Psychology of Addictive Behaviors 2005, Vol. 19, No. 1, 94 –98
Copyright 2005 by the Educational Publishing Foundation 0893-164X/05/$12.00 DOI: 10.1037/0893-164X.19.1.94
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Heart Rate Increase to Alcohol Administration and Video Lottery Terminal (VLT) Play Among Regular VLT Players Sherry H. Stewart, Pamela Collins, James R. Blackburn, Mike Ellery, and Raymond M. Klein Dalhousie University The authors examined heart rate responses to video lottery terminal (VLT) play and alcohol intake. Forty-four VLT players were randomized to an alcohol (mean blood alcohol concentration ⫽ 0.06%) or a control beverage condition. Heart rate was recorded at pre- and postdrinking baseline and during VLT play. Alcohol participants displayed elevated heart rates relative to controls at postdrinking and VLT play. Controls displayed elevated heart rates during VLT play relative to both pre- and postdrinking baselines, whereas alcohol participants displayed elevations at post- relative to predrinking and at VLT play relative to postdrinking. Heart rate increases from predrinking to VLT play were greater among alcohol participants relative to controls. Results provide novel information that the combination of VLT play and alcohol further intensifies heart rate increase relative to either alone. Implications for pathological gambling and alcohol use disorder comorbidity are discussed.
and the orbital frontal cortex; e.g., Blackburn, Pfaus, & Phillips, 1992) that results in increased susceptibility to reward motivation (e.g., Comings et al., 1996; Potenza, 2001). Some research suggests the possibility of a psychophysiological marker of such reward susceptibility. Resting baseline heart rate increases in response to alcohol intake (e.g., Stewart, Finn, & Pihl, 1992) are thought to reflect a psychomotor stimulant-like response to alcohol mediated through the dopamine reward system (Peterson et al., 1996). Heart rate increases to alcohol have been associated with increased positive mood states (Conrod, Peterson, & Pihl, 2001), alcoholic family history (Stewart et al., 1992), and increased alcohol use (Peterson, Pihl, Seguin, Finn, & Stewart, 1993). Alcohol may indirectly affect the dopamine reward system through stimulating endogenous opiate release (Peterson et al., 1996). Consistent with this, heart rate increase to alcohol correlates with beta-endorphin release to alcohol ingestion (Peterson et al., 1996). Heart rate increases have also been observed during gambling among regular gamblers (e.g., Coventry & Hudson, 2001; Griffiths, 1993). Our purpose was to investigate heart rate responses to a moderately intoxicating dose of alcohol, to VLT play, and to their combination among a sample of regular VLT players. It was hypothesized that alcohol would lead to increases in heart rate relative to both a predrinking baseline and a group administered no alcohol. It was also hypothesized that VLT play would increase heart rate relative to pre- and postdrinking baselines among those not consuming alcohol. Finally, we investigated whether the combination of VLT play and alcohol intake would result in further heart rate increases relative to either activity alone. Hypotheses were tested in a mixed-model design in which regular VLT players were randomly assigned to alcohol or a control beverage and heart rate was measured at pre- and postdrinking and during VLT play.
Alcohol use disorders and pathological gambling are commonly comorbid (Crockford & el-Guebaly, 1998). CunninghamWilliams, Cottler, Compton, and Spitznagel (1998) found that 44% of those with disordered gambling reported a lifetime history of alcohol use disorder—a rate that is substantially elevated relative to the 14% lifetime prevalence in the general population (Robins, Locke, & Regier, 1991). Alcohol disorder may cause pathological gambling or vice versa, or a third variable may cause both disorders (Grant, Kushner, & Kim, 2002). Disordered gambling and alcohol use are related not only at the syndrome level (i.e., comorbid diagnoses) but also at the event level (i.e., co-occurrence of gambling and drinking behavior) (Grant et al., 2002). A community survey study found that 74% of regular video lottery terminal (VLT) players reported drinking alcohol while playing VLTs (Focal Research, 1998). Similarly high rates of alcohol use during VLT play were obtained in an observational study (Stewart, McWilliams, Blackburn, & Klein, 2002). Consistent with the third-variable explanation of comorbidity, evidence suggests a common genetic vulnerability for alcoholism and pathological gambling (see Slutske et al., 2000). Some have speculated that both disorders may involve genetically mediated dysregulation in the dopamine reward system (a brain circuit consisting of the ventral tegmental area, the nucleus accumbens,
Sherry H. Stewart, Pamela Collins, James R. Blackburn, Mike Ellery, and Raymond M. Klein, Department of Psychology, Dalhousie University, Halifax, Nova Scotia, Canada. This research was supported by a generous grant from the Nova Scotia Gaming Foundation. Correspondence concerning this article should be addressed to Sherry H. Stewart, Department of Psychology, Dalhousie University, Halifax, Nova Scotia, Canada B3H 4J1. E-mail:
[email protected] 94
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Table 1 Means (and Standard Deviations) on Demographic and Addictive Behavior Variables as a Function of Beverage Condition Beverage condition Variable Age (years) Gender Female (n) Male (n) Marital status Married/cohabiting (n) Single/divorced/widowed (n) Annual income (1–7 scale) Years schooling Smoking status Smokers (n) Nonsmokers (n) Drinks per week SOGS total scores SOGS category Nonpathological (n) Probable pathological (n) Years playing VLTs Frequency VLT play (per week) Length of test play Full 30 min (n) Less than 30 min (n) Note.
No alcohol (n ⫽ 22)
Alcohol (n ⫽ 22)
F
35.68 (11.56)
33.40 (12.59)
0.39
7 15
7 15
2 17 2.91 (1.74) 14.52 (2.62)
7 15 3.75 (1.86) 14.26 (2.49)
7 15 10.11 (10.68) 5.04 (2.88)
9 13 9.82 (9.20) 5.22 (5.04)
11 11 7.04 (2.75) 2.07 (1.24)
11 11 6.40 (5.82) 2.18 (1.34)
8 14
14 8
2
p
0.00
ns ns
2.69
ns
0.39
ns ns ns
0.00
ns ns ns
1.64
ns ns ns
2.29 0.10
0.01 0.02
0.21 0.07
SOGS ⫽ South Oaks Gambling Screen; VLTs ⫽ video lottery terminals.
Method Participants Forty-four regular VLT players were recruited via newspaper advertisements.1 Respondents had to play VLTs at least once a month, be familiar with video poker, and consume alcohol at least once a month. Respondents were administered the Brief Michigan Alcoholism Screening Test (Pokorny, Miller, & Kaplan, 1972); those scoring 6 or above (possible problem drinkers) were excluded. We ensured that there was no medical reason that the individual should not consume alcohol, such as medication use or a medical condition for which alcohol is contraindicated and, for women, possible pregnancy or plans to conceive. Eligible individuals were instructed to fast for 4 hr, and to abstain from alcohol and drugs for 24 hr, before testing. Participants in the two beverage conditions did not differ on demographic or addictive behavior measures (see Table 1). We compared our sample with 711 regular VLT players in Nova Scotia on demographics and addictive behaviors (Focal Research, 1998). Our sample appeared representative of regular players, save that our participants were less likely to be married or cohabiting (21% vs. 57%), had played VLTs for longer (Ms ⫽ 6.7 vs. 3.6 years), and were more likely to be “problem gamblers” (50% vs. 16%).2
Materials Demographic and addictive behaviors information was obtained via questionnaires. The South Oaks Gambling Screen (Lesieur & Blume, 1987) assessed gambling problems. Subjective intoxication was measured using a 100-mm visual analogue scale (VAS). Blood alcohol concentrations (BACs) were measured using an Alcosensor III (Intoximeters, St. Louis, MO). Heart rate was collected with a photoplethysmograph and the ProComp⫹/Biograph psychophysiological data acquisition system (Thought Technology, Montreal, Quebec, Canada).
The photoplethysmograph was attached to the middle finger of the nondominant hand so as not to interfere with VLT play. At each testing time, mean heart rate was calculated via the ProComp⫹/Biograph program as the average interbeat interval, converted to beats per minute, across the entire recording interval.
