Heart rate increase to alcohol administration and video lottery terminal play among probable pathological gamblers and nonpathological gamblers
The authors examined heart-rate responses to alcohol consumption and video lottery terminal (VLT) play. Regular VLT players (30 probable pathological gamblers [PPGs]; 30 nonpathological gamblers [NPGs]) were randomized to an alcohol (mean postdrinking blood alcohol concentration = 0.056%) or placebo condition. Heart rate was recorded at pre- and postdrinking baselines and during VLT play. Consistent with an earlier study, alcohol-condition participants displayed elevated heart rates relative to placebo-condition participants only at postdrinking and VLT play. Moreover, alcohol-condition participants showed a greater heart rate increase to VLT play than did placebo-condition participants. However, PPGs were not more susceptible to alcohol- and/or VLT play-induced heart rate accelerations than were NPGs. Implications for gambling/alcohol-disorder comorbidity are discussed.
Heart Rate Increase to Alcohol Administration and Video Lottery Terminal
Play Among Probable Pathological Gamblers and
Sherry H. Stewart
Jordan B. Peterson
University of Toronto
Pamela Collins, Shondalee Eisnor, and Michael Ellery
The authors examined heart-rate responses to alcohol consumption and video lottery terminal (VLT)
play. Regular VLT players (30 probable pathological gamblers [PPGs]; 30 nonpathological gamblers
[NPGs]) were randomized to an alcohol (mean postdrinking blood alcohol concentration ⫽ 0.056%) or
placebo condition. Heart rate was recorded at pre- and postdrinking baselines and during VLT play.
Consistent with an earlier study (S. H. Stewart, P. Collins, J. R. Blackburn, M. Ellery, & R. Klein, 2005),
alcohol-condition participants displayed elevated heart rates relative to placebo-condition participants
only at postdrinking and VLT play. Moreover, alcohol-condition participants showed a greater heart rate
increase to VLT play than did placebo-condition participants. However, PPGs were not more susceptible
to alcohol- and/or VLT play-induced heart rate accelerations than were NPGs. Implications for gambling/
alcohol-disorder comorbidity are discussed.
Keywords: heart rate, alcohol, gambling, video lottery terminals, comorbidity
Many studies suggest elevated rates of alcohol use disorders
among those with pathological gambling disorders and vice versa
(Crockford & el-Guebaly, 1998; Stewart & Kushner, 2003). For
example, Kausch (2003) found that 66% of those with disordered
gambling reported a lifetime history of substance use disorder,
with alcohol being the most commonly abused substance in this
clinical sample. This rate is substantially elevated relative to life-
time prevalence in the general population (Robins, Locke, &
Regier, 1991). The overlap of alcohol and gambling occurs not
only at the diagnostic level but also at the behavioral level (i.e.,
frequent combining of these two activities). This behavioral over-
lap is evidenced in both survey (e.g., Focal Research, 1998) and
behavioral observation studies (e.g., Stewart, McWilliams, Black-
burn, & Klein, 2002). For example, in a lab-based experimental
study, 73% of regular gamblers assigned to a video lottery terminal
(VLT) play condition chose to purchase alcoholic beverages dur-
ing play as compared with only 40% of those regular gamblers
assigned to a control activity (Stewart et al., 2002). There are
several possible explanations for this high rate of co-occurrence.
First, heavy drinking might cause gambling problems (e.g., Ellery,
Stewart, & Loba, 2005). Second, gambling problems might cause
heavy drinking. Or, finally, some third variable might cause both
alcohol use disorders and pathological gambling (Grant, Kushner,
& Kim, 2002; Stewart & Kushner, 2003).
Researchers have begun to explore what types of third variables
might help explain the high comorbidity between alcohol use and
gambling disorders. For example, recent evidence suggests a com-
mon genetic vulnerability for pathological gambling and alcohol-
use disorders (Slutske et al., 2000). Others (e.g., Comings et al.,
1996; Potenza, 2001) have suggested that both disorders may
involve dysregulation of dopaminergic brain circuitry. This dys-
regulation may be genetically mediated or environmentally medi-
ated (e.g., as a consequence of chronic stress; Lin, Bruijnzeel,
Schmidt, & Markou, 2002) and is thought to result in increased
susceptibility to incentive reward motivation.
Research over the last few decades has suggested that heart rate
increase may constitute a psychophysiological marker of incentive
reward motivation susceptibility, at least under some conditions
(Fowles, 1980; Fowles, Fisher, & Tranel, 1982), as the cardiovas-
cular system steps up its output to prepare the body for motivated,
goal-directed action (Wright, Killebrew, & Pimpalapure, 2002).
Under conditions of high expectancy of eventual reward, this
increase appears particularly evident (Ladouceur, Sevigny, Blaszc-
zynski, O’Connor, & Lavoie, 2003). Incentive reward (i.e., tech-
nically, response to a cue for consummatory reward or to novelty;
Sherry H. Stewart, Pamela Collins, Shondalee Eisnor, and Michael
Ellery, Department of Psychology, Dalhousie University, Halifax, Nova
Scotia, Canada; Jordan B. Peterson, Department of Psychology, University
of Toronto, Toronto, Ontario, Canada.
Shondalee Eisnor is now at the Maritime School of Social Work,
Sherry H. Stewart is now at the Departments of Psychiatry and Psy-
chology, Dalhousie University.
This research was supported by a generous grant from the Nova Scotia
Gaming Foundation. Sherry H. Stewart is supported through an Investiga-
tor Award from the Canadian Institutes of Health Research.
Correspondence concerning this article should be addressed to Sherry H.
Stewart, Department of Psychology, Dalhousie University, Halifax, Nova
Scotia B3H 4J1, Canada. E-mail: firstname.lastname@example.org
Psychology of Addictive Behaviors Copyright 2006 by the American Psychological Association
2006, Vol. 20, No. 1, 53– 61 0893-164X/06/$12.00 DOI: 10.1037/0893-164X.20.1.53
Gray, 1982) appears mediated primarily by the dopaminergic
reward systems (Gray, 1982; Panksepp, 1999) originating in the
ventral tegmental area, and involving the extended amygdala, the
nucleus accumbens, and the orbital frontal cortex (Blackburn,
Pfaus, & Phillips, 1992) and/or anterior cingulate cortex (Kalivas
& McFarland, 2003). Activation of this system has been hypoth-
esized as the primary commonality linking drugs of abuse in
animals and humans (Wise, 1988).
Some have argued that heart-rate increases in response to alco-
hol intake in the resting state reflect a psychomotor stimulant-like
response to alcohol (similar to that observed for established stim-
ulant drugs like cocaine; e.g., Peterson et al., 1996). Peterson, Pihl,
Seguin, Finn, and Stewart (1993) hypothesized that the alcohol-
induced baseline resting heart rate increase characteristic of sons
of multigenerational alcoholics was a consequence of an enhanced
psychomotor stimulant response to alcohol. Among animal re-
searchers, it has been long known that alcohol is capable of
directly activating the dopamine reward system (e.g., Deminiere,
Piazza, LeMoal, & Simon, 1989; McBride, Murphy, Lumeng, &
Li, 1990). Further evidence for baseline heart rate increase as an
index of the reward properties of alcohol intake comes from a
variety of sources. For example, baseline heart rate increases to
alcohol have been associated with increased alcohol use (Peterson
et al., 1993), alcoholic family history (Stewart, Finn, & Pihl,
1992), and increases in positive mood states (Conrod, Peterson, &
Pihl, 2001). Furthermore, Boileau et al. (2003) recently directly
demonstrated that dopamine was in fact released in the ventral
striatum and nucleus accumbens as a consequence of alcohol
intake in humans (using [
C]raclopride positron-emission tomog
raphy scans), and that such release did correlate both with alcohol-
induced baseline heart-rate increase and impulsiveness. Such re-
lease may be a direct or first order consequence of alcohol’s effect
on the dopaminergic systems; alternatively, at least in some cases,
it might also be mediated indirectly via alcohol’s stimulation of
endogenous opiate release (Peterson et al., 1996), as alcohol-
induced baseline heart-rate increase can be reduced to zero as a
consequence of the coadministration of naltrexone, an opiate an-
tagonist (Peterson, Conrod, Vassileva, Gianoulakis, & Pihl, in
press). Although opiates are primarily regarded as analgesics,
cocaine also has potent analgesic properties, and opiates have
powerful psychomotor stimulant effects (Gianoulakis, 1996; Gray,
1982; Wise, 1988).
Incentive reward activation also appears to mediate at least
some of the pleasurable and addictive aspects of gambling. Grif-
fiths (1991) has contended that pathological gamblers engage in
gambling for its euphoric, arousal-enhancing consequences. In
indirect keeping with such a hypothesis, Zack and Poulos (2004)
have recently demonstrated that amphetamine, a potent dopamine
agonist, primes motivation to gamble in problem gamblers. Fur-
thermore, heart-rate increase characterizes regular gamblers during
gambling bouts (Coventry & Hudson, 2001; Griffiths, 1993) and
appears related to the excitement generated by the possibility of
winning money (Ladouceur et al., 2003) and to the similarity of the
testing situation to the real-world gambling context (Diskin, Hod-
gins, & Skitch, 2003). Taken together, such findings suggest the
possibility that heart-rate increase may represent a common psy-
chophysiological marker of susceptibility to reward from both
drinking and gambling and, thus, susceptibility to developing
gambling and/or drinking problems.
Until recently, however, no research had examined heart-rate
responses to alcohol and gambling in the same individuals within
the same study. Stewart, Collins, Blackburn, Ellery, and Klein
(2005) examined heart rate responses to VLT play and alcohol
consumption, alone and in combination. Forty-four regular VLT
players (i.e., a group including both probable pathological and
nonpathological gamblers) were randomly assigned to a moder-
ately intoxicating dose of alcohol or a control (mix only) beverage
condition. Heart rate was recorded at three times: at a predrinking
baseline, at a postdrinking baseline, and during VLT play. Through
comparison of degree of increases from pre- to postdrinking base-
line among gamblers assigned to the alcohol and control beverage
conditions, the results confirmed previous findings that alcohol
consumption alone increased heart rate (cf. Peterson et al., 1993,
1996; Stewart et al., 1992). The study also demonstrated that VLT
play alone increased heart rate, like other forms of gambling (cf.
Coventry & Hudson, 2001; Griffiths, 1993; Leary & Dickerson,
1985), among players in the control beverage condition, and that
the combination of VLT play and alcohol-intensified heart rate
increase, relative to either condition alone. Given the evidence
suggesting that baseline heart rate increases might index the in-
centive reward characteristics of certain forms of addictive activ-
ity, it appears that the combination of VLT play and alcohol use
might be particularly rewarding.
The current study was designed to replicate and extend Stewart
et al. (2005). We, therefore, investigated heart-rate responses to a
moderately intoxicating dose of alcohol, to VLT play, and to their
combination, among a sample of regular VLT players. We also
made a number of methodological improvements. First, because it
was not designed to examine expectancy effects, our earlier study
used a mix-only beverage rather than a placebo beverage in the
control beverage condition. To control for expectancy effects, we
used a placebo-beverage condition in the present study. Second,
during our original study, participants played a video poker game
on the VLT machines. In the present study we had participants
play a “spinning reels” game, which is a video-simulated slot
machine game. This particular game is popular with most VLT
players (Focal Research, 1998). Finally, the previous study did not
include a sufficient sample size to test whether the heart-rate
increases to alcohol, VLT play, and their combination were dif-
ferent among probable pathological gamblers (PPGs) and non-
pathological gambler controls (NPGs). Brunelle, Assaad, Pihl,
Tremblay, and Vitaro (2003) have recently demonstrated that
elevated scores on a measure of gambling problems (the South
Oaks Gambling Screen [SOGS]; Lesieur & Blume, 1987) were in
fact associated with greater sensitivity to alcohol-induced heart
rate increases. In the present study, we increased our sample size
so that we could determine whether PPGs, as identified on the
SOGS, might show comparatively increased heart rate to VLT
play, alcohol, and/or their combination, relative to NPGs.
In the present study, we used a 2 ⫻ 2 ⫻ 3 (Gambler Group ⫻
Beverage Condition ⫻ Testing Time) mixed-model design with
two between- and one within-subjects factor. We divided regular
VLT players into probable pathological versus nonpathological
gambler groups on the basis of scores on the SOGS (Lesieur &
Blume, 1987). Participants in each gambler group were randomly
assigned to an alcohol or a placebo– control beverage condition.
Heart rate was measured at three testing times: predrinking base-
line, postdrinking baseline, and during VLT play. We tested sev-
STEWART, PETERSON, COLLINS, EISNOR, AND ELLERY
eral hypotheses that follow from the idea that enhanced dopamine/
incentive–reward sensitivity underlies alcohol abuse/pathological
First, we expected a two-way Beverage Condition ⫻ Testing
Time interaction, consisting of the following three effects: (a) heart
rate increase to alcohol consumption alone, evidenced by an in-
crease in heart rate from pre- to postdrinking baseline in the
alcohol beverage condition (with no change in the placebo bever-
age condition) and by a greater heart rate in the alcohol beverage
condition relative to the placebo beverage condition at postdrink-
ing baseline (but no difference between beverage conditions at
predrinking baseline); (b) heart-rate increases to VLT play alone,
evidenced by an increase in heart rate from postdrinking baseline
to the VLT play phase in both the alcohol and placebo beverage
conditions and by an increase in heart rate from predrinking
baseline in the placebo beverage condition; and (c) heart rate
increase to the combination of alcohol intake and VLT play,
relative to either activity alone, evidenced by a greater heart rate in
the alcohol beverage condition relative to the placebo beverage
condition at VLT play (but no difference between beverage con-
ditions at predrinking baseline) and by a greater heart rate increase
to VLT play from predrinking baseline in those who had consumed
alcohol relative to those who had consumed placebo. Second, we
expected a three-way Gambler Group ⫻ Beverage Condition ⫻
Time interaction, such that all the effects listed above would be
greater for PPGs than for NPGs.
Sixty regular VLT players were recruited via newspaper and local cable
Half were PPGs, according to their SOGS scores; the
other half were NPGs. To be eligible for participation, respondents had to
play VLTs at least once a month, be familiar with a spinning reels game,
and consume alcohol at least once a month. These were the same inclusion
criteria used for our last study (Stewart et al., 2005). Because the study
involved alcohol administration, those scoring ⱖ6 on the Brief Michigan
Alcoholism Screening Test (Pokorny, Miller, & Kaplan, 1972), indicative
of possible problem-drinker status, were excluded (Stewart et al., 2005).
Those with medical contraindications to alcohol consumption were ex-
cluded (Stewart et al., 2005).
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, except that our partic-
ipants were less likely to be married or cohabiting (29% vs. 57%), had
played VLTs for longer (Ms ⫽ 6.8 vs. 3.6 years), and were more likely to
be probable pathological gamblers (50% vs. 16%).
Materials and Measures
Information on demographic characteristics and addictive behaviors was
obtained via author-compiled questionnaires. Subjective intoxication was
measured using a 100-mm visual analog scale (VAS). Gambler group
membership was determined by screening scores on the SOGS—a reliable
and valid screen for problem gambling. Those scoring ⱖ5 on the SOGS
were assigned to the PPG group and all others to the NPG group (cf.
Lesieur & Blume, 1987). Blood alcohol concentrations (BACs) were
measured using an Alcosensor III (Intoximeters, St. Louis, Missouri).
Heart rate was collected with a photoplethysmograph via the ProComp⫹/
Biograph psychophysiological data acquisition system (Thought Technol-
ogy, Montreal, Quebec, Canada). So as not to interfere with VLT play, the
photoplethysmograph was attached to the middle finger of the nondomi-
nant hand. Mean heart rate was calculated via the ProComp⫹/Biograph
program first as the average interbeat interval (IBI) at each testing phase,
across the entire recording interval. IBI was then converted to beats per
minute (bpm). Participants gambled on VLTs that were identical in all
respects to commercial VLTs appearing in licensed establishments in the
province of Nova Scotia (Stewart, Blackburn, & Klein, 2000). VLTs are
similar to slot machines in that both are electronic gaming machines that
operate using random number generators. Both VLTs and slot machines
can be used to play spinning reels-type games. However, VLTs do not
contain mechanical reels but rather use video-simulated reels.
For the purposes of telephone screening, we developed a standard
telephone script incorporating the scorable items from the SOGS (Lesieur
& Blume, 1987) to appropriately assign the participant to a condition
within the 2 ⫻ 2 design. PPGs were overrecruited (i.e., actively sought as
potential participants on the basis of the results of telephone screening) to
equate the n in each cell of the 2 ⫻ 2 (Beverage Condition ⫻ Gambler
Group) between-subjects design. This was accomplished by continuing to
recruit PPGs into the study after the two cells (i.e., alcohol and placebo) of
NPGs had been filled. Within each gambler group, random assignment to
one of the two beverage conditions was accomplished via lottery at the
time of participant screening. Eligible individuals were instructed to fast
for 4 hr and to abstain from alcohol and drugs for 24 hr prior to testing (cf.
Stewart et al., 2005).
Testing occurred during the afternoon in a laboratory modified to re-
semble a bar. The “bar-lab” contained a bar and two VLTs. Consent was
obtained, fasting was verified verbally, and participants were weighed to
determine alcohol dose. BAC was taken to verify abstinence from alcohol
and to provide a predrinking baseline measure. Participants were provided
$80 (Canadian) compensation. Questionnaires were administered. The
photoplethysmograph was attached and an 8-min habituation period fol-
lowed. Predrinking baseline heart rate was continuously recorded for 5
followed by administration of a demographics questionnaire.
Participants were provided with their assigned beverage (alcohol or
placebo) in 3–4 glasses, depending on total volume. Because this study
was also designed to test expectancy effects, all participants were informed
that they would be receiving a moderate dose of alcohol, consisting of the
equivalent of 3–4 mixed bar drinks. For those in the alcohol condition, the
alcohol dose was 1.55 mL 50% United States Pharmacopeia units of
Eighty-three people responded to recruitment advertisements. Of these,
67 met study inclusion criteria. Reasons for exclusion included possible
problem drinker status (i.e., scoring above the cutoff-point on the Brief
Michigan Alcoholism Screening Test), medical contraindications to alco-
hol ingestion, and lack of familiarity with the spinning reels game. Of the
67 eligible individuals who initially agreed to participate, 60 appeared as
scheduled; the rest were no-shows or cancellations.
The Focal Research (1998) report did not include measures of vari
ability to permit direct statistical comparisons with the present results. It
should also be noted that PPGs were defined differently in the two studies.
In the present study, PPGs were defined by SOGS scores (Lesieur &
Blume, 1987), whereas a more stringent measure, developed by the au-
thors, was used in the Focal Research study. Moreover, as noted in the
procedure section, probable pathological gamblers were purposely overre-
cruited in the present study to equate cell n in the 2 ⫻ 2 (Gambler Group ⫻
Beverage Condition) between-subjects design.
The length of the heart-rate recording interval at each of the two
baseline phases was increased from 90 s in our original study to 5 min in
the present study to allow for collection of a potentially more representa-
tive sample of heart rate within each baseline phase.
HEART RATE, ALCOHOL, AND VLT PLAY
alcohol/kg body weight for men (1.29 mL/kg for women), mixed 1:4 parts
alcohol to cranberry juice. The dose targeted a peak BAC of 0.055%
(Stewart et al., 2005). Placebo drinks (cranberry juice only) were matched
for volume with the alcohol drinks. To provide taste and smell cues of
alcohol for the placebo participants, we spread a small amount of vodka
around the rim of each glass and a few drops of vodka were placed on the
top surface of each drink (cf. MacDonald, Stewart, Hutson, Rhyno, &
Loughlin, 2001). No additional visual cues were provided, as recom-
mended by Ross and Pihl (1989), to avoid excessive experimental demand
characteristics. As in Stewart et al. (2005), beverages were consumed
steadily over 20 –25 min, depending on volume. Participants then rested for
20 –25 min to permit alcohol absorption. A postdrinking baseline heart rate
was continuously recorded for 5 min (see Footnote 3). Participants then
provided a postdrinking BAC reading and were asked to rate their subjec-
tive level of intoxication on the VAS scale.
Participants were invited to use their own money to play the spinning
reels game on one of two VLTs for up to 15 min.
