Taste aversion therapy with alcoholics: Techniques and evidence of a conditioned response

TASTE

AVERSION THERAPY WITH ALCOHOLICS: TECHNIQUES AND EVIDENCE OF A CONDITIONED RESPONSE TIMOTHY B. BAKER

and DALE S. CANNON

Alcohol Treatment Unit, Salt Lake Veterans Administration (Received

26 September

Hospital

1978)

Summary-Aversion therapy for alcoholism is based on the notion that aversion conditioning produces a conditioned response (CR) to alcohol that is antagonistic to subsequent alcohol ingestion. This study reports the first experimental evidence that aversion conditioning produces a CR to the taste and smell of alcohol. Two patients were given taste aversion therapy for alcoholism. While medically conservative, the taste-aversion procedures produced profound malaise and reliable emesis shortly after patients began drinking alcoholic beverages. Behavioral. attitudinal and psychophysiological indices all reflected the acquisition of an alcohol aversion as a function of conditioning.

Experimental reports of the effectiveness of electric shock aversion therapy for alcoholics have not been encouraging (Elkins, 1975; Hallam, Rachman and Falkowski, 1972; MacCulloch er al., 1966; Miller et al., 1973; Wilson, Leaf and Nathan, 1975; Wilson and Tracey, 1976). This may be because taste is more readily associated with illness than with electric shock (Garcia, Hankins and Rusiniak, 1974; Seligman, 1970). In support of this notion, Lamon, Wilson and Leaf (1977) found in an analogue study with humans that pseudocoriolis-induced nausea was more effective than shock in decreasing nonalcoholic beverage consumption. While theoretical support for taste aversion therapy for alcoholism may be relatively recent, non-experimental reports of the technique’s clinical efficacy are among the oldest in the behavior therapy literature (Kant, 1945; Lemere and Voegtlin, 1950; Thimann. 1943). These positive clinical reports encourage further evaluation of taste aversion therapy, but methodological weaknesses [e.g. no control groups, no verification of self-report data, cf. Franks (1966)] limit confidence in their results. Recently, the first truly experimental evaluative study of taste aversion therapy for alcoholism showed that patients given such conditioning were more likely to abstain from alcohol following treatment than control patients (Boland, Mellor and Revusky, 1978). This positive report underscores the importance of further research into taste aversion therapy for alcoholism. There is considerable disagreement regarding the appropriate emetic to employ in taste aversion therapy (cf. Elkins, 1975; Rachman, 1965; Revusky, 1973; Revusky and Gorry, 1973). The emetic used most frequently in alcohol aversion therapy in this country is emetine hydrochloride (Raleigh Hills, Inc., 1975). The regimen usually employed is a series of 5 inpatient treatment sessions at 48-hr intervals along with 5 outpatient ‘booster’ sessions spread over a 6-month period. The emetine dosage is increased from 52 mg i.m. and 100 mg orally during the first session to 78 mg i.m. and 100 mg orally by the fourth session, for a total i.m. dosage of 344.5 mg over the IO-day inpatient treatment period. Most of the 500 mg of oral emetine presumably is not absorbed (Rollo, 1970). This treatment regimen exceeds the maximum daily emetine dosage (60 mg i.m.) and, depending on how much of the oral emetine is absorbed, approaches or exceeds the maximum total dosage over a lO-day course (600 mg) recommended by Rollo (1970). The toxic effects of emetine include hypotension, precordial pain, tachycardia, dyspnea and ECG abnormalities (cf. Rollo, 1970). Kattwinkel (1949) reported a death following the injection of 750 mg of emetine over an 11-day course of aversion therapy treatments. 229

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TIMOTHYB. BAKER and DALE S. CANNON

A safer, more reliable emetic is syrup of ipecac (Bates and Grunwaldt, 1962; Robertson, 1962; Rollo, 1970). Voegtlin (1947) stated that ipecac was not as effective as emetine in producing alcohol aversions, but no documentation of this claim was provided. Other suggested UCS’s have serious drawbacks. Apomorphine hydrochloride produces a hypnotic effect which early investigators felt interfered with conditioning (cf. Franks, 1966). Lithium chloride has been recommended based upon its effectiveness in taste aversion conditioning with rats (Boland et al., 1978; Revusky, 1973). However, lithium is extremely toxic at high dosages (Schou, 1958, 1968) and is an unreliable emetic (Boland et al., 1978; Schou, 1958), a serious problem if alcoholics must regurgitate ingested alcohol during treatment sessions. EXPERIMENT

1

Experiment 1 describes a taste aversion therapy technique which is safe, easily standardized and is intended to produce distaste or nausea as conditioned responses discriminated on the taste of alcoholic beverages. The procedure is a modification of one used in programs that have produced much of the promising clinical data (Lemere and Voegtlin, 1950; Weins et al., 1976; Raleigh Hills, Inc., 1975). However, the present technique is somewhat more conservative medically. Evidence for its efficacy is presented. METHOD Subject

