challenge research (e.g., Feldner et al., 2003, 2006; Zvolensky, Eifert et al., 2001; Zvolensky, Feldner et al., 2001). 1.3.3. Physiological measures A J&J Engineering I-330-C2 system was used to digitally record physiological data on-line at a sample rate of 1024 samples per second across all channels using J&J Engineering Physiolab Software in order to measure skin conductance level (SCL). Skin conductance levels, converted to microsiemens (mS), was obtained using an RV-5 skin resistance lead connected to SE-35 electrodes placed on the middle segment of the middle finger. Indices of SCL were used to measure psychophysiological reactivity to the challenge procedure. 1.4. Physiologic stimulus and gas delivery A physiologic stimulus of 10% CO2-enriched air (10% CO2, 21% O2, and 69% N2) was used. Participants were equipped with a continuous positive pressure Downs C-PAP Mask (Vital Signs Inc., Model No. 9000). For a comprehensive description of the automated apparatus, see Lejuez, Forsyth, and Eifert (1998). Consistent with prior research (Feldner et al., 2006), participants were administered a single 5-min CO2 presentation. 1.5. Apparatus All participants completed the CO2 procedure and structured interviews in a 12 ft 14 ft experimental room containing a chair, desk, and computer. The experimenter was seated in an adjacent room containing a 40-cylinder CO2 tank filled with 10% CO2 compressed air and a J&J Engineering recording device transferring information onto a personal computer. The experimenter was able to continuously monitor and communicate with the participant via a two-way mirror, intercom system, and surveillance video. 1.6. Procedure Participants were first administered the screening portion of the SCID to initially assess for Axis I psychopathology, suicidality, and medication use. Upon meeting initial eligibility requirements, participants attended a laboratory-based individual session. During
B.O. Olatunji et al. / Journal of Anxiety Disorders 23 (2009) 420–428
423
Table 1 Descriptive information and correlations among measures immediately following the CO2 challenge by AS group Anxiety
Anxiety Valence Arousal Control SCL ASI Baseline, mean (SD)
Valence
Arousal
High
Low
High
Low
– – – – – – 2.70 (2.16)
– – – – – – 1.88 (1.96)
.81*** – – – – – 4.17 (1.40)
.54** – – – – – 3.42 (1.53)
High
Control Low
.21 .15
.46* .33 – – – – – – – – 3.87 (1.60) 3.79 (2.00)
Skin conductance
ASI
High
High
High
Low
.62** .79*** .11 – – – 4.39 (1.78)
.33 .06 .45* .06 .37 .08 .23 .02 .44* .03 .37 .07 – .03 .43 .08 – – – .13 – – – – 2.63 (1.58) 12.51 (6.35) 12.11 (6.35) 22.30 (4.75)
Low
Low .30 .48* .22 .08 .08 – 4.13 (1.92)
Note: *p < .05; **p < .01; ***p < .001. High = high AS group; Low = low AS group; SCL = skin conductance level; ASI = Anxiety Sensitivity Index.
this session, participants provided written informed consent that described likely effects of the CO2 (e.g., increased heart rate, shortness of breath). Upon obtaining informed consent, the SCID and medical screening interview were administered to further evaluate exclusionary criteria. Eligible participants completed a battery of self-report measures including the ASI. Upon completion of the questionnaires, participants then completed the CO2 procedure. During the CO2 procedure, individual participants sat in front of a computer in the experimental room. The researcher explained the physiological electrode placement procedures to ensure adequate participant comfort, as well as the use of the C-PAP mask, which was then fit to the participant. All participants were told if they wanted to end the procedure to raise their hand and the researcher would end the experiment without consequences to the participant. A total of 12 participants requested to stop the procedure early. The researcher left the room and began the procedure, continuously monitoring the participant via a two-way mirror, a video surveillance system, and a bi-directional intercom. Participants first completed a 10-min baseline period, which was immediately followed by a 5-min 10% CO2-enriched air administration. The SUDS and SAM were administered via computer at the beginning and end of the baseline period, immediately after the challenge procedure, and every 60 s during the 10-min recovery period. SCL was monitored throughout the procedure. After the challenge was completed, the researcher entered the room and removed the mask and electrodes. All participants were then debriefed and received $20 for their time and participation. 2. Results
high AS group (p’s < .05). In the low AS group, post-CO2 levels of anxiety were significantly correlated with valence, arousal, and skin conductance (p’s < .05). 