They were informed that
the odds of winning or losing were exactly the same as on any machine
they had played on previously in the province. They were told that they
could gamble as little or as much money as they wanted (up to a maximum
of the $80, which they had been provided at the onset of the study). This
maximum was set to ensure that participants did not spend money out of
their own pockets to play the VLTs in the lab. Participants were informed
that they would not be reimbursed for any money they lost while gambling.
Similarly, they were informed that they could keep or continue to play with
Heart rate was continuously recorded during this time.
Consistent with Stewart et al. (2005), 30 min after the beginning of the
VLT play session, participants provided a post-VLT play BAC reading and
completed a second VAS subjective intoxication measure. Smoking was
not permitted during testing. Participants were debriefed about their bev-
erage condition status, including an explanation to placebo participants as
to the nature and necessity of the placebo deception (cf. MacDonald et al.,
2001). If a participant was in the placebo condition, any winnings were
paid out and he or she was sent home. Alcohol participants remained until
BAC reached 0.04%. Taxi chits were available for transportation home if
a ride had not been previously arranged.
Demographic characteristics and addictive behavior measure
scores were examined in a set of 2 ⫻ 2 (Beverage Condition ⫻
Gambler Group) analyses of variance (ANOVAs) and chi-square
) analyses to ensure that random assignment to beverage con
dition was effective in balancing groups on potentially confound-
ing variables. Analyses revealed no significant main or interactive
effect of beverage condition and gambler group on age, gender,
marital status, educational history, annual income, years playing
VLTs, or number of drinks per week. As expected, a significant
main effect of gambler group was found for SOGS total score, with
those in the PPG group scoring significantly higher than those in
the NPG group (Ms ⫽ 8.8 vs. 1.6, respectively): F(3, 56) ⫽
150.43, p ⬍ .01. No other significant effects were revealed. Table
1 contains means and standard deviations on demographic and
addictive behavior variables as a function of Gambler Group ⫻
A2⫻ 3 (Gambler Group ⫻ Testing Time) mixed-model
ANOVA was performed on alcohol condition participants’ BACs.
Gambler group was included as a factor to ensure that the groups
did not differ in objective intoxication levels. The ANOVA re-
vealed only a testing time effect, F(2, 56) ⫽ 510.04, p ⬍ .01,
.948 (predrinking, M ⫽ .000%, SD ⫽ .000; postdrinking, M ⫽
.056%, SD ⫽ .012; and post-VLT play, M ⫽ .051%, SD ⫽ .009).
Post hoc tests revealed that relative to predrinking, BACs were
elevated at postdrinking, t(29) ⫽ 24.83, p ⬍ .01,
⫽ .955, and
post-VLT play, t(29) ⫽ 31.29, p ⬍ .01,
⫽ .971. BACs at
postdrinking and post-VLT play also differed, t(29) ⫽ 2.71, p ⬍
⫽ .140, with BACs falling slightly between the postdrink
ing assessment and the assessment following the completion of
VLT play. These results suggested that the experimental procedure
was quite successful in targeting the desired BAC of 0.055% at
postdrinking, and at keeping this BAC elevated close to the target
during VLT play.
A2⫻ 2 ⫻ 2 (Gambler Group ⫻ Beverage Condition ⫻ Testing
Time) mixed-model ANOVA was conducted on VAS scores at
postdrinking and post-VLT play. Again, gambler group was in-
cluded as a variable to ensure that groups did not differ in subjec-
tive intoxication levels. The ANOVA revealed only a testing time
main effect, F(1, 56) ⫽ 24.91, p ⬍ .01,
⫽ .948 (M ⫽ 31.80,
SD ⫽ 23.31, vs. M ⫽ 22.47, SD ⫽ 19.22, for postdrinking and
post-VLT play assessment times, respectively). The fact that there
were no beverage-condition effects on VAS scores supports the
supposition that the placebo manipulation was successful. Further-
more, although subjective intoxication scores decreased somewhat
from postdrinking to post-VLT play, t tests indicated that average
subjective intoxication was ⬎0 at both testing points, t(59) ⫽
10.57, p ⬍ .01,
⫽ .654, and t(59) ⫽ 9.06, p ⬍ .01,
We conducted a 2 ⫻ 2 ⫻ 3 (Gambler Group ⫻ Beverage
Condition ⫻ Testing Time) mixed-model ANOVA on heart rate at
the predrinking and postdrinking baseline measurement periods
and during VLT play. A testing time effect, F(2, 112) ⫽ 4.76, p ⫽
⫽ .078, emerged, along with the predicted Beverage
Condition ⫻ Testing Time interaction, F(2, 112) ⫽ 3.92, p ⬍ .05,
⫽ .065. Means and standard deviations for the hypothesized
Beverage Condition ⫻ Testing Time interaction are illustrated in
Figure 1. No other effects were revealed. In particular, the ex-
pected three-way interaction was nonsignificant, F(2, 112) ⫽ 1.21,
⫽ .021, providing no evidence for our hypothesis that
heart-rate increases to alcohol, VLT play, and their combination
would be greater among PPGs.
