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A retrospective study of the learning history origins of anxiety sensitivity

Anxiety sensitivity (AS; the fear of anxiety-related sensations) has been proposed as a risk factor for the development of panic disorder. The present study involved a conceptual replication of Ehlers' (1993, Behaviour Research and Therapy, 31,
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  PERGAMON Behaviour Research and Therapy 36 (1998) 505-525 BEH VlOUR RESE RCH ND THER PY A retrospective study of the learning history srcins anxiety sensitivity Margo C. Watt a *, Sherry H. Stewart a, Brian J. Cox b aDepartment of Psychology Dalhousie University Halifax Nova Scotia Canada B3H 4J1 bDepartment of Psychology University of Manitoba Manitoba Canada Received 3 October 1997 o bstract Anxiety sensitivity (AS; the fear of anxiety-related sensations) has been proposed as a risk factor for the development of panic disorder. The present study involved a conceptual replication of Ehlers' (1993, Behaviour Research and Therapy 31 269-278) study on childhood learning experiences and panic attacks, but also extended her work by investigating the relationship between early learning experiences and the development of AS, in a non-clinical sample. A sample of 551 university students participated in a retrospective assessment of their childhood and adolescent instrumental and vicarious learning experiences with respect to somatic symptoms (i.e. anxiety and cold symptoms, respectively) using an expanded version of Ehler's (1993) Learning History Questionnaire. AS levels were assessed using the Anxiety Sensitivity Index, and panic history was obtained using the Panic Attack Questionnaire, Revised. Contrary to hypotheses, the learning experiences of high AS individuals were not found to be specific to anxiety symptoms, but involved parental reinforcement of sick-role behavior related to somatic symptoms in general. High AS subjects reported both more anxiety and cold symptoms prior to age 18 than individuals with lower levels of AS. In addition, both cold and anxiety symptoms elicited more special attention and/or instructions from parents for high AS individuals to take special care of themselves. These findings are contrasted with the results for self-reported panickers who reported more learning experiences (modeling and parental reinforcement) specific to anxiety-related symptoms, than the non-panickers. The results suggest that higher-than-normal levels of AS may arise from learning to catastrophize about the occurrence of bodily symptoms in general, rather than anxiety-related symptoms in particular. © 1998 Elsevier Science Ltd. All rights reserved. Portions of the results of this study were presented as a new research poster at the 17th National Conference of the Anxiety Disorders Association of America, New Orleans, LA, March 1997. * Author for correspondence. 0005-7967/98/ 19.00 © 1998 Elsevier Science Ltd. All rights reserved. PII: S0005-7967(97) 10029-8  5 6 M.C. Watt et al. / Behaviour Research and Therapy 36 1998) 50~525 I Introduction According to the expectancy model of fear and anxiety proposed by Reiss and McNally (1985; Reiss, 1991), there are three fundamental fears or sensitivities that shape the development, maintenance, and severity of a variety of specific fears: fear of injury/death, fear of negative social evaluation, and anxiety sensitivity (AS). AS is defined as the fear of anxiety-related bodily sensations arising from beliefs that these sensations have harmful somatic, psychological, or social consequences (Reiss, 1991; Stewart et al., 1997). For example, a person with high AS might fear heart palpitations believing they portend a heart attack; fear dizziness believing it to signify insanity; and/or fear trembling in anticipation of rejection or ridicule by others. In contrast, a person low in AS would perceive such sensations to be transient and unpleasant, but otherwise harmless consequences of being in an anxious state. High levels of AS have been shown to be characteristic of the anxiety disorders, particularly panic disorder with or without agoraphobia (e.g. Stewart et al., 1992; Taylor et al., 1992). Prior to the proposition of Reiss expectancy model, many researchers viewed the fear of anxiety as a secondary consequence of panic attacks (e.g. Goldstein and Chambless, 1978). In contrast, expectancy theory posited that AS could precede panic attacks and even serve as a risk factor for the development of panic attacks, panic disorder, and other anxiety disorders (Reiss, 