2.3. Change across time during the post-CO2 challenge recovery To examine several specific research questions concerning decline in anxiety, arousal, uncontrollability, and valence during recovery from the challenge, regression analyses and their followup tests were conducted using hierarchical linear modeling (HLM; see Raudenbush & Bryk, 2002, for reviews). HLM is useful in analyzing repeated measures data (Level 1 data) nested within subjects (Level 2 data; Bryk, Raudenbush, & Congdon, 1996) and has been demonstrated to be more powerful than repeated measures analyses of variance for examining change in repeated measures across time (Muthe´n & Curran, 1997). HLM does not require the assumption of independence of observations, improves the estimate of effects within individual units, and has lower Type I error rates (Raudenbush and Bryk, 2002). Moreover, HLM allows for inclusion of both fixed factors (i.e., independent variable) and multiple random factors (e.g., individuals). It was used in this study to examine change across time with repeated measures for each individual (growth curve modeling). t-tests were used to examine whether y-intercepts of the regression lines were significantly different from zero, and whether differences between two regression lines (e.g., regression line for change in anxiety during recovery for high AS individuals versus regression line for change in anxiety during recovery for low AS individuals) were significant. In this example, ‘‘anxiety’’ (i.e., SUDS anxiety ratings) would be the Level 1 predictor, nested within ‘‘AS group’’ as the Level 2 variable.3
2.1. Participant characteristics
2.2. Post-CO2 challenge group differences
2.3.1. Initial anxiety and slopes Although anxiety immediately following the CO2 challenge significantly differed from zero for both the low AS group [b = 1.23, t(45) = 4.48, p < .001] and the high AS group [b = 2.00, t(45), p < .001], initial anxiety was marginally [t(45) = 1.86, p < .07] higher in the high AS group (see Table 1 for means and standard deviations). Significant decline in anxiety was observed in both the low AS group [b = 0.06, t(45) = 2.59, p < .05] and the high AS
One-way ANOVAs were conducted to assess for differences between high and low AS groups on the relevant measures immediately following the CO2 administration. Significantly lower perceived control [F(1, 45) = 12.97, p < .001] was observed among the high AS group compared to the low AS group. In addition, valence was marginally higher in the high AS group compared to the low AS group [F(1, 45) = 3.12, p = .08]. Table 1 provides the means and SDs for the post-CO2 measures as well as the correlations among these measures for both the high and low AS groups. As shown in Table 1, post-CO2 levels of anxiety were significantly correlated with valence and perceived control in the
3 In HLM, the majority of information for each of these analyses can be gathered with only one model. However, whether changes in the predictor variables are statistically significantly associated with changes in the DV is reported only for the reference group and then the comparison group is simply compared to the reference group. b coefficients in the ‘‘dummy’’ lines represent the difference between the reference and comparison group b coefficients. In order to assess whether these associations are statistically significant for the comparison group (through a t-test), the dummy codes must be reversed so that the comparison group is placed as the reference group in a second model. These t-tests are reported in the text. We chose not to report the full models for the reverse dummy coded analyses because this would have resulted in a significant amount of redundancy.
The high AS group (N = 23) was primarily female (65%), with a mean age of 20.87 (SD = 4.99). The low AS group (N = 24) was primarily male (75%), with a mean age of 27.33 (SD = 11.77). The low AS group was significantly older than the high AS group (t = 2.47, p < .05).
424
B.O. Olatunji et al. / Journal of Anxiety Disorders 23 (2009) 420–428
group [b = 0.08, t(45) = 2.68, p < .01] with no differences in slope of decline between AS groups (p = .65). 2.3.2. Initial arousal and slopes A similar pattern emerged with respect to the activation and subsequent decline of arousal. Initial arousal ratings significantly differed from zero in both the low AS group [b = 3.25, t(45) = 10.55, p < .001] and the high AS group [b = 3.39, t(45) = 14.00, p < .001] with no significant differences between groups (p = .72). As with anxiety decline, the low and high AS groups both showed significant arousal decline across time during the recovery period [b = 0.11, t(45) = 4.10, p < .001 and b = 0.10, t(45) = 3.23, p < .01, respectively], with no differences in slope of decline between the high and low AS groups (p = .94). 2.3.3. Initial perceived control and slopes Perceived control significantly differed from zero in the low AS group [b = 2.50, t(45) = 7.55, p < .001]. However, initial perceived control in the high AS group [b = 3.99, t(45) = 13.60, p < .001] was significantly lower (i.e., higher ratings) than that of the low AS group [t(45) = 3.36, p < .01]. Perceived control significantly increased in both the low AS group [b = 0.07, t(45) = 3.16, p < .01] and the high AS group [b = 0.12, t(45) = 4.03, p < .001] during the recovery period, with no significant differences in slope of recovery between AS groups (p = .16). 2.3.4. Initial valence and slopes Immediately following CO2 administration, those in both the low AS and high AS groups reported valence ratings that significantly differed from zero [b = 3.24, t(45) = 12.44, p < .001 and b = 3.97, t(45) = 17.33, p < .001, respectively]. However, those in the high AS group reported significantly higher initial negative valence than those in the low AS group [t(45) = 2.11, p < .05]. In contrast to the aforementioned variables, valence did not significantly change across time for either group (p’s > .75).
Fig. 1. Relation between anxiety (SUDS) and arousal by AS group during recovery when controlling for valence.
