Eehac. Res. Thu. Vol. 26, No. 5. pp. 369-381, 1988 ON357967188 53.00 + 0.

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Printed in Great Britain Pergamon Press plc

INVITED ESSAY
ALCOHOL AND ANXIETY

G. TERENCE WILSON
GSAPP, Rutgers University, Box 819, Piscataway, NJ 08854, U.S.A.

(Receiced 4 Murch 1988)

INTRODUCTION

Readers who watch the American television show Dallus might recall the following episode: A
public altercation at a major social reception at the Ewing ranch causes conflict, embarrassment
and tension. J. R. Ewing, speaking to his father, Jock, sees a passing waitress with champagne and
says something in the order of, “Here, you need one of these” as he reaches for a glass of bubbly.
Jock replies that he needs “something a lot stronger than that.” The two go off to a local bar, get
intoxicated, reappear happy, laughing and relaxed, and drive home intoxicated but safely. This
vignette, aside from exemplifying the unfortunate modeling of a destructive drinking pattern
(Wilson, in press), illustrates the widely shared conviction that alcohol reduces tension or anxiety.
This, of course, is the well-known tension or anxiety reducing theory of alcohol use and abuse.
It is not surprising that television would portray this function of alcohol. One of the most striking
features of the anxiety reduction theory is how widely it is believed. Both social and problem
drinkers subscribe to the belief, the latter even more strongly than the former (Edwards, 1972;
Goldman, Brown and Christiansen, 1987). Therapists who treat alcoholism also hold to this view
(Cappell, 1975). Even such erstwhile foes as psychoanalysis and learning theory agree on this
putative property of ethanol. The superego has been defined as that part of the psyche that is
soluble in alcohol. Learning theorists have looked to alcohol’s anxiety reducing effects as a negative
reinforcer of maladaptive behavior. Not insignificantly, English literature and poetry contain some
of the classic statements of alcohol’s anxiety reducing effects.
Almost as striking as how commonly held this belief in alcohol’s anxiolytic effects has been, is
first, the influence of the anxiety reduction theory of alcohol on the behavior of researchers across
disciplines; and second, the difficulty we have ‘encountered in consistently demonstrating such
effects in people in the experimental laboratory.
Since it was formally spelled-out by Conger (1956), the tension or anxiety reducing theory has
had a profound impact on research on alcohol. Three decades later it continues to generate studies
and stir debate. The global terms “anxiety” and “tension” can be used roughly synonymously.
Attempts to draw finer distinctions have not been successful. Stress reduction is another common
and broadly comparable term. Most recently, Levenson and Sher have introduced the term “stress
response dampening” to describe alcohol’s effects. Although it is narrower in scope, there is
probably little to be accomplished by trying to distinguish the stress response dampening model
from what has come to be known as the tension reduction theory (Blane and Leonard, 1987). Sher
(1987) himself characterizes the stress response dampening model as “a modest, pared-down
tension reduction hypothesis” (p. 234).
It is not difficult to understand why the anxiety reducing theory has had such broad and lasting
appeal. Demonstrating robust anxiolytic effects of alcohol would help elucidate the causes of
alcohol abuse and steer us towards what would need to be put right in order to help alcoholics.
But the theory promised more than a plausible account of the development and maintenance of
alcohol abuse. Potentially, alcohol’s commonly observed actions on a range of everyday activities
might be explained. As Neal Miller, one of the pioneers of research in this area put it, “alcohol
has a perplexing variety of effects, making some aggressive, others amorous, some tearful, and
others talkative” (1964). However, if we assume that the diverse behavior that follows alcohol
consumption was previously inhibited by anxiety-a plausible assumption in many instances-then
369
370 G. TERENCE
WILSON

these apparently unrelated effects can all be explained by a single mechanism of action-that of
anxiety reduction.
Unfortunately, however, as several reviewers of the field have observed, controlled experimental
studies have often yielded conflicting and inconclusive findings. Alcohol has variously been shown
to decrease anxiety, increase it, or simply have no effect (Cappell and Greeley, 1987; Pohorecky
and Brick, 1983; Sher, 1987). Rather than serving as the single mechanism that can help explain
other phenomena, the interaction between alcohol and anxiety is itself in need of explanation.

ANIMAL STUDIES

There are really two parts to the anxiety reduction theory. The first is that alcohol reduces
anxiety, the second that this action motivates drinking. My focus here is on the first, and perhaps
more fundamental component-that intoxication does indeed reduce anxiety.’ Although my
emphasis is on human research, I must first note the substantial literature on animal studies of
ethanol’s effects on stress.
Overall, these studies have shown that alcohol attenuates the neuroendocrine response to stress,
For example, Brick and Pohorecky (1983) have shown that a low dose of ethanol reduces the
stress-induced increase of corticosterone and nonesterified fatty acids in rats. They found this
protective effect of ethanol in response to both physical and psychological stressors. Similarly,
Vogel and DeTurck (1983) reported that the elevations in plasma and brain catecholamines in rats,
due to immobilization, were prevented by prior administration of ethanol.
Although the stress-attenuating effect of alcohol at the neuroendocrine level has been reliably
demonstrated in rats, the mechanism(s) of this interaction have yet to be established. Brick and
Pohorecky (1983, 1985) argue for a mechanism at the level of the central nervous system. Most
recently, research on the compound imidazodiazepine (Ro-15-45 13) suggests that the stress-
reducing and intoxicating effects of alcohol are mediated by central GABA receptors. Ro-15-45 13
acts at GABA receptors. Pretreatment of rats with Ro-15-4513 blocks the anxiety-reducing effect
of alcohol-but not pentobarbital-as well as the behavioral intoxication at high doses of alcohol
(Suzdak, Glowa, Crawley and Schwartz et al., 1986).
In contrast to these studies of neuroendocrine response, controversy has marked the inter-
pretation of behavioral studies of alcohol’s effects on tension operationalized as fear and avoidance
responses. Although Cappell, in his much cited 1975 review, asserted that the evidence was
equivocal or negative, