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  • Anxiety disorders tend to run in families, but not everyone who has one passes it on to their children. Neither you nor your child is at fault, and an anxiety disorder diagnosis is not a sign of weakness or poor parenting. Anxiety and related disorders in children The term “anxiety disorder” refers to a group of mental.
  • Anxiety is a medical problem when it is persistent, overwhelming, and interferes with your day-to-day functioning. Symptoms of anxiety commonly include unrealistic fears and worries, physical complaints, such as upset stomach or rapid heart rate, and the avoidance of anxiety producing situations. Over 19 million American adults struggle with.

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Anxiety is undoubtedly an unpleasant feeling, but it is something that everyone experiences. Of course, some people experience anxiety more regularly than others, but it is a completely natural experience that is part and parcel of daily life. Due to the unpleasant nature of anxiety, people often worry that experiencing it is harmful.

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Pergamon
Journal of Anxiety Disorders, Vol. 13, No. 6, pp. 575–589, 1999 Copyright  2000 Elsevier Science Ltd Printed in the USA. All rights reserved 0887-6185/99 $–see front matter
PII S0887-6185(99)00024-9
The Efficacy of Habituation in Decreasing Subjective Distress Among High Anxiety-Sensitive College Students Michele M. Carter, Ph.D., Nancy Watt Marin, B.A., and Karen L. Murrell, B.A. American University, Washington, DC, USA
Abstract—While there is mounting evidence that the concept of anxiety sensitivity (AS) is linked to the expression of anxiety (specifically, panic), there has been little research comparing the efficacy of interoceptive exposure alone with interoceptive exposure coupled with cognitive restructuring among high AS participants. The present investigation addressed this issue in a sample of high anxiety-sensitive college students (scores above 29 on the Anxiety Sensitivity Index). Participants were randomly assigned to receive either five consecutive trials of voluntary hyperventilation or five consecutive trials of hyperventilation with cognitive restructuring instructions. It was expected that while repeated hyperventilation would be associated with a significant reduction in selfreported anxiety, catastrophic cognitions, and somatic sensations across trials, the greatest reduction in symptoms would occur with the addition of cognitive restructuring. These predictions were partially supported. As expected, high AS participants evidenced significant decreases in anxiety symptoms when habituation was accompanied by cognitive restructuring. Contrary to predictions, however, interoceptive exposure alone was not effective in reducing anxious symptoms. These results suggest that brief habituation alone may not be an effective strategy for high AS participants and are discussed as providing further support for a cognitive model of anxiety.  2000 Elsevier Science Ltd. All rights reserved. Keywords: Hyperventilation; Habituation; Anxiety sensitivity
In the last decade, the scientific community has amassed considerable evidence regarding the phenomenology of anxiety as well as its successful treatment (Barlow, 1988; Carter & Barlow, 1995; Craske & Barlow, 1993). Partly responsible for the advances made in this area are the variety of safe methods Requests for reprints should be sent to Michele M. Carter, Ph.D., Department of Psychology, American University, 321 Asbury Building, Washington, DC 20016-8062, USA.