The length of the VLT play session and associated heart-rate recording
interval was decreased from 30 min in our original study to 15 min in the
present study for several reasons. First, we felt a shorter heart rate record-
ing interval would be more comparable to the 5 min intervals used at the
two baseline phases (see Footnote 3). Second, when offered the opportu-
nity to play for up to 30 min in our previous study (Stewart et al., 2005),
only half of the regular gambler participants chose to play for the full
allotted time (range ⫽ 18 –30 min). To maintain ecological validity, we
still allowed participants to self-select length of VLT play but shortened the
maximal interval to 15 min to reduce variability in length of the VLT play
section. All but 2 of our 60 participants chose to play for the full 15 min
allotted (range ⫽ 8 –15 min).
Although participants were informed at study outset that large wins
(e.g., more than $250) would be paid via check rather than cash, no such
large wins occurred during the course of the study.
STEWART, PETERSON, COLLINS, EISNOR, AND ELLERY
The significant two-way interaction was followed up with sim-
ple effects analyses and post hoc tests
to test the three specific
hypotheses regarding the effects of alcohol, VLT play, and their
combination on heart rate. Analyses of the simple effects of
beverage condition at each testing time revealed that alcohol-
condition participants displayed elevated heart rates, relative to
placebo participants, at postdrinking, F(1, 58) ⫽ 5.22, p ⬍ .05,
⫽ .083, and during VLT play, F(1, 58) ⫽ 4.14, p ⬍ .05,
.067, but not at the predrinking baseline, F(1, 58) ⫽ 0.28, ns,
.005, consistent with our hypotheses of heart-rate increases to
alcohol alone, and to the combination of alcohol intake and VLT
play, respectively. Although significant simple effects of testing
time were revealed both in the alcohol, F(2, 58) ⫽ 3.98, p ⬍ .05,
⫽ .121, and placebo, F(2, 58) ⫽ 4.74, p ⬍ .05,
conditions, the pattern of heart-rate changes over testing times
varied by beverage condition. For placebo participants, contrary to
our prediction that there would be no change in heart rate follow-
ing placebo beverage ingestion, post hoc tests indicated that heart
rates were significantly lower at postdrinking than at predrinking
baseline, t(29) ⫽⫺2.81, p ⬍ .01,
⫽ .214. As covered more
extensively in the Discussion, this effect may reflect an antago-
nistic placebo response that can occur when the participant is
expecting but does not receive alcohol (see Newlin, 1985). Par-
tially consistent with our expectation of heart rate increases to
VLT play alone, in the placebo group, heart rates at VLT play were
higher than at postdrinking baseline, t(29) ⫽ 3.05, p ⬍ .01,
.243. However, inconsistent with expectation, in the placebo
group, heart rates at VLT play were not higher than at predrinking
baseline, t(29) ⫽ 0.54, ns,
⫽ .010. For alcohol-condition
participants, contrary to the hypothesis involving alcohol-induced
heart rate increases, post hoc tests indicated that heart rates were
not elevated at post relative to predrinking, t(29) ⫽⫺0.61, ns,
⫽ .013. However, consistent with the hypothesis involving
VLT play-induced heart-rate increases, in the alcohol condition,
heart rate was elevated at VLT play relative to both predrinking,
t(29) ⫽ 2.80, p ⬍ .01,
⫽ .213, and postdrinking, t(29) ⫽ 2.03,
p ⬍ .05,
⫽ .125, baselines.
To determine whether heart rate increases to VLT play varied by
beverage condition (i.e., to further test the hypothesis that heart
rate increases to the combination of VLT play and alcohol intake
would be greater than those to either activity alone), we submitted
Because this study is relatively exploratory (i.e., the first study to
examine, within the same study, potential differences between PPGs and
NPGs in their relative sensitivity to heart-rate increases to alcohol, VLT
play, and their combination), we made an a priori decision not to adjust
levels in our post hoc tests to maximize our chances of observing the
hypothesized effects if they do exist. Nonetheless, as covered in the
Discussion, this decision increases the probability of Type I error.
Means and Standard Deviations on Demographic and Addictive Behavior Variables as a
Function of Beverage Condition and Gambler Group
Placebo (n ⫽ 15) Alcohol (n ⫽ 15) Placebo (n ⫽ 15) Alcohol (n ⫽ 15)
M 36.67 40.20 35.33 37.53
SD 10.93 10.51 9.02 8.48
n female 9988
n male 6677
n married/cohabiting 4552
n single/divorced/widowed 11 10 10 13
Annual income (1–7 scale)
M 3.00 2.73 3.47 3.07
SD 1.73 1.58 2.20 1.94
Years of schooling
M 12.93 13.47 13.80 14.40
SD 2.22 3.33 3.03 3.06
Smoke while gambling
n smokers 5665
n nonsmokers 10 9 9 10
Drinks per week
M 7.27 10.18 9.93 9.67
SD 5.33 10.76 7.63 7.04
SOGS total scores
M 1.27 2.00 9.07 8.60
SD 1.22 1.46 2.60 3.20
Years playing VLTs
M 7.27 6.87 6.40 6.87
SD 4.75 4.75 2.84 3.21
Note. NPG ⫽ nonpathological gamblers; PPG ⫽ probable pathological gamblers; SOGS ⫽ South Oaks
Gambling Screen; VLT ⫽ video lottery terminal.
