Psychophysiological analysis of the anxiety model of bulimia nervosa

BEHAVIORTHERAPY 19, 1-9, 1988

Psychophysiological Analysis of the Anxiety Model of Bulimia Nervosa DONALD A . WILLIAMSON, ANTHONY J. GORECZNY, C . J . DAVIS, LAURIE RUOGIERO, AND SANDRA J. MCKENZIE Louisiana State University The anxiety model of bulimia nervosa was tested, using psychophysiological assessment of sympathetic arousal following eating. The experimental design included four groups-bulimia nervosa, obese, normals, and a normal control group who did not eat-assessed prior to and 60 min after eating. Five psychophysiological responses were measured throughout the session: heart rate, peripheral vasomotor response, skin temperature, skin resistance, and forearm electromyogram (EMG). Results produced mixed support for the anxiety model. Heart rate and EMG were both elevated for bulimics after eating. Other responses yielded patterns inconsistent with predictions from the anxiety model. These findings were discussed in terms of the utility of psychophysiological methods, relative to other approaches, for evaluating the anxiety model of bulimia nervosa. Suggestions for future studies in this area of research were also provided.

Several theoretical models of bulimia nervosa have postulated anxiety due to weight gain as a primary factor in the maintenance and development of bulimia nervosa (Mizes, 1985; Rosen & Leitenberg, 1982; Williamson, Prather, Goreczny, Davis, & McKenzie, in press). These models propose that binge eating produces anxiety and worry regarding weight gain and that purgative behavior, e.g., self-induced vomiting or laxative abuse, is motivated by reduction of such anxiety. In support of this model, Rosen and Leitenberg (1982) and Leitenberg, Gross, Peterson, and Rosen (1984) reported increased subjective ratings of anxiety in bulimics who ate rather large test meals and were unable to purge. Leitenberg et al. (1984) also reported heart rate increases after eating in two of the five subjects. In another test of the anxiety model, Rosen, Leitenberg, Gross, and Willmuth (1985) found that in test meals, when they were told that they could not purge, bulimics ate significantly less than normals. Finally, Janata, Klonoff, and Ginsberg (1985), using ambulatory monitoring of heart rate in naturalistic settings, reported increased heart rate after eating but decreased heart rate after purging in bulimics. Thus, psychophysiological, behavioral, and subjective rating data exist to support the anxiety model. Studies Requests for reprints should be addressed to Donald A. Williamson, Department of Psychology, Louisiana State University, Baton Rouge, LA 70803.

1 0005-7894/88/0001-000951.00/0 Copyright 1988 by Association for Advancementof Behavior Therapy All rights of reproduction in any form reserved.

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using psychophysiological methods have been uncontrolled because appropriate control groups have not been included, e.g., a normal control group and a group that does not eat, to control for the physiological effects of eating. Furthermore, earlier studies have used heart rate as the sole psychophysiological measure of anxiety. Our study was designed to overcome the limitations of that previous research. We compared bulimics who frequently purged (bulimia nervosa) with control groups of: 1) obese patients, 2) normals who ate a test meal, and 3) normals who did not eat a test meal. These control groups allowed comparing the psychophysiological reactions of bulimics with the obese group and with normals after eating a test meal. The control group of normals who did not eat were included to evaluate the physiological changes due to eating a test meal. A comprehensive psychophysiological assessment was used, spanning five measures that were recorded throughout the session: heart rate, peripheral vasomotor response (VMR), skin temperature, skin resistance, and forearm electromyogram (EMG). Using this methodology, strong support for the anxiety model would require the finding of generalized sympathetic arousal, i.e., heart rate acceleration, peripheral vasoconstriction, lowered skin temperature, decreased skin resistance, and increased EMG, which was specific to bulimia after eating a test meal.

METHOD Subjects Forty-eight Caucasian women served as research participants with 12 subjects in each of the four groups: 1) bulimia nervosa, 2) obese, 3) normals, and 4) normals who did not eat. The bulimics were diagnosed by clinical interviews: All had been referred for treatment to an eating disorders clinic. They were either community residents (n = 5) or college students (n = 7). To be included in the study, all bulimics met the DSM III criteria for bulimia (American Psychiatric Association, 1980) and reported, in the interview, purging via self-induced vomiting or laxative abuse at least once per week. Thus, bulimic subjects were assembled from consecutive referrals who met the research criteria. The obese group contained university undergraduates who did not meet or approach the DSM III criteria for bulimia but were at least 20% overweight (mean percent overweight = 280/o). The two normal groups were volunteers who were recruited from undergraduate classes in psychology, did not meet the DSM III criteria for bulimia, and had weights from - 10% to + 20070 under/overweight of population norms. Obese patients proved significantly heavier than each of the other three groups (p < .05), which did not differ and were of normal weight levels. No groups differed with regard to height or age. Mean heights ranged from 63.9 in to 64.4 in across groups. Mean ages ranged from 21.5 to 22.0 yrs. Age ranges within groups were also comparable, i.e., 17 to 28 yrs.