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(e.g., sodium lactate infusion, carbon dioxide inhalation, and hyperventilation) found to reliably induce anxiety symptoms among panic disorder patients (Sanderson & Wetzler, 1990). Such methods have allowed the systematic investigation of phenomena related to anxiety, such as the concept of safety (Carter, Hollon, Carson, & Shelton, 1995; Rapee, Telfer, & Barlow, 1991; Schmidt & Telch, 1994), and the import of catastrophic cognitions (Salkovskis & Clark, 1990). Although there is abundant evidence that provocation procedures are effective in inducing anxiety and/or panic among panic-disordered subjects, the exact mechanism of action for this effect remains unclear. Several theorists have posited that certain biological mechanisms are responsible for anxiety generated from challenge procedures. Some recently proposed mechanisms of action include adrenergic dysregulation (Charney, Heninger, & Breier, 1984), chemoreceptor sensitivity (Gorman, Liebowitz, Fyer, Fyer, & Klein, 1986; Margraf, 1993), serotonergic hypersensitivity (Targum & Marshall, 1989), and a false suffocation alarm reaction (Klein, 1993). One alternative theory contends that it is the manner in which the physiological sensations generated by challenge procedures are interpreted that is of primary importance (Barlow, 1988; Beck & Emery, 1985; Clark, 1986, 1993). From a cognitive perspective, the chief concern is not that challenge procedures can produce physiological sensations, but that the sensations are catastrophically misinterpreted (Clark, 1993). Salkovskis and Clark (1990), for example, manipulated subjects interpretations of hyperventilation and found the positive interpretation group experienced hyperventilation as pleasant, whereas the negative interpretation group experienced hyperventilation as unpleasant. Whether the genesis of the anxiety resulting from challenge procedures is primarily biological or cognitive in nature, there is ample evidence that psychological factors such as anxiety sensitivity (AS) can influence one’s response to various challenge procedures. Anxiety sensitivity is typically defined as a concern with the consequences of the physiological, evaluative, and cognitive concomitants of anxiety. Furthermore, it has been implicated as a potentially important moderator of anxious symptoms generated from biological challenge procedures, as well as a key predictor in the etiology and maintenance of anxiety disorders; notably panic disorder (Reiss, 1991; Taylor & Cox, 1998). An individual who exhibits elevated AS will be more likely to interpret symptoms of anxiety (racing heartbeat, sweating palms, dizziness, breathlessness, etc.) as signs of impending doom than someone who shows less sensitivity to their anxious sensations (Reiss & McNally, 1985). Based on a cognitive model of anxiety, individuals who characteristically make catastrophic interpretations of their bodily sensations should be more at risk for engaging in and maintaining a cycle of anxiety (Barlow, 1988). Several studies examining the relationship between AS and response to biological challenges (voluntary hyperventilation, CO2-inhalation, etc.) have
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reported that subjects with elevated anxiety sensitivity consistently evidence greater anxiety during challenge procedures than subjects low in AS (Asmundson, Norton, Wilson, & Sandler, 1994; Rapee & Medoro, 1994; Schmidt, Trakowski, & Staab, 1997; Whittal, Goetsch, & Suchday, 1994). For example, Holloway and McNally (1987) examined the relationship between AS and response to voluntary hyperventilation. Participants in this study were subjected to 5 minutes of voluntary hyperventilation and then asked to report on their sensations and level of subjective anxiety. Individuals with high AS reported more frequent and intense sensations, as well as more subjective anxiety than individuals with low AS. Similarly, Donnell and McNally (1989) used hyperventilation to compare the responses of nonclinical subjects with a history of panic attacks to nonclinical subjects with no history of panic. Individuals with a history of panic and high AS reported more sensations and greater subjective anxiety during hyperventilation than those who were high in AS with no history of panic, or low in AS with or without a history of panic. Furthermore, it was noted that AS was associated with significantly greater distress regardless of panic attack history, suggesting that AS may be a crucial determinant of response to hyperventilation. Rapee, Brown, Antony, and Barlow (1992) had participants hyperventilate for 90 seconds and undergo a 15-minute 5.5% CO2 challenge. The authors examined several variables and determined that the best predictor of response to each challenge procedure was participants’ level of AS. The greater the anxiety over somatic sensations, the greater the level of subjective distress. In a subsequent investigation, Rapee and Medoro (1994) reported that a significant portion of the variance in response to hyperventilation challenge procedures was accounted for by participants’ scores on the Anxiety Sensitivity Index (ASI; Reiss, Peterson, Gursky, & McNally, 1986), rather than scores on a general measure of trait anxiety. As well, there is some indication that repeated exposure to biological challenge procedures generally results in a reduction in responding (Wolpe, 1987). For example, Griez and van den Hout (1983) administered 35% CO2 to a single patient for 5 days, 10 sessions each day. Following 2 days, the authors reported the patient no longer experienced anxiety upon inhalation of the gas mixture. Similar results were reported by van den Hout, van der Molen, Griez, Lousberg, and Nansen (1987) who exposed participants to multiple 1-hour sessions of CO2 inhalations. The authors reported that panic patients evidenced a marked decrease over the course of repeated exposure to CO2. van den Hout and colleagues (1990) required subjects to engage in extreme hyperventilation for 2 minutes, and then kept their pCO2 55% below baseline for 30, 60, and 90 minutes. The authors reported that hyperventilating subjects experienced more anxious symptoms than normal ventilating subjects. They
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further noted that the anxiogenic effect of the continued hyperventilation decreased over time as subjects appeared to habituate to the symptoms (van den Hout, De Jong, Zandbergen, & Merckelbach, 1990). It would seem then, that behavioral methods for reducing anxiety (i.e., interoceptive exposure) would also be effective in reducing anxiety among high AS participants. However, there has been no investigation of the efficacy of interoceptive exposure alone in reducing anxiety symptomatology specifically among high AS participants. The present study was designed to investigate the comparative efficacy of interoceptive exposure alone versus interoceptive exposure in combination with cognitive restructuring in reducing anxiety among high AS participants. It was predicted that while high AS participants would evidence a decrease in subjective distress in either condition, those utilizing cognitive restructuring techniques would evidence the greatest decrease in anxiety symptomatology.