The patient was a 28-yr-old male alcoholic with a 5-yr history of heavy drinking, including a hospitalization for alcohol related gastritis, two arrests for driving while intoxicated, and delirium tremens during one of his three medical detoxifications. The patient indicated that during the 6 months preceding hospitalization his longest period of abstinence was 4-6 weeks, his longest continuous drinking bout was about 2 months. and he usually consumed a minimum of 750ml of 80” liquor or its equivalent per day when drinking. His favorite drinks were vodka and bourbon. Prior to treatment the patient was medically screened for cardiovascular disease, renal disease, esophagovaricies, hernias and hypertension, as taste aversion therapy is contraindicated for patients with any of these conditions. The patient was a volunteer and was fully informed of the nature of the treatment and his right to terminate at any time. Procedure

In addition to aversion therapy the patient received the standard 60-day inpatient regimen (e.g. group therapy, alcohol education, AA, etc.). Conditioning, psychophysiological and taste test sessions occurred in a simulated bar adjacent to the Alcohol Treatment Unit. Two psychophysiological recording sessions and two taste test sessions were conducted prior to the inpatient course of aversion treatments, and were repeated the week after it. The psychophysiological measurements were repeated just prior to and several days after each of the last two outpatient booster sessions. The quasi-experimental design used was an AB time series design with multiple measures and extended follow-up and booster treatments (cf. Hersen and Barlow, 1976; Campbell and Stanley, 1963). Psychophysiological sessions were intended to assess changes in psychophysiological responses to alcohol which could be considered components of a conditioned response. Skin conductance response (SCR) and heart rate response (HRR) were measured using a Grass model 7D polygraph with a 7P122B amplifier and a Grass 7P4F cardiotachometer. Resistance was recorded directly from two active sites (palm to palm, with Ag-AgCl electrodes) but was converted to SCR for data presentation. Heart rate was recorded off Lead II with Ag-AgC1 electrodes. After a lo-min habituation period, three nonalcoholic flavors-cola, a lemon-lime soft drink, and water and three of the S’s favorite alcoholic flavors-port wine, beer and vodka (spirits) were presented by squirt-

231

Taste aversiontherapy with alcoholics

ing 2 ml of beverage into the patient’s mouth from a syringe. Each flavor was presented twice, in random order. This procedure permits control over CS onset and magnitude and eliminates patient movement artifacts. The taste test sessions were modeled after those used by Miller and his colleagues (Miller er al., 1973). Such inpatient drinking assessments have been shown to predict outpatient drinking status (Baker, Udin and Vogler, 1975; Miller ef al., 1974). The patient tasted the same types of alcoholic and non-alcoholic beverages as he was presented in the psychophysiological sessions and he rated each drink using bipolar semantic differential checklists (Costello, Rice and Schoenfeld, 1974a, 1974b) and open-ended questions. The bipolar adjective pairs were: tasty-distasteful, relaxing-alarming, pleasant -unpleasant, safe-dangerous, appetitive-repulsive, harmless-harmful, good-bad (Costello, Rice and Schoenfeld, 1974a. 1974b). The patient rated each drink with respect to every adjective. The patient used a Likert scale (i.e. 1 = not at all, 2 = a little, 3 = some, 4 = extremely) to rate the appropriateness of each adjective to each drink. The patient was told that he could drink as much or as little of each drink as he needed in order to rate the drinks accurately but that he had to drink at least some of each. The ratings consituted a credible reason for the patient to drink alcohol so that the amount of alcohol consumed before and after conditioning could be surreptitiously determined. The inpatient regimen consisted of five conditioning sessions which were scheduled at least 48 hr apart to allow the patient to recuperate. To prevent interference with CS-UCS associations by other flavors and to reduce the risk of aspiration during emesis, sessions were conducted in midmorning and the patient was allowed only water from midnight the night before. Before each session the patient’s pulse and blood pressure were recorded. The patient was given 20 ml of syrup of ipecac*-an oral emetic, and an i.m. injection of pilocarpine nitrate, ephedrine sulfate and 40 mg emetine hyrochloride. Dosages of pilocarpine and ephedrine increased across sessions l-5 (9, 9, 12, 15 and 18 mg for pilocarpine and 25, 25, 40, 50 and 60 mg for ephedrine). Pilocarpine produces sialorrhea and diaphoresis, which early investigators felt aided conditioning (e.g. Voegtlin, 1940). It also constricts the pyloric sphincter, preventing alcohol absorption by the small intestine. [Some individuals experience undesirable reactions to pilocarpine (e.g. prolonged abdominal cramping, blurred vision) and in these cases the dosage is reduced.] Both pilocarpine and ephedrine are hypertensives and therefore protect against a rapid fall in blood pressure. Emetine is a nauseant and prolongs the iilness. Immediately after the patient swallowed the ipecac, he was given 30ml of his favorite liquor (vodka) to insure that the taste of liquor rather than ipecac was associated with the onset of illness. Five minutes after the injection the patient’s pulse was recorded, and he drank 600 ml of water. He then drank about 2400ml of a variety of alcoholic drinks within 20 min of the injection. He sniffed each beverage before tasting it and then swished the drink in his mouth before swallowing. An additional 600ml of water was given at the close of each session. The patient was able to drink such large amounts since he was regurgitating throughout a session. He was given water before and after the sessions to prevent dry vomiting. The final 600 ml of water resulted in a cessation of emesis. Distilled spirits were diluted (2 parts spirits/l part water) while wine and beer were not. All beverages were served either warm (beer) or at room temperature (wine and spirits) since cold fluids are not regurgitated easily. Beer was served flat since effervescence interferes with emesis. Although it was not required, the patient’s stomach would have been lavaged to prevent the absorption of large amounts of alcohol had he not regurgitated most of the alcohol within 20 min of the injection. [We have never had to use gastric lavage * It stronger

is

vital that syrup of ipecac be used rather than extract of ipecac and a substitution may be fatal (Batesand Grunwaldt,1962).

as the latter

is about

14 times

232

TIMOTHYB. BAKER and DALE S. CANNON

with any patient (n = 14) using this treatment procedure.] The patient was restricted to his bed for 4 hr following a session and his pulse and blood pressure were monitored frequently. Twenty minutes after a conditioning session the patient was given 2 oz of beer which contained 24 mg potassium antimony tartrate to prolong the nausea. A washcloth soaked in various types of alcoholic drinks was placed near the patient’s head as long as he remained ill. During this time the patient was instructed to think about the problems drinking had caused him. In-person follow-up interviews and additional conditioning sessions were conducted at 2-weeks and 1, 2, 4 and 6 months following discharge. An additional in-person interview was held at 9 months, and frequent telephone contact was maintained throughout the follow-up period. Verification of the patient’s follow-up reports was obtained from his spouse and a friend with whom he had frequent contact. RESULTS The patient regurgitated from 17 to 29 times during and after each session, and his first emesis usually occurred about 8 min after he was given ipecac. The patient reported that he did not begin feeling ill until just prior to his first emesis. The patient usually gagged himself with a tongue depressor at the end of a session to completely evacuate his stomach contents. Neither this patient nor any of our other patients have ever felt any signs of alcohol intoxication during or after treatment. The patient’s pulse at. the beginning of sessions was usually about 70-75 bpm but increased to 12@-140bpm by the end of a session. The patient’s only physical complaint following sessions was intermittent nausea that lasted up to several hours. Since we employ a low emetine dosage, this treatment produced none of the side-effects associated with emetine poisoning: e.g. diarrhea, fatigue or ECG abnormalities. Taste rest session measures. The patient’s mean post-treatment (Taste Test Sessions 3 and 4) consumption of alcoholic beverages was about 50% of baseline (Taste Test

b. 182

TASTE TEST

384

SESSIONS

Fig. la and 1 b. Figure la shows mean alcoholic and nonalcoholic beverage consumption. Figure lb displays the mean negative ratings (distasteful, alarming, repulsive, harmful, unpleasant, dangerous and bad) of alcoholic and nonalcoholic flavors according to a Likert scale where 1 = not at all, 2 = a little, 3 = some. 4 = extremely. Both consumption and attitudinal ratings are averaged for the preconditioning taste test sessions (Sessions 1 and 2) and for the postconditioning taste-test sessions (Sessions 3 and 4). Responses for the three nonalcoholic flavors are averaged for clarity of presentation.