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Apparatus and Psychophysiological Recording Psychophysiological measurements were made using a Grass Model 7 polygraph interfaced with Med Associates logic and physiological integration components. All responses were recorded continuously throughout the session and scored in 10-see intervals. Heart rate was recorded using a 7P5 preamplifier with output from the driver amplifier connected to a Med Associates (ANL-300) threshold comparator to count the R wave o f each ventricular contraction. Heart beats were computed every 10 sec. Periods with artifact due to movement were discarded. Electrode placements were two active electrodes on the left arm and right ankle. The ground electrode was placed on the left ankle. Peripheral VMR was recorded from the volar surface o f the thumb o f the left hand using a reflectance photoplethysmograph. A 7P1 preamplifier was used for recording VMR. Peak-to-trough amplitudes o f VMR were sampled and scored by hand at 10-sec intervals. The VMR was then converted to a percentage change score from baseline, i.e., (period minus baseline divided by baseline) × 100. This conversion is necessary since VMR is not an absolute measure and is interpretable only as a relative change from baseline. Skin temperature was measured from the volar surface of the index finger of the left hand using a Yellow-Springs temperature thermistor. It was recorded in degrees centrigrade using a Med Associates (ANL-410) skin temperature module and continually integrated using a Med Associates (ANL-610) analogto-digital integrator. Skin temperature was also displayed on the polygraph using a 7P1 preamplifier. Skin resistance was recorded from the volar surface of the third and fourth fingers of the left hand using two silver-silver/chloride electrodes. It was recorded using a 7P1 preamplifier and was handscored every 10 sec with a sensitivity allowing scoring in increments o f .5 K ohms. Forearm E M G was recorded from the dorsal side of the left forearm using three silver-silver/chloride electrodes. It was recorded using a 7P3 preamplifier with the output integrated using a Med Associates (ANL-610) analog-to-digital converter.

P roced u re Subjects were isolated from the recording equipment in a sound-attenuated chamber. All subjects were seated in a recliner and electrodes and transducers were attached. Following a 10-min adaptation period, subjects who ate the test meals were presented a lunch o f a sandwich, potato chips, and a nondiet drink. This meal consisted of approximately 620 calories. They were instructed to eat the meal in the next 15 min. The experimenter checked with the subject approximately every 5 min to prompt eating if the subject was not complying with the instructions to eat. All subjects ate at least 75°7o o f the meal. Groups did not differ in the amount o f food consumed. The no-eating normal con-

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trois simply sat quietly during this 15-min period. Data during this interval were not scored due to potential artifacts from subjects' movements during eating and arousal due to the experimenter checks. After the eating period, subjects were asked to sit quietly during the next 60 min. This phase allowed for assessment of psychophysiological arousal after eating as predicted by the anxiety model of bulimia, in which bulimics were allowed to eat, but not purge. RESULTS Data were summarized in terms of means in each five-rain period, resulting in 13 periods, i.e., baseline and 12 periods following eating. Psychophysiological data were analyzed using a 4 (Group) × 13 (Period) Multivariate Analysis of Variance (MANOVA). Univariate analysis of variance (ANOVA) was used to analyze changes for each psychophysiological response using the same 4 × 13 design. Interaction effects were further analyzed using orthogonal contrasts of specific response profiles between groups. The MANOVA yielded a statistically significant Group × Period interaction, F (180, 2612) = 1.88, p < .0001. Univariate ANOVAs for each psychophysiological measure also yielded significant Group × Period interactions, Fs (36, 528) as follows: heart rate = 1.73, p < .006; vasomotor response = 1.78, p < .004; skin temperature = 2.99, p < .0001; skin resistance = 1.75, p < .005; forearm EMG = 1.60, p < .02. In order to evaluate baseline differences, groups were compared at baseline for each response. Group differences were found for EMG, F (3, 44) = 3.91, p < .02, but all other analyses proved nonsignificant. Figure 1 presents the findings for heart rate. Both the bulimic and obese groups responded with increased heart rate after eating the test meal. Or-

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FIG. 2. Meanchangesin vasomotorresponse(expressedas percentagechange from baseline) for each group across five-minute intervals. thogonal contrasts of these two patterns of heart rate acceleration showed that they were statistically different (p < .05). The bulimic group responded to eating with immediate heart rate acceleration whereas heart rate in the obese group increased about 30 min after eating. Both the obese and bulimic groups differed from the normal control group, which responded to eating with heart rate deceleration. Differences among the bulimic group and normals who did not eat approached significance (p < .10), using orthogonal contrasts as the statistical test.