Procedure Testing occurred during the afternoon in a laboratory modified to resemble a bar. The “bar-lab” contained a bar and VLTs that were identical in all respects to commercial VLTs appearing in licensed establishments in Nova Scotia. Consent was obtained, fasting was verified, and participants were weighed to determine alcohol dose. BAC was taken to verify abstinence and to provide a predrinking baseline. Participants were provided $30 (Canadian) compensation. Questionnaires were administered. Partici-
1
In all, 84 people responded to recruitment advertisements. Of these, 68 met study inclusion criteria. Of the 16 excluded individuals, reasons for exclusion included possible problem drinker status, medical contraindications to alcohol ingestion, and lack of familiarity with the video poker game. All 68 eligible individuals initially agreed to participate. Of the 68 who were booked for testing, 44 appeared as scheduled; the rest were “no shows” or cancellations. 2 The Focal Research (1998) report did not include measures of variability to permit direct statistical comparisons with the present results. It should also be noted that “problem gamblers” were defined differently in the two studies. In the present study, problem gamblers were “probable pathological gamblers” defined by scores of 5 or more on the South Oaks Gambling Screen (Lesieur & Blume, 1987), whereas in the Focal Research study, problem gamblers were defined using a more stringent measure developed by the authors.
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Figure 1. Mean heart rate in beats per minute as a function of beverage condition and testing time. Bars represent standard deviations. VLT ⫽ video lottery terminal.
pants were randomly assigned to beverage conditions (n ⫽ 22 per cell). The photoplethysmograph was applied, and an 8-min habituation followed. Predrinking baseline heart rate was continuously recorded for 90 s (with the experimenter absent). Participants were provided with their assigned beverage in 3– 4 glasses, depending on volume. Because this study was not designed to test expectancy effects, all participants were accurately informed of their beverage condition. The alcohol dose was 1.55 mL 50% USP units of alcohol/kg body weight for men and 1.29 mL/kg for women, mixed 1:4 parts alcohol to orange juice. The dose targeted a peak BAC of 0.06% (cf. MacDonald, Baker, Stewart, & Skinner, 2000). Control drinks (orange juice only) were matched for volume with the alcohol drinks. Beverages were consumed steadily over 20 –25 min, depending on volume. Participants rested for 20 –25 min to permit absorption. VAS and BAC measures were obtained. Postdrinking baseline heart rate was continuously recorded for 90 s (with the experimenter absent). Participants were invited to use their own money to play a video poker game on one of two VLTs for up to 30 min.3 Heart rate was continuously recorded during the entire period that each participant played the VLT. The experimenter unobtrusively recorded VLT play time. Talking during VLT play was discouraged. A third BAC was obtained 15 min into VLT play. Smoking was not permitted during testing. Alcohol participants remained until BAC fell below 0.04%; taxis were available for transportation home.
Results A one-way (testing time) repeated measures analysis of variance (ANOVA) was performed on alcohol condition participants’ BACs, which revealed a testing time effect: F(2, 42) ⫽ 146.03, p ⬍ .001; means (and SDs) were .000% (.000), .052% (.019), and .057% (.012) at predrinking, postdrinking, and VLT play, respectively. Relative to predrinking, BACs were elevated at postdrinking, t(21) ⫽ 12.85, p ⬍ .001, and at VLT play, t(21) ⫽ 24.03, p ⬍ .001. BACs at postdrinking and VLT play did not differ, t(21) ⫽ 0.83, ns. A one-way (beverage condition) ANOVA on VAS scores
at postdrinking revealed a beverage condition effect: F(1, 42) ⫽ 66.59, p ⬍ .001; means (and SDs) were 39.68 (20.53) versus 2.07 (6.75) for alcohol and no alcohol, respectively. A 2 ⫻ 3 (Beverage Condition ⫻ Testing Time) mixed-model ANOVA was performed on heart rate. A testing time effect, F(2, 84) ⫽ 97.00, p ⬍ .001, and a Beverage Condition ⫻ Testing Time interaction, F(2, 84) ⫽ 16.46, p ⬍ .001, emerged (see Figure 1). Analyses of simple effects revealed that alcohol participants displayed elevated heart rates relative to no-alcohol controls at postdrinking, F(1, 42) ⫽ 14.89, p ⬍ .01, and at VLT play, F(1, 42) ⫽ 13.51, p ⬍ .01, but not at predrinking, F(1, 42) ⫽ 2.25, ns. Although simple effects of testing time were revealed in both the alcohol, F(2, 42) ⫽ 61.23, p ⬍ .001, and no-alcohol, F(2, 42) ⫽ 48.14, p ⬍ .001, conditions, the pattern of heart rate changes over testing times varied by condition. For no-alcohol controls, heart rates at VLT play were higher than at both predrinking, t(21) ⫽ 7.66, p ⬍ .001, and postdrinking, t(21) ⫽ 8.73, p ⬍ .001, whereas heart rates at pre- and postdrinking did not differ, t(21) ⫽ 0.93, ns. For alcohol condition participants, heart rates were elevated at post- relative to predrinking, t(21) ⫽ 5.75, p ⬍ .001, and at VLT play relative to both pre-, t(21) ⫽ 11.21, p ⬍ .001, and postdrinking, t(21) ⫽ 5.17, p ⬍ .001. To determine whether heart rate increases to VLT play varied by beverage condition, heart rate change scores (i.e., heart rate at VLT play minus heart rate at predrinking) were submitted to a one-way (beverage condition) ANOVA. A beverage condition effect, F(1, 3 Variable lengths of VLT play were permitted to maximize ecological validity. Half (50%) of the participants chose to play for the maximum of 30 min allotted, and all chose to play for at least some of the allotted time (range ⫽ 18 –30 min). Beverage conditions did not differ significantly in the proportion of participants choosing to play for the full 30 min.