(p = .97). Changes in valence significantly predicted changes in anxiety in the high AS group [b = 0.51, t(45) = 4.73, p < .001] and were significantly more predictive of anxiety decline in this group (p < .001) as compared to the low AS group, in which change across time in valence only marginally predicted change in anxiety [b = 0.09, t(45) = 1.74, p < .09]. Although the slope of decline in valence ratings was statistically more significantly associated with the slope of decline in anxiety in the high AS group, changes in anxiety were independent of the predictor variables (i.e., the collective changes in valence and arousal) in the high AS group [b = 0.05, t(45) = 2.00, p = .05], whereas decline in anxiety was not independent of valence and arousal in the low AS group (p = .56). This suggests that other mechanism not included in the model may be at work with the high AS group. 2.5. AS and association between perceived control and anxiety during the post-CO2 challenge recovery
2.3.5. Initial SCL and slopes Initial SCL following the CO2 challenge was significantly different from zero in both the low AS group [b = 13.03, t(42) = 8.78, p < .001] and the high AS group [b = 11.93, t(42) = 9.08, p < .001], with no differences between AS groups (p = .58). Skin conductance level significantly declined across the recovery period in both the low AS group [b = 0.33, t(42) = 3.31, p < .01] and the high AS group [b = 0.33, t(42) = 4.05, p < .001], with no significant differences in slope of decline between AS groups (p = .94).
A similar two-level HLM was conducted as described above, with perceived control entered as a Level 1 predictor instead of arousal. Fig. 2 shows the relation between perceived control and anxiety for both AS groups after adjusting for valence (full model provided in Table 3). Change across time in perceived control (i.e., increase in perceived control) was not significantly associated with change in anxiety in the low AS group (p = .23). In contrast, the perceived control slope significantly predicted anxiety slope in the high AS group [b = 0.43, t(45) = 4.47, p < .001], such that decreases
2.4. AS and association between arousal and anxiety during the postCO2 challenge recovery
Table 2 Final model examining change in arousal as a predictor of change in anxiety after controlling for valence
A two-level HLM was conducted with anxiety (i.e., SUDS ratings) as the dependent variable. Valence, arousal, and ‘‘minute’’ were all entered as Level 1 predictors, with ‘‘minute’’ indicating the time period across the 10 min of assessment. Group (high versus low AS) was entered as the between-groups Level 2 predictor. A significant effect of ‘‘minute’’ indicates that the dependent variable is at least partially independent of the predictor variables entered into the model (i.e., valence and arousal), as a significant amount of variance in the dependent variable is unaccounted for by the predictor variables. Fig. 1 shows the relation between arousal and anxiety in the high and low AS groups after adjusting for valence (full model provided in Table 2). Rate of decline in arousal ratings was significantly positively associated with anxiety decline in both the low [b = 0.31, t(45) = 3.04, p < .01] and high [b = 0.31, t(45) = 3.44, p < .01] AS groups, with no significant differences between groups
Fixed effect
b
SE
t (df)
Intercept Intercept Dummy
0.12 1.06
0.27 0.41
0.44 (45) 2.58 (45)*
Minute slope Intercept Dummy
0.01 0.03
0.02 0.03
0.60 (45) 0.95 (45)
Valence slope Intercept Dummy
0.09 0.42
0.05 0.12
1.74 (45)t 3.52 (45)***
Arousal slope Intercept Dummy
0.31 0.006
0.10 0.14
3.04 (45)* 0.042 (45)
Note: low AS is the reference group. Intercept = line represents information for reference group; dummy = line represents the difference between the groups. p < .10; *p < .05; ***p < .001.
t
B.O. Olatunji et al. / Journal of Anxiety Disorders 23 (2009) 420–428
Fig. 2. Relation between anxiety (SUDS) and perceived control by AS group during recovery when controlling for valence.
in anxiety over time were associated with increases in perceived control during recovery. As with the previous model, change in valence was marginally associated with anxiety decline slope in the low AS group [b = 0.16, t(45) = 1.94, p < .06] and significantly associated with change in anxiety in the high AS group [b = 0.39, t(45) = 3.46, p < .001]. In the low AS group, the slope of anxiety decline was not independent of the marginally associated slope of decline in valence (p = .13). In contrast, changes in anxiety were marginally independent of changes in valence and perceived control in the high AS group during the recovery period [b = 0.03, t(45) = 1.79, p = .08]. 2.6. AS and association between physiology and anxiety during the post-CO2 challenge recovery A two-level HLM was conducted with anxiety as the dependent variable, SCL, and ‘‘minute’’ as Level 1 predictors, and AS group (high versus low) as the Level 2 predictor. Fig. 3 shows the relation between SCL and anxiety for both AS groups (full model provided in Table 4). The slope of decline in SCL was not significantly associated with slope in anxiety in the low AS group (p = .49). In contrast, slope of decrease in SCL did predict slope of decrease in anxiety in the high AS group [b = 0.16, t(42) = 2.24, p < .05]. Furthermore, the slope of anxiety in the high ASI group was not independent of the skin conductance slope (p = .53). As above, to assess whether this finding continued to emerge after controlling for valence, a second model was created with all of the same variables and the addition of the valence ratings. This Table 3 Final model examining change in perceived control as a predictor of change in anxiety after controlling for valence Fixed effect
b
SE
t (df)
Intercept Intercept Dummy
0.10 1.37
0.50 0.65
0.21 (45) 2.14 (45)*
Minute slope Intercept Dummy
0.04 0.01
0.03 0.03
1.56 (45) 0.36 (45)
Valence slope Intercept Dummy
0.16 0.24
0.08 0.14
1.94 (45)t 1.69 (45)
Control slope Intercept Dummy
0.18 0.25
0.15 0.18
1.22 (45) 1.42 (45)
Note: low AS is the reference group. Intercept = line represents information for reference group; dummy = line represents the difference between the groups. t p < .10; *p < .05.