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Changes in VMR are illustrated in Figure 2. All groups responded to eating with immediate vasoconstriction. The VMR response of the bulimics differed from all other groups (p < .05). The pattern of the bulimics' VMR response suggested reduced vasoconstriction 20 rain after eating; in contrast, all other groups continued with further vasoconstriction. The VMR response patterns among nonbulimic groups did not differ statistically. Figure 3 presents the results for skin temperature. All groups responded with

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decreased temperature. The most marked reduction in temperature was observed in those normals who did not eat a test meal, and who differed from all other groups (p < .05). Skin temperature in the obese group was higher than for all other groups (p < .05). Bulimics and normals who ate the test meal did not differ. Figure 4 illustrates changes in skin resistance. Bulimics differed from all other groups (p < .05), because the bulimics responded to eating with an immediate increase in skin resistance followed by a decline (see Figure 4). Unlike both normal groups, obese subjects showed decreased skin resistance, and the obese group differed from normals who ate the test meal (p < .05). Figure 5 presents the findings for forearm EMG. In addition to the interaction effect noted earlier, an overall group effect was found F (3, 44) = 2.72, p < .05, but it simply reflected baseline differences, higher in the normal controls, who maintained higher levels of EMG throughout the session. Since a test of the experimental hypothesis involved examination of the interaction effect, orthogonal contrasts were used to compare the response patterns of the four groups across the experimental session: these comparisons showed that the bulimics differed from both normal groups (p < .05), but not from the obese group. Bulimics responded to eating with increased EMG, whereas both normal groups had decreased EMG across the experimental session.

DISCUSSION Our data provide only mixed support for an anxiety model of bulimia. Such a view predicts that bulimics should respond with anxiety, i.e., sympathetic arousal, to eating when given no opportunity to purge. Sympathetic arousal may be defined, for the variables under investigation, as heart rate acceleration, peripheral vasoconstriction, lowered skin temperature, decreased skin resistance, and increased EMG. Examination of Figures 1 through 5 confirms that, with the possible exception of skin resistance, the bulimic group showed this pattern of response. For skin resistance there was an immediate increase after eating followed by a decline. Therefore, the pattern of results was supportive of the anxiety prediction. However, except for heart rate and forearm EMG, normals responded similar to bulimics or, as in the case of VMR and skin resistance, the bulimics responded in a manner suggestive of less anxiety than normals. For heart rate, bulimics, after eating, displayed average heart rate increases of about 4 to 5 beats per min. The obese group showed a heart rate acceleration of like magnitude, but delayed in time. For EMG, a similar pattern was found with bulimics increasing EMG after eating, as did the obese group, but not both groups of normals. It is possible that the bulimics' reduced vasoconstriction after 20 rain may reflect compensatory cardiovascular changes in order to lower blood pressure after sustained heart rate acceleration. In order to evaluate the normal effects of eating upon psychophysiological responses, one must compare normals who ate the test meal with normals who did not eat. Skin temperature was the only variable which was significantly affected by eating, and eating had the effect of producing a relative increase