HEART RATE, ALCOHOL, AND VLT PLAY
heart rate change scores (i.e., heart rate at VLT play minus heart
rate at predrinking baseline) to a 2 ⫻ 2 (Gambler Group ⫻
Beverage Condition) between-subjects ANOVA. The analysis re-
vealed only a beverage condition effect, F(1, 56) ⫽ 4.55, p ⬍ .05,
⫽ .075. As hypothesized, alcohol participants showed a greater
magnitude heart-rate increase to VLT play than did placebo con-
trols (M ⫽ 2.99 bpm, SD ⫽ 5.85, vs. M ⫽⫺0.75 bpm, SD ⫽ 7.62,
respectively). Again, the predicted Beverage Condition ⫻ Gam-
bler Group interaction was nonsignificant, F(1, 56) ⫽ 2.01, ns,
⫽ .035, providing no evidence that heart-rate increases to the
combination of VLT play and alcohol intake would be greater
among PPGs than among NPGs.
The present study was designed to investigate the existence of a
potential common reward mechanism that may underlie the rein-
forcing effects of drinking and gambling behavior among regular
VLT players. In effect, we set out to replicate and extend our
earlier study on this issue (i.e., Stewart et al., 2005) by investigat-
ing heart-rate responses to a moderately intoxicating dose of
alcohol, to VLT play, and to their combination, among a sample of
regular VLT players, half of whom were given alcohol and half of
whom received a mix-only control beverage. The two main
changes from our original study were the use of a placebo bever-
age to control for expectancy effects in the present study and the
use of a larger sample size that allowed us to investigate whether
regular gamblers identified as PPGs would show greater heart-rate
increases in response to alcohol and/or gambling. We hypothesized
that alcohol would lead to increases in heart rate relative to both
heart rate at the predrinking baseline and heart rate in the group
administered placebo. We also hypothesized that VLT play would
increase heart rate relative to pre- and postdrinking baselines even
among those consuming placebo and that the combination of VLT
play and alcohol intake would result in further heart rate increases
relative to either activity alone. Finally, we hypothesized that the
above effects would prove stronger among PPGs relative to NPGs.
In the current study we were able to partially replicate Stewart
et al. (2005) with respect to the effects of alcohol. Previous
research shows that alcohol consumption increases heart rate rel-
ative to placebo (cf. Peterson et al., 1993, 1996; Stewart et al.,
1992) and we expected to see heart rate elevations in those ad-
ministered alcohol relative to those administered placebo in the
present study at postdrinking baseline. This hypothesis was sup-
ported in that participants in the alcohol condition displayed ele-
vated heart rate relative to participants in the placebo condition at
postdrinking but not at the predrinking baseline.
We were also able to partially replicate Stewart et al. (2005)
with respect to the effects of VLT play, extending our previous
findings of heart rate increase with a video poker game to the more
popular type of spinning reels VLT game. All players, regardless
of beverage condition, showed elevated heart rates at VLT play,
relative to postdrinking baseline. However, heart rates were ele-
Figure 1. Mean heart rate in beats per minute (bpm) as a function of beverage condition and testing time.
VLT ⫽ video lottery terminal. Error bars represent standard deviations.
STEWART, PETERSON, COLLINS, EISNOR, AND ELLERY
vated during VLT play relative to predrinking baseline only among
those administered alcohol, suggesting that the effects of gambling
on heart rate interacted with beverage condition. We examined this
interactive effect of drinking and VLT play more directly by
comparing the degree of increase from predrinking baseline to
VLT play in each beverage condition in a supplementary set of
statistical analyses. As hypothesized, and consistent with our ear-
lier study (Stewart et al., 2005), we did see that the degree of
increase from predrinking to VLT play was greater for those in the
alcohol condition. Thus, the combination of VLT play and alcohol
consumption does appear to be linked to an additional heart-rate
increase, compared with the heart rate increase associated with
engaging in either addictive behavior alone, which may help
explain the frequent pairing of these two activities in both clinical
and nonclinical populations (Focal Research, 1998; Stewart &
Kushner, 2003; Stewart et al., 2002).
Although most aspects of our original study (Stewart et al.,
2005) were replicated, there were some important differences as
well. For example, contrary to hypothesis, alcohol participants
showed no significant increase in heart rate from pre- to postdrink-
ing baselines. This was surprising given that several studies (e.g.,
Stewart et al., 1992, 2005) have shown that alcohol increases heart
rate from resting baseline. We also found placebo participants
actually had higher heart rates at predrinking than at postdrinking
baseline. It appears most likely that this was a consequence of a
conditioned compensatory response. Newlin (1985) found an au-
tonomic response in placebo-condition participants that was op-
posite in direction to the effects of alcohol among a sample of male
social drinkers. In effect, the cues associated with drinking alcohol
(e.g., bar setting, smell of vodka) may have elicited a conditioned
compensatory response, causing heart rate to decrease in anticipa-
tion of receiving the beverage, resulting in heart rate deceleration
in the placebo-condition participants from the pre- to the post-
drinking baseline. This conditioned compensatory response was
presumably not operative in our last study because we used a
control beverage rather than a placebo beverage in the latter
(Stewart et al., 2005). This explanation could also be used to
account for the lack of change between pre- and postdrinking
baselines in the alcohol group in the present study. Specifically, a
conditioned compensatory heart rate deceleration in the alcohol-
condition participants could have countered the expected stimulant
effects of alcohol, resulting in no net change from pre- to post-
drinking baseline in this beverage condition.