425
Fig. 3. Relation between anxiety (SUDS) and skin conductance by AS group.
model provided in Table 5 shows the full model. In this model, a different pattern emerged. After controlling for valence, slope of decline in SCL was not associated with anxiety decline for either the low (p = .78) or high (p = .84) AS groups, with no betweengroup differences (p = .95). As with the previous analyses, decreases in valence predicted decreases in anxiety for both the low and high AS groups [b = 0.29, t(42) = 4.76, p < .001 and b = 0.57, t(42) = 4.68, p < .001, respectively], with valence significantly more predictive of anxiety in the high AS group (p < .05). Similar to the pattern observed in the previous analyses, anxiety Table 4 Final model examining change in skin conductance as a predictor of change in anxiety Fixed effect
b
SE
t (df)
Intercept Intercept Dummy
0.50 0.20
0.61 0.88
0.83 (42) 0.23 (42)
Minute slope Intercept Dummy
0.04 0.03
0.03 0.04
1.72 (42)t 0.66 (42)
SC slope Intercept Dummy
0.03 0.13
0.05 0.09
0.70 (42) 1.46 (42)
Note: low AS is the reference group. Intercept = line represents information for reference group; dummy = line represents the difference between the groups; SC = skin conductance. t p < .10.
Table 5 Final model examining changes in skin conductance as a predictor of changes in anxiety controlling for valence Fixed effect
b
SE
t (df)
Intercept Intercept Dummy
0.14 0.54
0.36 0.56
0.40 (42) 0.96 (42)
Minute slope Intercept Dummy
0.05 0.003
0.03 0.03
1.92 (42)t 0.11 (42)
Valence slope Intercept Dummy
0.30 0.28
0.06 0.14
4.76 (42)*** 2.05 (42)*
SC slope Intercept Dummy
0.01 0.003
0.03 0.04
0.28 (42) 0.07 (42)
Note: low AS is the reference group. Intercept = line represents information for reference group; dummy = line represents the difference between the groups; SC = skin conductance. t p < .10; *p < .05; ***p < .001.
426
B.O. Olatunji et al. / Journal of Anxiety Disorders 23 (2009) 420–428
was independent of valence in the high AS group [b = 0.05, t(42) = 2.36, p < .05] and only marginally independent of valence in the low AS group [b = 0.05, t(42) = 1.92, p = .06]. 3. Discussion The present study assessed anxiety, valence, arousal, and perceived control among high and low AS individuals every 60 s during a 10-min recovery period (following a 5 min administration of 10% CO2-enriched air). Significant declines in anxiety, arousal (self-reported and indexed via SCL), and uncontrollability were observed in both the low and high AS groups during the recovery period. However, valence (i.e., how positive or negative) ratings during recovery did not significantly decline for low or high AS participants. These findings suggest that although high and low AS participants generally ‘recovered,’ as indicated via reductions in anxiety ratings, arousal and SCL and increased perceived control post-CO2 administration, they generally did not report changes in pleasantness (or valence) during the 10-min recovery period. It is unclear why significant reductions were observed in anxiety, arousal, and uncontrollability and not valence. It is possible that appraisals of valence during recovery may be intertwined with appraisals of the initial provocation (‘‘it was bad’’), whereas evaluations of anxiety, arousal, and control are perhaps more sensitive to responding after the provocation. Alternatively, participants remained in an experimental setting and were fitted with the C-PAP mask and electrodes throughout the recovery period. Thus, participants may have continued to experience generally negatively valenced affect throughout the procedure, with relatively little change during the recovery period. The present study also examined differences in the association between arousal, control, and anxiety during recovery as a function of AS. As a relatively stringent test of these associations, valence was statistically controlled. Consistent with prior research, decline in arousal was significantly associated with decline in anxiety among low and high AS participants (i.e., Schmidt, Lerew et al., 1997; Schmidt, Trakowski et al., 1997). In contrast, increase in perceived control predicted decreased anxiety during the recovery period in the high AS group but not in the low AS group. Thus, selfreported reductions in autonomic arousal significantly corresponded with self-reported reductions in anxiety independent of pre-existing levels of AS. In contrast, self-reported increase in perceived control significantly corresponded with self-reported reductions in anxiety only among those high in AS. In combination, this pattern suggests that AS may mark a propensity to misinterpret physical arousal as dangerous, but not necessarily a tendency to experience more physical arousal per se (Bouton, Mineka, & Barlow, 2001; Forsyth, Lejuez, & Finlay, 2000). For high AS individuals that do misinterpret bodily sensations, perceived control over those sensations may uniquely influence their ability to cope with the sensations by altering the perceived dangerousness of the sensations which can result in less anxietyrelated distress. This is consistent with theoretical models positing that individuals who perceive limited control over aversive physical or environmental events are at increased susceptibility to anxiety-related distress (Chorpita & Barlow, 1998; Mineka & Zinbarg, 2006), particularly panic disorder (Rapee, Mattick, & Murrell, 1986; Sanderson et al., 1989). An important finding from the present study was that in the model examining the association between arousal and anxiety during recovery and the association between perceived control and anxiety during recovery, valence emerged as a more significant covariate within the high AS group. In fact, the SCL decline during the recovery period was also associated with decreases in anxiety in the high AS group but not the low AS group. However, this effect
became nonsignificant when controlling for valence. This suggests that perhaps for individuals who are fearful of the symptoms of anxiety and experience abrupt increases in bodily arousal, recovery may be influenced by both appraisals of valence (e.g., how bad it was) and perceived control, and it is this combination that determines level of anxiety. Anxiety symptoms experienced during recovery from a panic attack may directly inform expectancies about coping with future panic episodes, which has important implications for the development of panic spectrum problems (Barlow, 2002). There is evidence suggesting that panic attacks that occur in less controllable situations are associated with more anxiety than panic attacks that occur in more controllable conditions (Craske, Miller, Rotunda, & Barlow, 1990). Among those that consider physical symptoms themselves to be dangerous (high AS), persistent concerns about having a future panic attack may be partially attributed to continuing to experience high levels of anxiety during recovery from previous panic