METHOD Participants Participants were 24 undergraduate students at American University who were selected based on their scores on the ASI (.29). Twenty-nine was selected based on the ASI manual indicating the mean for college students is approximately 20, with a standard deviation of 9 (Peterson & Reiss, 1993). We chose students whose scores fell 1 standard deviation above the mean reported by Peterson and Reiss (1993) for college students to represent high AS participants. Each participant received course credit in exchange for their participation. Data from these participants were part of a larger investigation (Carter & Watt, 1999) conducted to compare the efficacy of cognitive restructuring, habituation, and distraction in reducing anxiety symptoms. Only nonoverlapping data relevant to this investigation is reported. Measures Anxiety Sensitivity Index. The ASI (Reiss et al., 1986) is a 16-item question that measures an individual’s fear of the symptoms of anxiety. The ASI has excellent construct validity and adequate test-retest reliability at r 5 .74 (Reiss et al., 1986). Agoraphobics Cognition Questionnaire. The Agoraphobics Cognition Questionnaire (ACQ; Chambless, Caputo, Bright, & Gallagher, 1984) is a 15-item questionnaire measuring the frequency of occurrence of catastrophic thoughts commonly reported by panic patients. The instructions for the original ACQ
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were modified to assess those thoughts occurring during the challenge procedure. The Hyperventilation Questionnaire. The Hyperventilation Questionnaire (HQ; Rapee & Medoro, 1994) is a 33-item questionnaire designed to measure cognitive, affective, and somatic concerns commonly reported during periods of hyperventilation. Participants rate each item from 0 (not at all) to 3 (strongly). This measure has demonstrated internal consistency for each subscale. Cognitive subscale, a 5 .80; Anxiety subscale, a 5 .88; Somatic subscale, a 5 .92. State-Trait Anxiety Inventory-State version. The State-Trait Anxiety Inventory-State version (STAI-S; Spielberger, Gorsuch, & Lushene, 1970; Knight, Waal-Manning, & Spears, 1983) is a 20-item questionnaire designed to assess participants anxiety in the moment. The STAI has demonstrated adequate internal consistency among college populations (a 5 .91) Medical History Questionnaire. The Medical History Questionnaire (MHQ) asked participants to report medication use, as well as past and present medical conditions that may make hyperventilation contraindicated. For example, individuals with a history of respiratory disorders, such as severe asthma, were excluded from the study. Seven participants were excluded for medical reasons, and none were currently taking anxiolytic medications. Procedure Each participant first completed the ASI, HQ, and STAI-S. Participants scoring above 29 on the ASI were then randomly assigned to one of two conditions: (a) repeated hyperventilation, or (b) repeated hyperventilation with cognitive restructuring. Habituation condition. After completing the initial measures, participants were instructed to breathe faster and deeper as if blowing up a balloon for a period of 90 seconds. Consistent with instructions provided by Rapee and Medoro (1994), no information about the effects of hyperventilation were provided to participants at this time except that it was not dangerous and that the effects could be different for each person. To assure all participants inhaled at the same rate, a taped voice repeated the words “in” and “out” at the rate of 45 breaths per minute. Specific instructions were as follows: We will now begin the fast breathing portion of our study. Please stand while I read you the instructions. I am going to play a tape that will tell you how
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fast to breathe. The voice on the tape will say “IN” when you should inhale and “OUT” when you should exhale. You should breathe in and out as hard as you can, like you are blowing up a balloon. You should look like this when you breathe [the experimenter modeled the breathing intensity]. It is important that you breathe deeply and that you breathe when the tape tells you to do so. At the end of 90 seconds the tape will say stop, and at this point you should begin breathing as you normally do. Do you have any questions? Before you begin the fast breathing I will ask you to stand quietly while I take a baseline pulse rate for two minutes. Then you will do the fast breathing exercise for 90 seconds, and when you are finished, I will ask you to remain standing while you fill out more questionnaires and I take another two minute post pulse rate.