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Sessions 1 and 2) while his mean consumption of nonalcoholic drinks did not change (Fig. la). The consumption of nonalcoholic drinks has been averaged for clarity of presentation (interflavor response variability was slight). After treatment we told the patient that we wanted to ensure that he understood why he had participated in the various experimental treatments and measures. He was asked to describe the experimental procedures and give rationales for them. He did not guess that the taste test sessions were designed to measure fluid intake. Figure 1b shows the patient’s mean attitude ratings of the alcoholic and nonalcoholic drinks before and after treatment according to the semantic differential technique. As noted previously, options in the Likert rating scale were assigned numerical values where 1 = not at all, 2 = a little, 3 = some and 4 = extremely. Figure 1b shows that the mean ratings of the negative adjectives (distasteful, alarming, unpleasant, dangerous. repulsive, harmful, bad) increased for all three alcoholic drinks from preconditioning to postconditioning taste test sessions while negative ratings of nonalcoholic drinks showed a slight decrease. The mean correlation coefficient between ratings of members of a pair of adjectives (one positive and one negative, e.g. good-bad) was rxy = - 0.62. Skin conductance response. Figure 2 depicts the mean amplitude of the patient’s SCR to spirits, wine and nonalcoholic drinks within 40 set of drink presentation. The patient’s SCR to beer is not plotted in Fig. 2 since the patient was never able to identify its flavor in psychophysiological sessions and showed no psychophysiological response to that flavor. Peak SCR was determined by subtracting pre-flavor skin conductance from the skin conductance peak during the 40 set immediately following a flavor presentation. A longer post-flavor interval was used for SCR determination than for HR since the latency to the peak SCR response was considerably longer. The patient’s initial large magnitude responses to both alcoholic and nonalcoholic flavors during baseline was probably due to a general high level of arousal in early sessions. Tonic skin conductance levels (SCL’s) decreased somewhat across psychophysiological sessions. Figure 2 shows that conditioning consistently resulted in an increase in the patient’s SCR to spirits and wine relative to his SCR to nonalcoholic flavors. In all three postconditioning sessions (Psychophysiological Sessions 3, 6, and 8) the magnitude of the SCR relative to preconditioning values was greater for alcoholic flavors. By the last psychophysiological session (Psychophysiological Session 8) the patient’s SCR to alcoholic flavors exceeded his SCR to nonalcoholic flavors by about 0.65 pmhos. Heart rate response. Figure 3 shows the mean HRR to spirits and wine and to nonalcoholic flavors within 10 set of the flavor presentation. As with SCR, beer responses 1.5- INPATIENT CONMTIONING BOOSTER 4 Pre I Post Pre’ Post

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Fig. 2. Mean skin conductance response to wine, spirits and after the five inpatient conditioning sessions (Psychophysiological physiological Sessions 3 and 4). the 18-week booster session and 6) and the 26week booster session (Psychophysiological flavor responses are averaged for clarity of B.R.T.I7 3-f

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nonalcoholic flavors before and Sessions 1 and 2 and Psycho(Psychophysiological Sessions 5 Sessions 7 and 8). Nonalcoholic presentation.

TIMOTHY B. BAKER and DALE S. CANNON

234

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Fig 3. Mean heart rate response to wine. spirits and nonalcoholic flavors before and after the five inpatient conditioning sessions (Psychophysiological Sessions 1 and 2 and Psychophysiological Sessions 3 and 4). the 18-week booster session (Psychophysiological Sessions 5 and 6) and the 26-week booster session (Psychophysiological Sessions 7 and 8). Nonalcoholic flavor responses are averaged for clarity of presentation.

are omitted since the patient was unable to discriminate that flavor in psychophysiological sessions. Prior to conditioning (i.e. in Psychophysiological Session 2) the patient’s mean HRR to alcoholic flavors was about 2 bpm greater than for nonalcoholic flavors. However, the patient’s HRR to alcoholic flavors increased after each occurrence of conditioning, and those HRR increases tended to be maintained over the 6-month course of the booster sessions. Thus, after the final booster session the mean HRR was about 7 bpm greater for alcoholic than nonalcoholic flavors (cf. Psychophysiological Session 8). Heart rate tended to increase to both alcoholic (wine and spirits) and nonalcoholic drinks following conditioning sessions, suggesting a general sensitization effect. However. the HRR increase was greater for spirits and wine than for nonalcoholic beverages and stayed elevated throughout postconditioning psychophysiological sessions. Outpatient follow-up status. The patient’s post-discharge drinking status and outpatient adjustment have been followed for 9 months. For the first 3 months after discharge the patient drank no alcohol at all. During the next 4 months he drank on 29 days and was abstinent for 103. He drank only beer and usually only on weekends. He never consumed more than 3 beers/day. The patient reported that even though he drank beer, wine and spirits remained unappealing and distasteful to him. He attributed this effect to the aversion conditioning and so continued to participate in outpatient conditioning (booster) sessions. His pattern of controlled drinking has been corroborated by collateral informants. About 2 months after the patient’s last booster conditioning session he went on a 7-day binge during which he drank approximately 750 ml/day of bourbon. He discontinued drinking without medical assistance and was abstinent the remaining 41 days of the follow-up period. Thus, during the 9 months follow-up period, the patient was abstinent for 238 days, drank moderately for 29 days and was drunk on 7 days.