episodes coupled with the appraisal that the experience of panic are uncontrollable. Thus, whether the physical sensations experienced during a panic episode and during recovery from that episode among high AS individuals is perceived as controllable may influence the severity of the anxiety attributed to that episode and potentially the extent of avoidance of situations where panic sensations are likely to occur. Future naturalistic work that addresses the relations between avoidance behavior and affective components of responses to panic attacks would help to further inform these theoretical postulations and aid in the development of corresponding prevention programs. Despite significant progress made toward identifying unique risk factors for panic development, there remains a large degree of unexplained variance in understanding the maintenance of panic (Barlow, 2002). Inhalations of high concentrations of CO2-enriched air produce a wide range of autonomic and psychological effects that mirror symptoms associated with panic attacks and reactivity to such challenges prospectively predict panic development (Schmidt & Zvolensky, 2007). Examining the distinctiveness of the relations among response styles that have been identified as potential risk factors for panic development during recovery from inhalation of CO2-enriched air may speak to important maintenance processes. Indeed, the present findings suggest decline in anxiety during recovery was generally independent of the decline in arousal and perceived control (and valence) in the high AS but not in the low AS group. Thus, reductions in levels of arousal appears to be necessary and sufficient for recovery from a biological challenge among those low in AS, whereas reductions in levels of arousal and increases in perceived control appears to be necessary but not entirely sufficient for recovery among those high in AS. These studies may highlight more symmetry among low AS individuals, compared to high AS individuals, in reductions in negative affective systems associated with a panic episode during recovery from that episode. The disconnect between high and low AS individuals in the degree to which arousal, control, and anxiety change jointly during recovery may point to fundamental differences in emotion regulating strategies employed. Insight into such strategies may have important implications for better understanding maintenance processes associated with panic disorder. Panic disorder patients have been found to rigidly attempt to escape, avoid, suppress or otherwise limit the duration of somatic responses (Feldner, Zvolensky, & Leen-Feldner, 2004). However, such inflexible emotion regulation strategies may facilitate anxiety-related responding over time (Olatunji, Forsyth, & Feldner, 2007). In support of this idea, experimental research has shown that suppressing emotional responses to CO2 resulted in
B.O. Olatunji et al. / Journal of Anxiety Disorders 23 (2009) 420–428
greater anxious responding than merely observing such responses among vulnerable individuals (Feldner et al., 2003). One extension of this work has shown that emotion suppression resulted in greater self-reported anxiety and less willingness to participate in a second CO2 trial than emotion acceptance (Levitt, Brown, Orsillo, & Barlow, 2004). More recent work has also shown that emotion suppression during biological challenge resulted in impaired recovery in terms of heart rate among those high in AS (Feldner et al., 2006). The independence of decline in anxiety from decline in arousal and uncontrollability during recovery among high AS individuals may also reflect disproportionate utilization of avoidant-based (versus problem-focused) coping strategies (see Feldner, Zvolensky, & Leen-Feldner, 2004 for review). Studies have shown that individuals with panic disorder perceive avoidance-oriented coping as the most effective way to deal with anxiety sensations (Cox, Endler, Swinson, & Norton, 1992). However, avoidance-oriented coping has also been shown to predict increased physical panic symptoms and anxiety in response to panic-relevant interoceptive arousal (Karekla, Forsyth, & Kelly, 2004; Spira, Zvolensky, Eifert, & Feldner, 2004). This pattern of findings suggests that perhaps during recovery from a panic attack, inflexible emotion regulation strategies such as suppression and avoidance-oriented coping may impede emotional processing that may not allow for habituation to naturally take its course (Foa & Kozak, 1986). By engaging in such maladaptive coping strategies, high AS individuals may not allow themselves the opportunity to learn during recovery that reductions in arousal and increases in perceived control indicate the ‘danger’ has passed. The present findings are largely consistent with contemporary theory highlighting the central role of arousal and low perceived control in the development of panic problems (Barlow, 2002; Bouton et al., 2001). Although the present study represents a novel extension of work examining processes associated with reactivity to panic-related responding to the recovery period, inferences made based on these findings should be considered within the confines of the study limitations. Importantly, the current study examined the association between affect indicators and anxiety during recovery from a biological challenge among healthy individuals. Longitudinal research is clearly needed to determine the extent to which specific patterns of associations in affect among vulnerable individuals (i.e., high AS) during recovery from a panic-relevant episode is central to the development of panic disorder. It is also possible that the observed effects were due to potential gender and age differences in composition of the AS groups. Indeed, the high AS group was predominantly women and the low AS group consisted of mostly men who were significantly older than participants in the high AS group. The predominance of females in the high AS group is consistent with previous findings reporting higher levels of AS among women relative to men (i.e., Stewart, Taylor, & Baker, 1997) and prior work has documented lower AS levels among older adults than in a young adult comparison group (Mohlman & Zinbarg, 1997). However, future research with larger samples will be needed to examine the extent to which gender or age may moderate the association between AS and emotional responding during recovery from a panic-relevant episode. The small sample size and the relatively homogenous nature of the sample are also important limitations of the present study. Although the present findings highlight important differences between high and low AS individuals in the relationship between arousal, control, and anxiety during recovery from a biological challenge, observation of similar findings among patients with panic disorder is needed as this will ultimately bolster confidence in these preliminary findings.