1991). Theorists such as Clark (1986), Reiss and McNally (1985; Reiss, 1991) and Taylor (1995) suggested that AS can contribute to anxiety amplification, which may progress into panic attacks when AS is sufficiently elevated. Consistent with this latter suggestion are the findings of a longitudinal study by Maller and Reiss (1992) which showed that the AS levels of university student Ss in 1984 could predict the number, frequency, and intensity of their panic attacks in 1987. In addition, high AS Ss in 1984 were five times more likely to develop an anxiety disorder during the 3-yr follow-up than low AS Ss. Ehlers (1995) also found that AS levels predict both the maintenance and onset of panic attacks in a 1-yr follow- up study. For example, individuals who experienced their first panic attack during the 1-yr follow-up had shown higher levels of AS at initial assessment than continued non-panickers. Little is known about the srcins of AS. Expectancy theory posits AS to be acquired through learning and/or influenced by genetic factors (Reiss and McNally, 1985). With respect to genetic influences, it has been suggested that people who are highly autonomically reactive may develop greater concerns about becoming anxious, than less reactive people (Reiss and McNally, 1985). There is considerable evidence for genetic influences on normal fear and anxiety, on anxiety disorders in general, and on panic and obsessive-compulsive disorders, agoraphobia, and blood-injury phobia in particular (see review by Marks, 1986). However, little is known about how these genetic factors might operate, or how they might be modified by learning experiences. No research to date has examined the role of learning experiences in contributing to the development of AS. The application of learning theory to the etiology and maintenance of behavior rests on three primary learning mechanisms: (1) classical conditioning, (2) instrumental learning, and (3) vicarious conditioning. Classical conditioning has been implicated in the development of many specific fears. Similarly, it could be speculated that AS might develop through classical conditioning, or more specifically, interoceptive conditioning . If bodily arousal symptoms, such as dizziness or heart palpitations (CS), are paired with some  M.C. Watt et al. / Behaviour Research and Therapy 36 1998) 505-525 5 7 intrinsically frightening event, such as an unexpected panic attack coming out of the blue (UCS), then an individual might learn to fear (CR) the occurrence of bodily arousal symptoms in the future (Forsyth et al., 1996; Rapee, 1987). However, in a study of 425 college students, Donnell and McNally (1990) found that two-thirds of the high AS students had never experienced a panic attack (see also Cox et al., 1991), arguing against classical conditioning as the sole explanation for the development of AS, and standing in contrast to notions that AS is merely a secondary consequence of panic attacks (e.g. Goldstein and Chambless, 1978). With instrumental learning, also referred to as operant conditioning, the individual s behavior is instrumental in getting something he/she wants (i.e. positive reinforcement) or removing something he/she does not want (i.e. negative reinforcement). Reinforcement increases the probability that the behavior will occur in the future. In contrast, punishments (aversive consequences) decrease the probability that a behavior will occur again in the future. Instrumental learning could contribute to the development of AS if a child s display of, or complaints about, anxiety symptoms were rewarded in some way, such as being allowed to miss school (i.e. negative reinforcement) or being afforded special attention (i.e. positive reinforcement). If, on the other hand, a child s anxiety displays/complaints were met with parental disapproval or punishment, the symptoms would more likely be suppressed in the future, thereby theoretically contributing to lower AS levels. Vicarious conditioning or observational learning refers to learning by watching others (Bandura, 1986). According to Bandura, learning is not dependent on direct reinforcement--it typically occurs by observing the consequences of models behavior. Information acquired through vicarious learning can be conveyed through either physical demonstration or verbal transmission. Observational learning could account for the development of AS if a parent modeled and was rewarded for, fear reactions to their own anxiety-related symptoms in the presence of their child, and/or verbally transmitted their beliefs about the harmfulness