DISCUSSION:

EXPERIMENT

1

Experiment 1 presents a detailed description of a taste aversion therapy procedure as well as some evidence regarding its efficacy. One of the most important considerations in taste aversion therapy involves-the selection of an appropriate UCS. Our use of ipecac in conjunction with low doses of emetine avoids the dangers of emetine toxicity (Kattwinkel, 1949; Rollo, 1970) and yet ensures adequate nausea and emesis. Thus

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far we have used these procedures with over a dozen patients with no serious medical complications. The psychophysiological and taste test data suggest the development of wine and whiskey aversions, but the data for beer are problematic. There was a decrease in beer consumption in the drinking tests following the inpatient course, but there was no psychophysiological evidence of an aversion. It is unclear whether the lack of psychophysiological evidence was due to the measurement procedure (the patient’s inability to taste beer during psychophysiological sessions) or to the lack of an aversion. The drinking pattern during the fourth to the seventh month suggest the absence of an effective beer aversion. It is possible that the controlled beer intake weakened the whiskey aversion, making the subsequent whiskey drinking episode more probable. The presence of an altered psychophysiological response to alcohol following conditioning is notable since conditioned responses have been difficult to demonstrate with shock aversion conditioning (Hallam et al., 1972; cf. Busch and Evans, 1977; Evans and Busch, 1974; Evans and Kagehiro, 1977). Experiment 1 does not prove that changes in the patient’s functioning following treatment were due to the alcohol-illness contingency. While unlikely, it is possible that changes in the patient’s beverage consumption, attitude ratings, HRR, and SCR were all due to events that were temporally correlated with conditioning. Clinical considerations, however, discouraged us from using a reversal design or employing a gicater number of psychophysiological or taste test sessions. The conditioning procedure is so arduous that we did not wish to institute a reversal to achieve a higher degree of experimental control. Also, we viewed each taste test and psychophysiological session as an extinction trial since basic research has shown that preconditioning taste familiarity or nonreinforced taste presentations attenuate taste aversion learning (Elkins, 1973; Fenwick, Mikulka and Klein, 1975; Grote and Brown, 1973; Kalat, 1974; Vogel and Clody, 1972). EXPERIMENT

2

The promising results of Experiment 1 suggested that the effects of taste aversion conditioning should be investigated using a design with greater internal validity (Campbell and Stanley, 1963). In order to avoid the clinical drawbacks of an ABAB reversal design (Gelfand and Hartmann, 1975; Hersen and Barlow, 1976) Experiment 2 employed a single subject design with multiple baselines across alcoholic beverages. Dependent measures were the same as in Experiment 1 (i.e. psychophysiological and drinking measures). The objective of Experiment 2 was to determine whether a flavor-illness contingency per se can produce changes in a patient’s psychophysiological and consummatory responses to alcohol. While Experiment 1 employed a taste aversion conditioning technique as it is used to produce a maximal therapeutic effect (cf. Weins et al., 1976) Experiment 2 employed a design that achieved greater control, but possibly produced less robust conditioned responses. This design should also demonstrate whether alcohol aversions are discriminated on the flavors of particular alcoholic beverages, or on the taste of ethanol per se. The findings of Quinn and Henbest (1967) suggest that the former is the case. METHOD Subject

The subject was a 29-yr-old white male inpatient on the Salt Lake VA Hospital Alcohol Treatment Unit. His admitting diagnosis was alcohol addiction, chronic. He reported that he began drinking at less than 16 yr of age and that alcohol had been a serious problem for 3-5 yr. He reported four arrests for alcohol related offenses in the 6 months prior to admission. His preferred beverages were beer and bourbon. The subject volunteered for the study after being medically screened and informed of its nature.

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TIMOTHYB. BAKERand DALE S. CANNON Table 1. Sequence of experimental sessions Conditioning session Target beverages

Sessions Psychophysiological Taste Test l-4 Conditioning 1 Psychophysiological Taste Test 5 Conditioning