427
References Apfledorf, W. J., Shear, M. K., Leon, A. C., & Portera, L. (1994). A brief screen for panic disorder. Journal of Anxiety Disorders, 8, 71–78. Barlow, D. H. (2002). Anxiety and its disorders: The nature and treatment of anxiety and panic (2nd Ed.). New York: Guilford Press. Beck, J. G., Shipherd, J. C., & Zebb, B. J. (1996). Fearful responding to repeated CO2 inhalation: A preliminary investigation. Behaviour Research and Therapy, 34, 609– 620. Bouton, M. E., Mineka, S., & Barlow, D. (2001). A modern learning theory perspective on the etiology of panic disorder. Psychological Review, 108, 4–32. Bradley, M. M., & Lang, P. J. (1994). Measuring emotion: The self-assessment manikin and the semantic differential. Journal of Behavior Therapy & Experimental Psychiatry, 25, 49–59. Bryk, A. S., Raudenbush, S. W., & Congdon, R. T., Jr. (1996). HLM: Hierarchical linear and nonlinear modeling with the HLM/2L and HLM/3L programs. Chicago, IL: Scientific Software International. Chorpita, B. F., & Barlow, D. H. (1998). The development of anxiety: The role of control in the early environment. Psychological Bulletin, 124, 3–21. Cox, B. J., Endler, N. S., Swinson, R. P., & Norton, G. R. (1992). Situations and specific coping strategies associated with clinical and nonclinical panic attacks. Behaviour Research and Therapy, 30, 67–69. Craske, M., Miller, P., Rotunda, R., & Barlow, D. (1990). A descriptive report of features of initial unexpected panic attacks in minimal and extensive avoiders. Behaviour Research and Therapy, 28, 395–400. Davidson, R. J. (2000). Affective style, psychopathology, and resilience: Brain mechanisms and plasticity.. American Psychologist, 55, 1196–1214. Davidson, R. J., Jackson, D. C., & Kalin, N. H. (2000). Emotion, plasticity, context, and regulation: Perspectives from affective neuroscience. Psychological Bulletin, 126, 890–909. Feldner, M. T., Zvolensky, M. J., Eifert, G. H., & Spira, A. P. (2003). An experimental manipulation of experiential avoidance of emotional responses to a carbon dioxide-enriched air biological challenge. Behaviour Research and Therapy, 41, 403– 411. Feldner, M. T., Zvolensky, M. J., & Leen-Feldner, E. W. (2004a). A critical review of the literature on coping and panic disorder. Clinical Psychology Review, 24, 123–148. Feldner, M. T., Zvolensky, M. J., & Schmidt, N. B. (2004b). Prevention of anxiety psychopathology: A critical review of the empirical literature. Clinical Psychology: Science and Practice, 11, 405–424. Feldner, M. T., Zvolensky, M. J., Stickle, T. R., Bonn-Miller, M. O., & Leen-Feldner, E. W. (2006). Anxiety sensitivity as a moderator of the emotional consequences of emotion suppression during biological challenge: An experimental test using individual growth curve analysis. Behaviour Research and Therapy, 44, 249– 272. Feldner, M. T., Zvolensky, M. J., Babson, K. A., Leen-Feldner, E. W., & Schmidt, N. B. (2008). An integrated approach to panic prevention targeting the empiricallysupported risk factors of smoking and anxiety sensitivity: Theoretical basis and evidence from a pilot project evaluating feasibility and short-term efficacy. Journal of Anxiety Disorders, 22, 1227–1243. First, M. B., Spitzer, R. L., Gibbon, M., & Williams, J. B. W. (1995). Structured clinical interview for DSM-IV Axis I disorders—Non-patient edition. New York: New York State Psychiatric Institute. Foa, E. B., & Kozak, M. J. (1986). Emotional processing of fear: Exposure to corrective information. Psychological Bulletin, 99, 20–35. Forsyth, J. P., Palav, A., & Duff, K. (1999). The absence of relation between anxiety sensitivity and fear conditioning using 20% versus 13% CO2-enriched air as unconditioned stimuli. Behaviour Research and Therapy, 37, 143–153. Forsyth, J. P., Eifert, G. H., & Canna, M. A. (2000a). Evoking analogue subtypes of panic attacks in a non-clinical population using carbon dioxide-enriched air. Behaviour Research and Therapy, 38, 559–572. Forsyth, J. P., Lejuez, C., & Finlay, C. (2000b). Anxiogenic effects of repeated administrations of 20% CO2-enriched air: Stability within sessions and habituation across time. Journal of Behavior Therapy & Experimental Psychiatry, 31, 103–121. Karekla, M., Forsyth, J. P., & Kelly, M. (2004). Emotional avoidance and panicogenic