of these symptoms to the child. Consistent with this possibility, Donnell and McNally (1990) found that a family history of panic was associated with elevated AS levels among their student sample, suggesting that high AS may develop as a consequence of children being exposed to parental models who have displayed fear responses to their own (the parents ) anxiety experiences. Other studies have supported the roles of vicarious and instrumental learning in contributing to the development of sick-role behaviors. Turkat (1982) found that the frequency of hospital stays and illness-related work absence in adult diabetics correlated with patients retrospective reports of their degree of childhood exposure to parents not completing their (the parents ) housework, canceling other activities, and/or receiving special attention or support when ill. In a retrospective study involving 351 nurses and schoolgirls, Whitehead et al. (1986) found a certain correlational specificity relating the current symptoms reported by the Ss to specific childhood and adolescent instrumental and vicarious learning experiences. Those daughters who had been rewarded for adopting sick-role behavior with respect to menses, or whose mothers had modeled distress in response to their own (the mothers ) menses, reported significantly more menstrual symptoms, sought more medical help for their menstrual discomfort, and more frequently missed work/school due to menstrual symptoms. Similarly, those daughters encouraged to adopt sick-role behavior for colds, or who grew up in the presence of a chronically  5 8 M.C. Watt et al. / Behaviour Research and Therapy 36 1998) 505-525 ill family member, reported more medical visits and work/school absenteeism for non- gynecological symptoms. Daughters reports of their mothers behavior were validated by the mothers responses to the Learning History Questionnaire (LHQ) items (Whitehead et al., 1986). Ehlers (1993) used a modified version of Whitehead et al. s (1986) LHQ to explore the relationship between retrospectively reported childhood and adolescent learning experiences and panic attack development. LHQ scales were reworded to target anxiety-related somatic symptoms relevant for panic disorder patients (e.g. dizziness, shortness of breath, racing heartbeat). Whitehead et al. s (1986) scale assessing parental encouragement of sick-role behavior related to colds was retained as a comparison scale on which panickers were not expected to differ from normal controls, since previous research had shown that panic patients do not rate non-anxiety related bodily symptoms (e.g. toothache, itching) as more threatening than controls (Ehlers, 1991). Ehlers (1993) S groups included panic disorder patients and infrequent panickers, patients with other anxiety disorders, and normal controls. Ehlers found that the panickers and other anxiety disorder patients differed from normal controls in their self-reported learning experiences in childhood and adolescence with regard to anxiety symptoms. All anxiety groups reported more childhood instrumental and vicarious learning experiences related to parental and personal anxiety symptoms than normal controls. In contrast, no differences between the anxiety groups vs normal controls were found in reported parental encouragement of sick-role behavior related to childhood cold symptoms, indicating a specificity in learning experiences relevant to anxiety symptoms (cf. Whitehead et al., 1986). Ehlers (1993) also found that all anxiety groups compared to controls, reported more frequent exposure to parental uncontrolled behavior (e.g. due to drunkenness or anger)--a category of learning experiences included due to clinician impressions of a relation between anxiety patients concerns about loss of control and parental alcoholism (Ehlers, 1993). Panickers reported significantly more observations of parental sick-role behavior related to parental anxiety symptoms, and a greater number of chronically ill family members, than patients with other anxiety disorders and normal controls. Ehlers (1993) also examined the relations between specific childhood learning experiences and the degree of fear of fear in the panickers. Correlations were performed between scores on the LHQ scales and scores on two fear of fear measures: the Body Sensations Questionnaire (BSQ) and the Agoraphobic Cognitions Questionnaire (ACQ) (Chambless et al., 1984). Scores on all the LHQ scales, save the scale assessing parental encouragement of sick role behavior in response to the child s cold symptoms, correlated significantly