2

Conditioning

3

Psychophysiological Taste Test 6 Conditioning

4

Conditioning

5

Psychophysiological Taste Test 7

l-4 Bourbon

5.6

7.8

Bourbon Wine Bourbon Wine

9. 10

Bourbon Wine Beer Bourbon Wine

Procedure

As in Experiment 1, all treatment and testing sessions occurred in a simulated bar adjacent to the Alcohol Treatment Unit. Psychophysiological and taste test sessions occurred just as in Experiment 1 except that in psychophysiological sessions 3 ml of a beverage was squirted in the patient’s mouth, rather than 2ml. This change was intended to permit more accurate flavor discriminations. The three non-alcoholic flavors presented in psychophysiological and taste test sessions were cola, a lemon-lime soft drink and water, while the three alcoholic flavors were sherry wine, beer, and spirits (bourbon). Four psychophysiological and taste test sessions were conducted to establish stable baselines prior to treatment. Taste aversion conditioning sessions were run the same as in Experiment 1 except that since Experiment 2 is a multiple baseline design not all alcoholic flavors were presented in each conditioning session. The sequence of experimental events is presented in Table 1. Alcoholic flavors were conditioned in a randomly determined sequence. The patient started receiving bourbon during the first conditioning session, while wine was added in the second and third sessions and beer in the fourth and fifth (Table I). RESULTS Taste rest session measures. Consumption data for the four baseline taste test sessions and the taste test sessions following the first, third and fifth conditioning sessions are presented in Fig. 4a. For clarity of presentation, the consumption of nonalcoholic drinks is averaged for each session. The baseline consumption of alcoholic beverages is quite high (Jz = 78 ml/flavor) and relatively stable except for a decrease during Taste Test Session 3. The results of Taste Test Sessions 6, 8 and 10 indicate increasing aversion with repeated conditioning; mean consumption for all three alcoholic beverages for Taste Test Sessions 6, 8 and 10 was 67, 35 and 18 ml respectively. It is important to note that the amount of each alcoholic flavor consumed in Taste Test Sessions 5-7 is negatively correlated with the number of conditioning trials to each flavor. The sooner a flavor was introduced in conditioning sessions the smaller its consumption in subsequent taste test sessions. As in Experiment 1, this patient did not guess that beverage consumption was assessed in taste test sessions. Figure 4b complements Fig. 4a in that the patient’s negative taste ratings are negatively correlated with the amount of alcoholic beverage consumed in each postconditioning taste test session (Taste Test Sessions 5-7). Negative taste ratings show consistent increments as a function of the introduction of each flavor into conditioning sessions

Taste aversion therapy with alcohol&

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Fig. 4a and 4b. Figure 4a and b depict the mean alcoholic and nonalcoholic beverage consumg tion and negative attitude ratings to flavors before conditioning (Taste Test Sessions l-4) after conditioning to bourbon (Taste Test Session 5). after conditioning to bourbon and wine (Taste Test Session 6). and after conditioning to bourbon, wine and beer (Taste Test Session 7). Negative attitude adjectives were distasteful, alarming. repulsive. harmful. unpleasant, dangerous and bad and they were rated with Likert scales where I = not at all, 2 = a little. 3 = some, 4 = extremely. Responses for the three nonalcoholic flavors are averaged for clarity of presentation.

and the number of times flavors occurred in conditioning sessions. The mean correlation coefficient between ratings of members of a pair of adjectives (one positive and one negative, e.g. good-bad) was - 0.72. Skin conductance response. There was a marked decrease in tonic SCL’s across sessions. In all but Psychophysiological Session 2, SCL ranged from 1l-24 pmho during baseline, but was typically in the ~2-6 pmho range thereafter. A Pearson product-moment correlation revealed that the mean SCR ma~itude of a session was correlated with SCL at the inception of a session at rX,,= 0.91. Apparently, the tonic level of arousal of this patient partly determined the magnitude of his SCR (cf. Lykken, 1968). It is for this reason that his SCR’s are generally higher during baseline sessions than during subsequent psychophysiological sessions. Since some SCR values were quite extreme (e.g. the patient’s SCR to bourbon after its initial pairing with illness), values were converted to common log scores to permit their graphical representation [a constant (2) was added to log scores to avoid negative or zero values]. Figure 5 shows the SCR‘s to alcoholic and nonalcoholic flavors across the 10 psychophysiological sessions. Responses to nonalcoholic flavors are averaged for clarity of presentation (inter-flavor response variability was slight). During baseline, the SCR’s were fairly stable across sessions and were comparable for alcoholic and nonalcoholic flavors. Following the first bourbon conditioning session, the SCR to bourbon was quite large in Psychophysiological Session 5 but disappeared during Session 6. In Psychophysiological Session 7, following two bourbon and sherry conditioning sessions, there were SCR’s to both conditioned flavors, but these responses were not present in Psychophysiological Session 8. There was a small SCR to bourbon in Psychophysiological Session 9, but none to the other two conditioned flavors. The patient was unable to identify any flavor he was presented in Session 9 and he reported that he had not been attending to their tastes. Therefore, prior to Psychophysiological Session 10 the subject was instructed to be sure to attend to the flavors, and a large response to

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TIMOTHY B. BAKER and DALE S. CANNON 1.5

0 BOURBON

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PSYCHOPHYSIOLOGICAL

SESSIONS

Fig. 5. Mean skin conductance response (common log hmho/cm 2 + 2) to alcoholic and nonalcoholic drinks before conditioning (Psychophysiological Sessions I-4). after conditionjng to bourbon (Psychophysiological Sessions 5 and 6). after conditioning to bourbon and wine (Psychophysiological Sessions 7 and 8), and after conditioning to bourbon, wine. and beer (Psychophysiological Sessions 9 and 10). Responses to the three nonalcoholic flavors were averaged for clarity of presentation.

bourbon and a small response to sherry were observed. After Session 10 he was able to name all flavors presented except beer. There was no evidence of stimulus generalization across alcoholic flavors. Responses to nonalcoholic flavors and to beer were negligible from Test Session 5 on. Heart rate response. Increases in HRR following flavor presentations are shown in Fig. 6. As for SCR, nonalcoholic flavor responses are averaged across the three flavors for clarity of presentation. Heart rate responses during baseline were stable with no differences between responses to alcoholic and nonalcoholic flavors. There were large HRR’s to bourbon in Psychophysiological Sessions 5, 7, 8, 9 and 10. There was no evidence of a HRR to wine after its first two pairings with illness (in Psychophysiological Sessions 7 and 8) but there was some evidence of a HRR during Psychophysiological Session 10. As was the case with SCR, the patient showed little HRR during Psychophysiological Session 9. While -2 0

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Fig. 6. Mean heart rate response to alcoholic and nonalcoholic drinks before conditioning (Psychophysiological Sessions 14). after conditioning to bourbon (Psychophysiological Sessions 5 and 6). after conditioning to bourbon and wine (Psychophysiological Sessions 7 and 8). and after conditioning to bourbon. wine. and beer (Psychophysiological Sessions 9 and IO). Responses to the nonalcoholic flavors were averaged for clarity of presentation.

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he showed some evidence of a HRR to bourbon he was unable to identify the flavors he had been presented in that session. He showed large magnitude HRR’s to both bourbon and wine during Psychophysiological Session IO. His .HRR’s to bourbon and wine were 20 and 18 bpm respectively while his fairly stable HRR to nonalcoholic flavors was about 10 bpm. Again, as with SCR, the patient showed no HRR to beer, a flavor he was never able to identify in psychophysiological sessions. DISCUSSION:

EXPERIMENT

2

The overall pattern of results of Experiment 2 supports the conclusion that the flavorillness contingency produced conditioned taste aversions: the drinking consumption and attitudinal data show a pattern which parallels the sequence in which the flavors were conditioned, as does the pattern of SCR increases across Psychophysiological Sessions 5 and 7. The increase in HRR to bourbon in Psychophysiological Session 5 is consistent with the other measures, but the failure to observe a HRR to wine in Psychophysiological Session 7 is not. However, there was a wine HRR in Psychophysiological Session 10. After conditioning, therefore, the patient showed enhanced psychophysiological responses to both identifiable alcoholic flavors. The stability of all dependent measures for nonalcoholic flavors across the test sessions also strongly supports the conclusion that the changes observed with alcohol flavors was due to the flavor-illness contingency. The patient was able to identify the nonalcoholic flavors in most sessions. The decline in SCL across sessions is indicative of habituation to the testing procedure. That this habituation was evident even though the testing sessions took place in the same setting as conditioning sessions is consistent with the usual finding in the animal taste aversion literature that exteroceptive stimuli-illness associations are not readily made (e.g. Garcia et ul., 1974). Habituation to the testing procedure may account for another aspect of the SCL data. In Psychophysiological Sessions 5 and 7 there were SCR’s to conditioned flavors which were not evident the following day, i.e. in Psychophysiological Sessions 6 and 8. The rapid decline in these sessions might be attributed either to habituation or to extinction, but the increase in SCR’s from Session 9 to 10 argues for an attentional or orienting mechanism. Prior to Session 10, the subject was asked if he could identify any of the flavors given the day before. He replied.he could not inasmuch as he “wasn’t really paying attention”. He was then told he would be asked to name the flavors given in Session 10 after it was over. He was able to do so with the exception of beer. Thus it is possible that the decreased responding in Sessions 6, 8 and 9 is simply due to failure to attend to the flavor stimuli following habituation to the procedure. Even if the rapid declines in SCR were due to extinction, it is likely that such rapid extinction would not occur under more favorable conditions (e.g. as in Experiment 1). The extensive CS exposure just prior to conditioning (the psychophysiological and taste test baseline sessions) and the CS exposures interspersed between conditioning sessions should all attenuate conditioning. Bourbon evidenced the strongest aversion on all three dependent measures; sherry, an intermediate aversion: and beer, the weakest aversion. As number of flavor-illness pairings was confounded with conditioning sequence, it is not possible to determine which variable is prepotent. Strength of taste aversion has been shown to be a function of number of conditioning trials in the animal literature (e.g. Cannon er a/., 1975). Also, in studies of the compound CS ‘blocking effect’, Kamin (1968, 1969) has shown that in conditioned suppression training initial pairing of one component of a compound CS with the UCS retards the acquisition of associations between the second CS component and the UCS. If presenting multiple flavors during an illness experience can be conceived of as a compound CS, then Kamin’s data are relevant. The failure to observe conditioned SCR’s and HRR’s to beer may be due to a number of factors. First, beer received the fewest conditioning trials and was the third component of a compound stimulus. It is also likely that the subject’s inability to identify beer during psychophysiological sessions attenuated his psychophysiological response. A