responding to a biological challenge procedure. Behavior Therapy, 35, 725–746. Lang, P. J. (1980). Behavioral treatment and bio-behavioral assessment: Computer applications. In: J. B. Sidowski, J. H. Johnson, & T. A. Williams (Eds.), Technology in the health care delivery system (pp. 119–137). Norwood, NJ: Ablex. Lang, P. J. (1984). Cognition in emotion: Concept and action. In: C. E. Izard, J. Kagan, & R. B. Zajonc (Eds.), Emotions, cognitions, and behavior (pp. 192–228). New York: Cambridge. Leen-Feldner, E. W., Feldner, M. T., Bernstein, A., McCormick, J. T., & Zvolensky, M. J. (2005). Anxiety sensitivity and anxious responding to bodily sensations: A test among adolescents using a voluntary hyperventilation challenge. Cognitive Therapy and Research, 28, 593–609. Lejuez, C. W., Forsyth, J. P., & Eifert, G. H. (1998). Devices and methods for administering carbon dioxide-enriched air in experimental and clinical settings. Journal of Behavior Therapy & Experimental Psychiatry, 29, 239–248. Levitt, J. T., Brown, T. A., Orsillo, S. M., & Barlow, D. H. (2004). The effects of acceptance versus suppression of emotion on subjective and psychophysiological response to carbon dioxide challenge in patients with panic disorder. Behavior Therapy, 55, 747–766. McNally, R. J. (1996). Anxiety sensitivity is distinct from trait anxiety. In: R. M. Rapee (Ed.), Current controversies in the anxiety disorders (pp. 214–227). New York: Guilford.
428
B.O. Olatunji et al. / Journal of Anxiety Disorders 23 (2009) 420–428
McNally, R. J., & Lorenz, M. (1987). Anxiety sensitivity in agoraphobics. Journal of Behavior Therapy & Experimental Psychiatry, 18, 3–11. Mineka, S., & Zinbarg, R. (2006). A contemporary learning theory perspective on the etiology of anxiety disorders: It’s not what you thought it was. American Psychologist, 61, 10–26. Mohlman, J., & Zinbarg, R. E. (1997). Anxiety in the older adult-conceptualization and treatment issues. Poster presented at the annual meeting of the Association for the Advancement for Behavior Therapy. Muthe´n, B. O., & Curran, P. J. (1997). General longitudinal modeling of individual differences in experimental designs: A latent variable framework for analysis and power estimation. Psychological Methods, 2, 371–402. Olatunji, B. O., Forsyth, J. P., & Feldner, M. T. (2007). Emotion regulation: Implications for the shift from normative fear-relevant learning to anxiety-related psychopathology. American Psychologist, 62, 257–259. Osgood, C., Suci, G., & Tannenbaum, P. (1957). The measurement of meaning. Urbana, IL: University of Illinois. Peterson, R. A., & Reiss, S. (1992). Anxiety sensitivity index manual (2nd Ed.). Worthington, OH: International Diagnostic Systems. Rapee, R., & Medoro, L. (1994). Fear of physical sensations and trait anxiety as mediators of the response to hyperventilation in nonclinical subjects. Journal of Abnormal Psychology, 4, 693–699. Rapee, R., Mattick, R., & Murrell, E. (1986). Cognitive mediation in the affective component of spontaneous panic attacks. Journal of Behaviour Therapy & Experimental Psychiatry, 17, 245–253. Rapee, R. M., Brown, T. A., Antony, M. M., & Barlow, D. H. (1992). Response to hyperventilation and inhalation of 5.5% carbon dioxide-enriched air across the DSM-III-R anxiety disorders. Journal of Abnormal Psychology, 101, 538–552. Raudenbush, S. W., & Bryk, A. S. (2002). Hierarchical linear models: Applications and data analysis methods. Thousand Oaks, CA: Sage Publications. Reiss, S. (1991). Expectancy model of fear, anxiety, and panic. Clinical Psychology Review, 11, 141–153. Reiss, S., & McNally, R. J. (1985). The expectancy model of fear. In: S. Reiss & R. R. Bootzin (Eds.), Theoretical issues in behavior therapy. 