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42) ⫽ 17.79, p ⬍ .001, revealed that alcohol participants showed a greater heart rate increase to VLT play than no-alcohol controls: Means (and SDs) were 14.7 (6.1) versus 7.7 (4.7) beats per minute, respectively.
Discussion We replicated previous findings (e.g., Griffiths, 1993; Stewart et al., 1992) that alcohol and gambling alone cause heart rate increases. In addition, we showed that the combination of alcohol and VLT play leads to further heart rate increases relative to each activity alone. Assuming this exaggerated heart rate response might reflect increased activation of the reward system (Peterson et al., 1996), this finding might help explain alcohol disorder and pathological gambling comorbidity (Crockford & el-Guebaly, 1998) as well as why most regular VLT players drink while gambling (Focal Research, 1998). The neural systems implicated in the heart rate response to alcohol involve dopamine and the endogenous opiates (e.g., Peterson et al., 1993, 1996). Future research might test the degree to which beta-endorphin release is associated with heart rate increases during VLT play. Future work should include a larger sample to determine whether heart rate increases during VLT play are greater in pathological gamblers. Because increased heart rate can reflect states of uncertainty and fear as well as anticipated reward (Stewart et al., 1992), future studies should examine heart rate responses during anticipation of VLT wins versus losses and how these interact with alcohol. Given that heart rate increases to alcohol are maximal during the ascending limb of the BAC curve (Conrod, Peterson, Pihl, & Mankowski, 1997), further work should examine interactions of alcohol with VLT play at various phases of the BAC curve. Future studies might also test whether heart rate increases to alcohol and gambling alone and in combination correlate with positive mood states. Possible study limitations include our failure to control for movement artifact during VLT play, and our failure to counterbalance the drinking versus drinking-and-gambling phases. Another potential limitation involves the variable lengths of VLT play, which resulted in variable gambling “doses.” Additionally, although our sample appeared fairly representative of regular VLT players in the community (cf. Focal Research, 1998), self-selection resulted in chronic and problem gamblers being overrepresented, which could impact generalizability. Finally, because we did not use a placebo, heart rate increases to alcohol could have been due to expectancies.4 If future research shows heart rate increases to VLT play and alcohol to be mediated by the dopamine reward system, our findings may have important treatment implications. For example, naltrexone (an opioid antagonist that prevents alcohol reinforcement by inhibiting dopamine release in the nucleus accumbens; O’Malley, 1996) might prove efficacious in treating comorbid gambling and alcohol disorders.
4
Expectancies appear an unlikely explanation for the heart rate increases to alcohol observed in the present study, as previous research suggests that individuals consuming placebo alcohol display baseline heart rate responses opposite in direction (i.e., heart rate deceleration) to those observed in response to actual alcohol ingestion (e.g., Newlin, 1985; Stewart et al., 1992).