240

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DALE S. CANNON

related factor to this point is the finding that taste salience is an important determinant of taste aversion learning (Kalat. 1974). Perhaps beer (which has the lowest alcohol content) was simply a less salient flavor than wine or bourbon and therefore was less likely to become associated with illness. The modest amount of generalization of aversions across the three alcoholic flavors permitted the demonstration of the effect of the flavor-illness contingency. However, it also suggests that to be clinically effective, an alcohol aversion therapy treatment should include a wide variety of alcoholic beverages (Quinn and Henbest. 1967). CONCLUSIONS

The rationale for alcohol aversion therapy is straightforward; the treatment is intended to develop a conditioned response to alcohol, and the conditioned response in turn is supposed to lower the probability of subsequent drinking. In spite of the simplicity of the rationale and the fact that alcohol aversion therapy has been in use for nearly 40 years (e.g. Voegtlin, 1940; Thimann, 1943) the rationale has not been validated. Although there are anecdotal reports of alcohol aversions following treatment (cf. Hammersley, 1957), efforts to obtain experimental evidence of aversions have been unsuccessful (Hallam et a/., 1972). There have been reports of decreased drinking following aversion therapy (e.g. Voegthn and Lemere, 1942; Weins et al., 1976), but in the absence of evidence of conditioned aversions these clinical improvements have been attributed to such variables as cognitive changes, dissonance reduction, guilt expiation and placebo effects (cf. Hallam and Rachman, 1972; Rachman, 1977; for a review of non-conditioning theories). There is disagreement among investigators of Pavlovian conditioning as to what constitutes a ‘conditioned’ SCR (Stern and Walrath, 1977; Grings. 1977; Furedy and Poulos, 1977; Prokasy, 1977). The first two papers cited contend a distinction should be made between ‘orienting responses’ or ‘first interval responses’ and ‘conditioned responses’, while the second two papers disagree. The present data do not meet the rigorous criteria of conditioned responses proposed in the first two papers, but the differential response to alcoholic as opposed to nonalcoholic flavors and the sequence of SCR increases to bourbon and wine across Test Sessions 5 and 7 argue for a functional relationship between the taste-illness contingency and the observed response. Thus, the definition of a ‘conditioned response’ proposed by Prokasy (1977) has been met. Therefore, the results of Experiments 1 and 2 are the strongest validation to date of the first aspect of the rationale for alcohol aversion therapy, i.e. that aversion therapy results in conditioned alcohol aversions. Further research is needed to assess the validity of the second aspect of the rationale, i.e. that there is a relationship between conditioned alcohol aversions and the probability of subsequent drinking. ~~~ow~e~ge~~~nts-we thank the staff of the Salt Lake V.A. Hospital Alcohol Treatment Unit for their help throughout this research and Dr. Gary Stephenson and Essie Droubay, R.N., for their medical support. We thank Jeanette Farris and Linda Baker for their assistance in manuscript preparation. Reprints are avnilable from Timothy B. Baker. Department of Psychology, W. J. Brogden Psychology Building, 1202 West Johnson Street, University of Wisconsin-Madison, WI 53706. U.S.A. REFERENCES BAKERT. B., UDIN H. and V~CLER R. E. (1975) The effects of videotaped modeling and self-confrontation on the drinking behavior of alcoholics. Inc. J. Addict. 10, 779-793. BATEST. and GR&WALDT E. (1962) Ipecac poisoning. Am. J. Dis. Child. 103. 91-95. E~OLAND F. J.. MELLORC. S. and REVUSKYS. (1978) Chemical aversion treatment of alcoholism: lithium as the aversive agent. Behau. Rex Ther. 16, 401-&!2. BUSCHC. J. and EVANS I. M. (1977) The effectiveness of electric shock and foul odor as unconditioned stimuli in classical aversive conditioning. Behov. Res. Ther. 15. 167-175. CAMPEEL~D. T. and STANLEYJ. C. (1963) Experimental and Quasi-Experimental Designs for Research. Rand McNally & Co., Chicago. CANNOND. S., BERMANR. F., BAKERT. B. and ATKINSONC. A. (3975f Effect of pr~onditioning unconditioned stimuius experience on learned taste aversions. J. Exp. Psychof.: Animal Behau. Proc. 104. 27G-284. CCI~TELLO R. M.. RICE D. P. and SCHOENFELD L. S. (1974a) Attitude ambivalence with alcoholic respondents. J. consult. clin. Psycho/. 42, 303-304.

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