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. Behaviour Research and Therapy, 24, 1–8. Sanderson, W. C., Rapee, R. M., & Barlow, D. H. (1989). The influence of illusion of control on panic attacks induced by 5.5% carbon dioxide enriched air. Archives of General Psychiatry, 46, 157–162. Schmidt, N. B., & Lerew, D. R. (2002). Prospective evaluation of perceived control, predictability, and anxiety sensitivity in the pathogenesis of panic. Journal of Psychopathology and Behavioral Assessment, 24, 207–214. Schmidt, N. B., & Zvolensky, M. J. (2007). Anxiety sensitivity and CO2 challenge reactivity as unique and interactive prospective predictors of anxiety pathology. Depression and Anxiety, 24, 527–536. Schmidt, N. B., Lerew, D. R., & Jackson, R. J. (1997a). The role of anxiety sensitivity in the pathogenesis of panic: Prospective evaluation of spontaneous panic attacks during acute stress. Journal of Abnormal Psychology, 106, 355–364. Schmidt, N. B., Trakowski, J. H., & Staab, J. P. (1997b). Extinction of panicogenic effects of a 35% CO2 challenge in patients with panic disorder. Journal of Abnormal Psychology, 106, 630–638. Schmidt, N. B., Eggleston, A. M., Woolaway-Bickel, K., Fitzpatrick, K. K., Vasey, M. W., & Richey, J. A. (2007). Anxiety sensitivity amelioration training (ASAT): A long-
itudinal primary prevention program targeting cognitive vulnerability. Journal of Anxiety Disorders, 21, 302–319. Spira, A., Zvolensky, M. J., Eifert, G., & Feldner, M. T. (2004). The relation of anxiety sensitivity and coping strategy to CO2-induced anxious and fearful responding. Journal of Anxiety Disorders, 18, 309–323. Spitzer, R. L., Williams, J. B. W., Gibbon, M., & First, M. B. (1989). User’s guide for the structured clinical interview for DSM-III-R. New York: New York Psychiatric Institute. Stein, M. B., Jang, K. L., & Livesley, W. J. (1999). Heritability of anxiety sensitivity: A twin study. American Journal of Psychiatry, 156, 246–251. Stewart, S. H., Taylor, S., & Baker, J. M. (1997). Gender differences in dimensions of anxiety sensitivity. Journal of Anxiety Disorders, 11, 179–200. Stewart, S. H., Taylor, S., Jang, K. L., Cox, B. J., Watt, M. C., Fedoroff, I. C., et al. (2001). Causal modeling of relations among learning history, anxiety sensitivity, and panic attacks. Behaviour Research and Therapy, 39, 443–456. Taylor, S. (Ed.). (1999). Anxiety sensitivity: Theory, research, and treatment of the fear of anxiety. Mahwah, NJ: Lawrence Erlbaum. Telch, M., Silverman, A., & Schmidt, N. (1996). Effects of anxiety sensitivity and perceived control on emotional responding to caffeine challenge. Journal of Anxiety Disorders, 10, 21–35. White, K. S., Brown, T. A., Somers, T. J., & Barlow, D. H. (2006). Avoidance behavior in panic disorder: The moderating influence of perceived control. Behaviour Research and Therapy, 44, 147–157. Wolpe, J. (1958). Psychotherapy by reciprocal inhibition. Stanford, CA: Stanford University Press. 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. Zvolensky, M. J., & Eifert, G. H. (2000). A review of psychological factors/processes affecting anxious responding during voluntary hyperventilation and inhalations of carbon dioxide-enriched air. Clinical Psychology Review, 21, 375–400. Zvolensky, M. J., Lejuez, C. W., & Eifert, G. H. (1998). The role of control in anxious responding: An experimental test using repeated administrations of 20% CO2enriched air. Behavior Therapy, 19, 193–209. Zvolensky, M. J., Eifert, G. H., Lejuez, C. W., & McNeil, D. W. (1999). The effects of offset control over 20% carbon dioxide-enriched air on anxious responding. Journal of Abnormal Psychology, 108, 624–632. Zvolensky, M. J., Eifert, G. H., & Lejuez, C. W. (2001a). Emotional control during recurrent 20% carbon dioxide-enriched air induction: Relation to individual difference variables. Emotion, 2, 148–165. Zvolensky, M. J., Feldner, M. T., Eifert, G. H., & Stewart, S. H. (2001b). Evaluating differential predictions of anxiety-related reactivity during repeated 20% carbon dioxide-enriched air challenge. Cognition and Emotion, 15, 767–786. Zvolensky, M. J., Goodie, J. L., Ruggiero, K. J., Black, A. L., Larkin, K. T., & Taylor, B. K. (2002). Perceived stress and anxiety sensitivity in the prediction of anxiety-related responding: A multichallenge evaluation. Anxiety Stress and Coping, 15, 211–229. Zvolensky, M. J., Leen-Feldner, E. W., Feldner, M. T., Bonn-Miller, M. O., Lejuez, C. W., Kahler, C., et al. (2004). Emotional responding to biological challenge as a function of panic disorder and smoking. Journal of Anxiety Disorders, 18, 19–32. Zvolensky, M. J., Schmidt, N. B., Bernstein, A., & Keough, M. E. (2006). Risk factor research and prevention programs for anxiety disorders: A translational research framework. Behaviour Research and Therapy, 44, 1219–1239.