Following hyperventilation, participants were allowed 5 minutes rest, part of which was used to complete the HQ, ACQ, and STAI-S for what they experienced during the hyperventilation period. Following completion of the measures, participants were instructed to repeat the hyperventilation procedure four additional times. This procedure was repeated until each participant had completed five trials of hyperventilation. Cognitive restructuring condition. Participants in the cognitive restructuring condition underwent a similar procedure, except that the two most troublesome thoughts from the ACQ were targeted for restructuring. Once identified, the investigators utilized cognitive restructuring techniques consistent with the Panic Control Treatment of Barlow and Cerny (1988). Following each postassessment period, the two most troublesome (severely rated) thoughts were identified by the experimenter for restructuring. The restructuring followed the procedure described by Barlow (1988) and others for the treatment of panic disorder and consisted of having participants evaluate the accuracy of the thoughts in terms of the likelihood the thoughts will come true (probability overestimation), and the catastrophic nature of those thoughts (decatastrophizing). For detailed accounts of cognitive challenging the reader is referred to Barlow and Cerny (1988), Carter and Schultz (1998), and Craske and Barlow (1993). Finally, participants were asked to write down each thought and each challenge that was issued in response. Following the last trial of hyperventilation, all participants were fully debriefed.
RESULTS Demographic Information Demographic information is presented in Table 1. Participants were predominately female with a mean age of 19.11. A chi-square and analysis of variance (ANOVA) indicated that the groups were comparable with respect to gender distribution, x2(1) 5 .36, p 5 .54; and age, F(1, 23) 5 .07, p . .78. An
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THE EFFICACY OF HABITUATION
TABLE 1 Demographic Information by Condition
Habituationa
Gender Female Male Age ASI STAI-S HQ Somatic subscale Cognitive subscale Affective subscale
Cognitive Restructuringa
n
(%)
n
(%)
11 1 M 19.17 34.70 40.50
(91.7) (8.3) (SD) (1.47) (6.06) (8.93)
10 2 M 19.00 32.50 39.08
(83.3) (16.7) (SD) (1.48) (3.96) (7.12)
5.08 1.08 4.66
(3.34) (1.83) (2.93)
4.50 .58 4.33
(1.83) (.66) (1.92)
Note. ASI 5 Anxiety Sensitivity Index; STAI-S 5 State-Trait Anxiety Inventory-State version; HQ 5 Hyperventilation Questionnaire. a n 5 12.
overall multivariate ANOVA (MANOVA) conducted on state anxiety, anxiety sensitivity, catastrophic cognitions, and somatic sensations also indicated no significant group differences, F(5, 18) 5 .11, p 5 .82.