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in skin temperature, a change that might be predicted from the thermic effect of metabolism (Segal & Gutin, 1983). Therefore, it appears unlikely that the physiological effects of eating could explain the mixed results of our experiment. It is interesting that heart rate, one of the two psychophysiological responses giving positive results, is the only response measured in previous studies (Janata et al., 1985; Leitenberg et al., 1984). Our findings suggest that, although heart rate may be a good psychophysiological indicator of anxiety, it may not reflect generalized sympathetic arousal to eating which is postulated as specific to bulimia. Given these mixed results, what can one conclude about the validity of the anxiety model of bulimia? To answer this question, additional observations made during the study must be considered. One methodological weakness was our failure to include subjective ratings of anxiety as an alternative measure of anxiety. Obtaining this more subjective evaluation might have elucidated whether bulimics perceived greater anxiety than did the other groups. Additional studies reported by Williamson et al. (in press) have suggested such outcomes/results. Despite our failure to include subjective ratings, the impression of the experimenters was that, as a group, the bulimics were more distressed by the experimental protocol: they generally needed more coaxing to eat the test meal and required more extensive debriefing at the conclusion of the experiment. As noted below, these more behavioral indices of anxiety or emotional distress should be studied further. Another possible explanation for our mixed results has been posed by Leitenberg et al. (1984), who reported data suggesting that vomiting may result in decreased autonomic arousability. If this is confirmed, it may be especially difficult to find a generalized sympathetic arousal response in bulimia. Given these considerations and the data presented by others (e.g., Janata et al., 1985, Leitenberg et al., 1984; Rosen & Leitenberg, 1982; WiUiamson et al., in press), it seems probable that there is appreciable validity to the anxiety model of bulimia; however, the question remains, how should such anxiety best be measured? Based upon the results of a series of experiments using similar methodology, Williamson et al. (in press) concluded that there are some limitations in using psychophysiological methods to assess the anxiety model. First, it is often difficult to get bulimics to eat foods which they consider to be "forbidden" (Ruggiero, Williamson, Davis, Schlundt, & Carey, in press), and which might, in theory, arouse more anxiety. Second, presenting either large quantities of food or "forbidden" foods as the test meal may demand considerably more "coaxing" to get bulimics to consume as much as normals. It seems probable that such coaxing may inadvertently cause greater sympathetic arousal and emotion, thus contaminating the results. Third, psychophysiological assessment is quite complex, involving influences due to individual and situational variables (Ray & Raczynski, 1981; Williamson, Waters, and Hawkins, 1986) which create considerable variability in psychophysiological data. One effect of such variability is that only very "strong" effects can be established using this methodology. In the case of testing the anxiety model of bulimia, it is hard to control for other potential influences upon psychophysiological responses, e.g., amount eaten prior to the experimental session and anxiety

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anticipatory to the experimental situation itself. These other "secondary" variables may interfere with the detection of anxiety by psychophysiological methods. Given these considerations, it might be more fruitful to apply other assessment procedures in addition to psychophysiological assessment in order to evaluate the anxiety model. For example, Rosen et al. (1985) used direct behavioral observation of bulimics' eating behavior that supported the anxiety model. Others have reported subjective ratings of anxiety after eating (Leitenberg et al., 1984; Rosen & Leitenberg, 1982; Williamson et al., in press) and data from self-report inventories related to eating different types of foods (Ruggiero et al., in press) which were in support of the anxiety model. Future studies should integrate these other types of assessment with psychophysiological results to evaluate the intriguing anxiety theory of bulimia nervosa.

REFERENCES American Psychiatric Association. (1980). Diagnostic and statistical manual o f mental disorders (3rd ed.). Washington, DC: Author. Janata, J. W., Klonoff, E. A., & Ginsberg, A. J. (1985, November). Psychophysiological arousal and urges to binge and purge in adolescent bulimics monitored in vivo. Paper presented at the annual convention of the Association for Advancement of Behavior Therapy, Houston, TX. Leitenberg, H., Gross, H., Peterson, H., & Rosen, J. (1984). Analysis of an anxiety model in the process of change during exposure plus response prevention treatment of bulimia nervosa. Behavior Therapy, 15, 3-20. Mizes, J. S. (1985). Bulimia: A review of its symptomatology and treatment. Advances in Behavior Research and Therapy, 7, 91-142. Ray, W. J., & Raczynski, J. M. (1981). Psychophysiological assessment. In M. Hersen & A. S. Bellack (Eds.), Behavioral assessment: A practical handbook (pp. 175-214). New York:Pergamon Press. Rosen, J. C., & Leitenberg, J. (1982). Bulimia nervosa: Treatment with exposure and response prevention. Behavior Therapy, 13, 117-124. Rosen, J. C., Leitenberg, H., Gross, J., & Willmuth, M. (1985). Standardized test meals in the assessment of bulimia nervosa. Advances in Behavior Research and Therapy, 7, 181-197. Ruggiero, L., Williamson, D. A., Davis, C. J., Schlundt, D. G., & Carey, Mo P. (in press). Forbidden food survey: Measure of bulimics' anticipated emotional reactions to specific foods. Addictive Behaviors. Segal, K. R., & Gutin, B. (1983). Thermic effects of food and exercise in lean and obese women. Metabolism, 32, 581-589. Williamson, D. A., Prather, R. C., Goreczny, A. J., Davis, C. J., & McKenzie, S. J. (in press). Psychopathology of bulimia. In W. G. Johnson (Ed.) Advances in Eating Disorders, Greenwich, CT: JAI Press, Inc. Williamson, D. A., Waters, W. E, & Hawkins, M. E (1986). Physiologic variables. In R. O. Nelson & S. C. Hayes (Eds.) Conceptual foundations o f behavioral assessment (pp. 297-327). New York: Guilford Press. RECEIVED; December 8, 1986 FINAL ACCEPTANCE: March 24, 1987