with panickers scores on the BSQ and/or ACQ. Thus, Ehlers preliminary work suggests significant associations between levels of fear of fear in adulthood, and anxiety-specific learning experiences in childhood and adolescence. However, Ehlers examined these relations only in panic disorder patients and infrequent panickers, leaving the question open as to whether similar relations would be observed in non- clinical Ss. Moreover, it remains unknown as to whether these relations would persist using a more commonly-used measure of fear of fear (Cox, 1996a)--the Anxiety Sensitivity Index (ASI: Peterson and Reiss, 1992). Of further interest is whether the learning history srcins of a proposed risk factor for panic disorder (i.e. AS; Reiss, 1991) would be the same as those identified for panickers (Ehlers, 1993). The present study involved a retrospective assessment of university students childhood and adolescent learning experiences as a means of discerning the relationship between these  M.C. Watt et al. / Behaviour Research and Therapy 36 1998) 505-525 509 experiences and the development of AS in a non-clinical sample. We predicted that students with high levels of AS would report more parental modeling and encouragement of sick-role behavior in regard to anxiety symptoms than students with low and moderate levels of AS. We did not expect to find differences between high AS vs low or moderate AS Ss with respect to learning experiences associated with childhood cold-related symptoms because high AS young adults, by definition, are concerned with a specific set of arousal-related bodily symptoms (e.g. racing heartbeat, dizziness, shortness of breath). We further expected that chronic illnesses in family members and parental uncontrolled behavior would present more frequently in families of high AS, rather than lower AS, students since high AS individuals are afraid of serious illness consequences of anxiety, and of losing control over their behavior when anxious (Reiss, 1991; Stewart et al., 1997). In addition, we attempted to validate Ss' accounts of their childhood learning experiences by inviting parents to complete comparable versions of the LHQ. Using Ehlers' (1993) version of the LHQ, Jager (1988) found moderate to high positive correlations between the responses of 16 infrequent panickers and those of their parents. 2 Method 2.1. Participants Five-hundred and fifty-one undergraduate students at Dalhousie University (N = 238) and the University of Manitoba (N -- 313) served as participants. The mean (SD) ASI score for the entire sample was 18.1 (9.1). l A high AS (HAS) group (N = 88) was created by selecting those students scoring at least one SD above the sample mean on the ASI (> 27). A low AS (LAS) group (N = 88) was created by selecting those students scoring at least one SD below the ASI sample mean (< 9). In addition, a moderate AS (MAS) group (N = 112) was created by selecting a comparably-sized group consisting of all those Ss whose ASI scores closely surrounded the sample mean (+0.25 SD; ASI range, 16-20). An MAS comparison group was included in addition to the LAS group due to suggestions that LAS individuals form not just a good group against which to contrast HAS individuals but, in fact, appear to be an extreme group that often behave/score differently than MAS individuals (e.g. Cox, 1996b; Shostak and Peterson, 1990; Stewart and Pihl, 1994). The mean (SD) ASI scores of the HAS, MAS, and LAS groups were 33.1 (6.4), 17.9 (1.4), and 6.3 (2.3), respectively. Ninety parents (73 mothers; 17 fathers) of the Dalhousie students (i.e. 38 ) also participated in the project by filling out a parent version of the LHQ. 2 Students from the University of Manitoba reported higher ASI scores overall than Dalhousie University students (Ms (SDs) = 19.5 (9.1) vs 16.2 (8.6), respectively; t(541) = 4.29, P < 0.001; two-tailed test). Although statistically significant, the difference was not considered to be of practical significance since both means were well within the range of normative ASI means for university samples (Peterson and Reiss, 1992). Consequently, the two samples were combined for all further analyses involving ASI scores. 2 The mean ASI score of Dalhousie students whose parents completed the questionnaire did not differ from the mean ASI score of the remaining Dalhousie students (Ms (SDs)= 16.8 (8.9) vs 15.8 (8.4), respectively; t(229) = 0.61, NS), suggesting that the 90 parent-child validation pairs were representative of the larger sample of Dalhousie students.
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