Hyperventilation Manipulation To determine whether hyperventilation was effective in producing anxiety, Group (habituation, cognitive restructuring) 3 Time repeated measures ANOVAs were conducted. These analyses involved comparisons of prehyperventilation scores to scores following the first trial of hyperventilation. Analyses indicated there was a significant effect for time on the STAI, F(1, 22) 5 47.02, p , .001; somatic sensations, F(1, 22) 5 106.08, p , .001; catastrophic cognitions from the HQ, F(1, 22) 5 37.70, p , .001; anxiety from the HQ, F(1, 22) 5 21.23, p , .001. The absence of an interaction or main effect involving group suggests both groups experienced comparable elevations in the symptoms of anxiety. To further assess whether the manipulation was differentially effective between groups, a separate MANOVA was conducted on scores from Trial 1. The results indicated that the initial effect of hyperventilation was equivalent between groups, F(4, 18) 5 .52, p 5 .71.
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M. M. CARTER, N. WATT MARIN, AND K. L. MURRELL
Fig. 1. State-Trait Anxiety Inventory (STAI). State anxiety change across hyperventilation trials. Solid line: cognitive restructuring; broken line: habituation.
Change Across Trials To examine the impact of repeated hyperventilation on the symptoms of anxiety, Group (habituation, cognitive restructuring) 3 Time repeated measures ANOVAs were conducted. For these analyses, time refers to changes from Trial 1 through Trial 5 of hyperventilation. The series of Group 3 Time repeated measures ANOVAs indicated a significant interaction on the STAI-S, F(4, 88) 5 23.80, p , .001; and somatic sensations, catastrophic cognitions, and anxiety as measured by the HQ, F(4, 88) 5 17.62, p , .001; F(4, 88) 5 14.09, p , .001; F(4, 88) 5 22.64, p , .001, respectively. To aid in the interpretation of this finding, separate repeated measures ANOVAs were conducted for each group (see Figures 1–4). Results indicated that the cognitive restructuring group evidenced a significant reduction in state anxiety across trials as measured by the STAI-S, F(4, 44) 5 35.74, p , .001. The cognitive restructuring group also evidenced a significant reduction in somatic sensations, F(4, 44) 5 28.19, p , .001; catastrophic cognitions F(4, 44) 5 19.98, p , .001; and anxiety, F(4, 44) 5 30.95, p , .001, as measured by the respective subscales of the HQ. As depicted in Figures 1 through 4, the results from the analyses of the data from the habituation group were generally nonsignificant. Specifically, there
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Fig. 2. Hyperventilation Questionnaire (HQ). Somatic sensations change across hyperventilation trials. Solid line: cognitive restructuring; broken line: habituation.
was no change in the intensity of catastrophic cognitions, F(4, 44) 5 1.57, p 5 .22; somatic sensations, F(4, 44) 5 .61, p 5 .55; and anxiety, F(4, 44) 5 1.93, p 5 .15, across trials as measured by the respective subscales of the HQ. There was, however, a significant increase in anxiety as measured by the STAI-S, F(4, 44) 5 4.32, p , .05. To further understand this finding, a series of t tests between Trial 1 and subsequent trials were conducted. Results indicated that the significant increase on the STAI-S occurred from Trial 1 to Trial 3, t(11) 5 24.45, p , .01, and from Trial 1 to Trial 4, t(11) 5 22.94, p , .05. No other comparisons were significant, indicating that anxiety rose by the third trial, but had started to decline by the fifth trial. Point of Change In an effort to determine if all symptom indices changed at a similar point, a series of pairwise comparisons with Bonferroni’s correction were conducted on each measure for the cognitive restructuring group. Analyses indicated that participants in this condition evidenced a significant change in state anxiety, t(11) 5 3.51, p , .01; somatic sensations, t(11) 5 5.51, p , .001; anxiety, t(11) 5 6.84, p , .001; and catastrophic cognitions, t(11) 5 12.13, p , .001, as measured by the HQ in the comparison between Trials 1 and 3. As indicated
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M. M. CARTER, N. WATT MARIN, AND K. L. MURRELL
Fig. 3. Hyperventilation Questionnaire (HQ). Catastrophic cognitions change across hyperventilation trials. Solid line: cognitive restructuring; broken line: habituation.
in the figures, subsequent comparisons between Trial 1 and Trials 4 and 5 were also significantly different for the cognitive restructuring group (all ps , .001).