97 References
Blackburn, J. R., Pfaus, J. G., & Phillips, A. G. (1992). Dopamine functions in appetitive and defensive behaviors. Progress in Neurobiology, 39, 247–279. Comings, D. E., Rosenthal, R. J., Lesieur, H. R., Rugle, L. J., Muhleman, D., Chiu, C., et al. (1996). A study of the dopamine D2 receptor gene in pathological gambling. Pharmacogenetics, 6, 223–234. Conrod, P. J., Peterson, J. B., & Pihl, R. O. (2001). Reliability and validity of alcohol-induced heart rate increase as a measure of sensitivity to the stimulant properties of alcohol. Psychopharmacology, 157, 20 –30. Conrod, P. J., Peterson, J. B., Pihl, R. O., & Mankowski, S. (1997). Biphasic effects of alcohol on heart rate are influenced by alcoholic family history and rate of alcohol ingestion. Alcoholism: Clinical and Experimental Research, 21, 140 –149. Coventry, K. R., & Hudson, J. (2001). Gender differences, physiological arousal and the role of winning in fruit machine gamblers. Addiction, 96, 871– 879. Crockford, D. N., & el-Guebaly, N. (1998). Psychiatric comorbidity in pathological gambling: A critical review. Canadian Journal of Psychiatry, 43, 43–50. Cunningham-Williams, R. M., Cottler, L. B., Compton, W. M., & Spitznagel, E. L. (1998). Taking chance: Problem gamblers and mental health disorders—results from the St. Louis Epidemiological Catchment Area (ECA) study. American Journal of Public Health, 88, 1093–1096. Focal Research. (1998). Nova Scotia Video Lottery Players’ Survey 1997/ 98. Halifax, Nova Scotia, Canada: Nova Scotia Department of Health, Problem Gambling Services. Grant, J., Kushner, M. G., & Kim, S. W. (2002). Pathological gambling and alcohol use disorder. Alcohol Research and Health, 26, 143–150. Griffiths, M. D. (1993). Tolerance in gambling: An objective measure using the psychophysiological analysis of male fruit machine gamblers. Addictive Behaviors, 18, 365–372. Lesieur, H. R., & Blume, S. B. (1987). The South Oaks Gambling Screen (SOGS): A new instrument for the identification of pathological gamblers. American Journal of Psychiatry, 144, 1184 –1188. MacDonald, A. B., Baker, J. M., Stewart, S. H., & Skinner, M. (2000). Effects of alcohol on the response to hyperventilation of participants high and low in anxiety sensitivity. Alcoholism: Clinical and Experimental Research, 24, 1656 –1665. Newlin, D. B. (1985). The antagonistic placebo response to alcohol cues. Alcoholism: Clinical and Experimental Research, 9, 411– 416. O’Malley, S. S. (1996). Opioid antagonists in the treatment of alcohol dependence: Clinical efficacy and prevention of relapse. Alcohol and Alcoholism, 31, 77– 81. Peterson, J. B., Pihl, R. O., Gianoulakis, C., Conrod, P., Finn, P. R., Stewart, S. H., et al. (1996). Ethanol-induced change in cardiac and endogenous opiate function and risk for alcoholism. Alcoholism: Clinical and Experimental Research, 20, 1542–1552. Peterson, J. B., Pihl, R. O., Seguin, J. R., Finn, P. R., & Stewart, S. H. (1993). Heart rate reactivity and alcohol consumption among sons of male alcoholics and sons of non-alcoholics. Journal of Psychiatry and Neuroscience, 18, 190 –198. Pokorny, A. D., Miller, B. A., & Kaplan, H. B. (1972). The Brief MAST: A shortened version of the Michigan Alcoholism Screening Test. American Journal of Psychiatry, 129, 342–345. Potenza, M. N. (2001). The neurobiology of pathological gambling. Seminars in Clinical Neuropsychiatry, 6, 217–226. Robins, L. N., Locke, B. A., & Regier, D. A. (1991). An overview of psychiatric disorders in America. In L. N. Robins & D. A. Regier (Eds.), Psychiatric disorders in America: The Epidemiologic Catchment Area Study (pp. 53– 81). New York: Free Press. Slutske, W. S., Eisen, S., True, W. R., Lyons, M. J., Goldberg, J., & Tsuang, M. (2000). Common genetic vulnerability for pathological
98
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gambling and alcohol dependence in men. Archives of General Psychiatry, 57, 666 – 673. Stewart, S. H., Finn, P. R., & Pihl, R. O. (1992). The effects of alcohol on the cardiovascular stress response in men at high risk for alcoholism: A dose-response study. Journal of Studies on Alcohol, 53, 499 –506. Stewart, S. H., McWilliams, L. A., Blackburn, J. R., & Klein, R. (2002). A laboratory-based investigation of relations among video lottery terminal
(VLT) play, negative mood, and alcohol consumption in regular VLT players. Addictive Behaviors, 27, 819 – 835.
Received January 2, 2002 Revision received April 12, 2004 Accepted April 12, 2004 䡲