Contrary to hypothesis, the present study also found no effects
of gambler group on degree of heart rate response to gambling,
drinking, or their combination. The failure to observe between-
groups differences in heart rate increases to these addictive activ-
ities was not secondary to differences in heart rate at the predrink-
ing resting baseline. This latter finding is in contrast to predictions
that would be made on the basis of Jacobs’s (1986) general theory
of addictions in which he postulates that abnormalities in physio-
logical resting state predispose people to persistent, uncontrolled
behavioral patterns involving both drinking and gambling. The
failure to find the hypothesized gambler group differences in heart
rate reactivity to gambling, alcohol, or their combination could be
due to several factors.
First, our control group consisted of regular gamblers who were
not preselected into groups at high or low risk for gambling
problems. Thus, some of those in the control group may have been
susceptible to heart rate increases to gambling (and/or alcohol)
because of their high-risk status, washing out any between-groups
differences. A second explanation pertains to the measurement
instrument used in the present study (i.e., the original SOGS;
Lesieur & Blume, 1987). Given problems recently identified with
the original SOGS as a measure of gambling problems (Strong,
Lesieur, Breen, & Stinchfield, 2004), future research should use an
alternative method for identifying PPGs (e.g., Canadian Problem
Gambling Index, Ferris & Wynne, 2001; DSM–IV-based question-
naire, Beaudoin & Cox, 1999) to ensure that our null findings are
not due to measurement problems. Third, given recent research on
the validity of subtyping gamblers (e.g., Blaszczynski & Nower,
2002; Stewart, Wall, Loba, Stuart, & Ellery, 2004), it is possible
that certain subtypes of gamblers might be more or less sensitive
to the heart rate effects of gambling and alcohol. In future research
it would be interesting to determine whether enhancement-
motivated gamblers (a subtype who self-report gambling specifi-
cally to increase positive affect; Stewart et al., 2004) or impulsive
gamblers (a subtype with difficulties regulating behavior in the
presence of cues for reward; Blaszczynski & Nower, 2002) show
increased sensitivity to the positively reinforcing effects of gam-
bling (and/or alcohol) indexed by degree of heart rate response to
these addictive activities, relative to other gambler subtypes.
Fourth, the findings may indeed be valid in that there may be no
greater sensitivity to heart rate increases among PPGs. In fact, a
similar lack of relation between heart rate response to gambling
and severity of pathological gambling has been observed in pre-
vious studies (e.g., Diskin & Hodgins, 2003; Meyer et al., 2000).
Finally, it is possible that the combination of VLT play and alcohol
intake might be particularly addicting to potential alcoholics who
gamble (and therefore show an exceptionally enhanced heart rate
in the combined condition), rather than to potential problem gam-
blers who drink.
Several potential limitations to the current study should be
noted. One possible limitation pertains to the heart rate recording
equipment used. We used a photoplethysmograph attached to a
finger on the nondominant hand to collect IBI data that were later
converted to bpm values. Although some would argue that a more
appropriate method for heart rate recording would be through the
use of an electrocardiogram and electrodes placed on the chest
(e.g., Stewart et al., 1992), others have argued for the value of IBI
measurements in studies on heart rate (e.g., Heslegrave, Ogilvie, &
Furedy, 1979). Another possible limitation pertains to the possi-
bility that heart rate measures may have been influenced by minor
movement artifact, particularly during the VLT play phase, which
involved some small degree of movement. Nonetheless, studies
that have included a movement baseline control condition have
showed that heart rate increases to gambling are larger than those
caused by the minimal movement involved in gambling activity
(Coventry & Norman, 1997) making this possible explanation of
our findings unlikely. A further possible limitation was the rela-
tively small sample size per group in the 2 ⫻ 2 (Gambler Group ⫻
Beverage Condition) between-subjects design that may have pre-
cluded observation of the predicted interaction between these
variables on heart rate. Nonetheless, observation of effect sizes
involved in the predicted interactions involving the gambler status
variable indicate that low power is unlikely to explain the absence
of differences in heart rate reactivity across the PPG versus NPG
groups. We should also caution that our choice not to adjust
HEART RATE, ALCOHOL, AND VLT PLAY
our post hoc tests (see Footnote 6) may have resulted in an
increased probability of Type I errors. Finally, the present inves-
tigation was an analogue study that carries with it the usual
concerns about ecological validity.
The present findings are consistent with the possibility that
alcohol consumption and VLT gambling are associated with heart
rate increases that might reflect activity of the incentive reward
system (Peterson et al., 1993). If future research were to establish
the involvement of the dopamine reward system in the heart rate
response to these two addictive activities, the drug naltrexone (an
opiate antagonist that inhibits dopamine release in the nucleus
accumbens, O’Malley, 1996 and that reduces alcohol consumption
by making alcohol ingestion less pleasurable and rewarding, Gi-
anoulakis, 1996) might prove useful in treating those with comor-
bid alcohol and gambling disorders. It would be interesting to
replicate and extend the present study, with the addition of a
naltrexone versus pill placebo manipulation (cf. Peterson et al., in
press) to determine whether this drug would block the observed
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Received June 18, 2004
Revision received December 21, 2004
Accepted December 27, 2004 䡲
HEART RATE, ALCOHOL, AND VLT PLAY