DISCUSSION As expected, the results from this investigation demonstrate that brief cognitive restructuring procedures can be effective in reducing the anxiety experienced from a biological challenge procedure among high AS participants. It was noted that although initial anxiety rose quite sharply, by the third trial participants reported a significant reduction in state anxiety, somatic sensations, and catastrophic cognitions. By the fifth trial, participants had returned to their approximate baseline levels of anxiety symptomatology. This finding is particularly impressive, given these participants were selected to exhibit a propensity toward fear when confronted with a biological challenge. This finding provides further evidence that challenging negative thoughts can have a dramatic impact on anxiety, even over the course of a relatively brief manipulation. There were also several interesting patterns to the data among the cognitive restructuring group. Specifically, all indices of anxiety rose sharply and then declined at similar rates. This is contrary to a general cognitive model
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Fig. 4. Hyperventilation Questionnaire (HQ). Anxiety change across hyperventilation trials. Solid line: cognitive restructuring; broken line: habituation.
concerning the treatment of anxiety. A cognitive model would contend that a change in negative thoughts precedes a decline in anxious symptoms (Barlow, 1988; Clark, 1986), rather than all indices changing simultaneously. It may be that experiencing a reduction in symptoms actually coincides with rather than follows a reduction in catastrophic cognitions. This seems unlikely, since the manipulation directly targeted the negative cognitions. Hence, it seems illogical that a reduction in other indices of anxiety would evidence a change at the same time. More likely, the cognitive challenging procedures were effective in the two targeted thoughts, but the occurrence of additional catastrophic cognitions (not targeted for restructuring) remained elevated. These thoughts may have inflated the overall cognitive score of participants in this condition, and remained unchanged until there was an associated change in state anxiety or somatic sensations. This interpretation is more consistent with a cognitive perspective, and serves to highlight the importance of targeting multiple thoughts for restructuring. Nonetheless, the results clearly provide support for a cognitive model of anxiety in that cognitive restructuring decreased the symptoms associated with anxiety as predicted by theorists such as Barlow (1988) and Beck and Emery (1985). Contrary to predictions, however, there was no support for the position that repeated interoceptive exposure would be effective in reducing the symptoms of anxiety among high anxiety-sensitive participants. In this study, anxiety rose quickly from pre- to post-Trial 1 hyperventilation and remained elevated on most indices for the interoceptive exposure alone group. Notably, on
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M. M. CARTER, N. WATT MARIN, AND K. L. MURRELL
the STAI, participants reported a significant rise in symptoms from Trial 1 to Trial 3 indicating the severity of symptoms continued to rise during the first few trials and did not level off (well above baseline) until latter exposures. While an interesting finding, this is contrary to previous studies that have found a decrease in symptoms from multiple repeated exposures to the symptoms of anxiety (e.g., Beck, Shipherd, & Zebb, 1997). One possible explanation for the discrepancy in findings may be subject selection. In this investigation, we selected those who were elevated on AS, and consequently, those most likely to have a predisposition to experience intense levels of fear when experiencing the symptoms of anxiety. As such, these participants may inherently experience more difficulty habituating to the symptoms of anxiety. Along these lines, it may require significantly more trials of exposure to produce the desired effects than was utilized in this investigation. It should be noted, in fact, that previous investigations demonstrating the efficacy of interoceptive exposure alone have done so with considerably more trials or longer durations of exposure. For example, Beck et al. (1997) utilized extended numbers of trials (n 5 12) within a session and included multiple sessions for each subject to produce habituation. It may simply be that multiple sessions are required to produce the desired impact from interoceptive exposure alone among high AS participants. Consistent with this interpretation, at least one measure (STAI) indicated a downward trend at Trial 5, possibly suggesting the interoceptive exposure alone group may have expereinced a comparable reduction in anxiety had the number of trials been extended. The results from this study, therefore, provide clear evidence that cognitive techniques can be effective in reducing anxiety among high AS participants, even when the exposures are relatively brief in number and duration. Despite these strong findings, there are several limitations that deserve mention. First, we utilized a college sample rather than a clinical one. It is possible that a clinical sample would respond in a different fashion, perhaps with neither brief intervention being effective. Second, we relied on brief exposures, and, as noted above, this may have biased the results against a primarily behavioral account. However, it should be noted that the finding that cognitive strategies are useful in a time frame that straightforward behavioral techniques are not remains important. Third, we used a relatively simple induction procedure. The results may change depending on the method chosen to induce anxiety. Fourth, the sample size is admittedly small (although the findings are robust) and predominantly female. The results await replication with a larger sample that includes a greater proportion of males. Fifth, is the absence of objective measures of hyperventilation (e.g., respiration depth and rate). While participants were instructed to and did follow a tape, it is possible they were not breathing sufficiently deeply to trigger the body’s response to carbon dioxide. The manipulation check indicating a dramatic increase in anxiety from pretrial to Trial 1 of
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hyperventilation, however, argues against this strongly influencing the initial results of this study. It still remains possible, however, that subsequent trials of hyperventilation may have been influenced by differential respiratory depth between groups. Finally, it will be important for future studies to consider the impact of participants’ panic history and/or anxiety disorder diagnosis on the results of similar investigations. Despite these limitations, we found clear support for a cognitive model and little evidence for a behavioral model in reducing anxiety from brief, repeated, hyperventilation challenges. This suggests that cognitive restructuring has the capacity for producing symptomatic change in a relatively short time frame, and argues that such procedures be used in conjunction with interoceptive exposure in the treatment of those with panic-related problems. Future studies may want to consider the above limitations, and to pay particular attention to the process of change (that is, whether cognitions indeed change prior to other symptom domains) from interoceptive exposure as well as other interventions.
REFERENCES Asmundson, G. J. G., Norton, G. R., Wilson, K. G., & Sandler, L. S. (1994). Subjective symptoms and cardiac reactivity to brief hyperventilation in individuals with high anxiety sensitivity. Behaviour Research and Therapy, 32, 237–241. Barlow, D. H. (1988). Anxiety and its disorders: The nature and treatment of anxiety and panic. New York: Guilford Press. Barlow, D. H., & Cerny, J. A. (1988). Psychological treatment of panic. New York: Guilford Press. Beck, A. T., & Emery, G. (1985). Anxiety disorders and phobias. New York: Basic Books, Inc. Beck, J. G., Shipherd, J. C., & Zebb, B. J. (1997). How does interoceptive exposure for panic disorder work? An uncontrolled case study. Journal of Anxiety Disorders, 11, 541–556. Carter, M. M., & Barlow, D. H. (1995). Learned alarms: The origins of panic. In W. O’Donohue, & L. Krasner (Eds.), Theories of behavior therapy: Exploring behavior change (pp. 209–228). New York: Oxford University Press. Carter, M. M., Hollon, S. D., Carson, R., & Shelton, R. C. (1995). Effects of a safe person on induced distress following a biological challenge in panic disorder with agoraphobia. Journal of Abnormal Psychology, 104, 156–163. Carter, M. M., & Schultz, K. M. (1998). Panic disorder with agoraphobia: Its impact on patients and their significant others. In J. Carlson & L. Sperry (Eds.), The disordered couple (pp. 29–56). Bristol, PA: Brunner/Mazel, Inc. Carter, M. M., & Watt, N. M. (1999). Cognitive restructuring facilitates habituation to repeated voluntary hyperventilation among nonclinical participants. Manuscript submitted for publication. Chambless, D. L., Caputo, G., Bright, P., & Gallagher, R. (1984). Assessment of fear in agoraphobics: The Body Sensations Questionnaire and the Agoraphobic Cognitions Questionnaire. Journal of Consulting and Clinical Psychology, 52, 1090–1097. Charney, D. S., Heninger, G. R., & Breier, A. (1984). Noradrenergic function in panic in panic anxiety. Archives of General Psychiatry, 41, 751–763. Clark, D. M. (1986). A cognitive approach to panic. Behaviour Research and Therapy, 24, 461–470. Clark, D. M. (1993). Cognitive mediation of panic attacks induced by biological challenge tests. Advances in Behavior Research and Therapy, 15, 75–84.
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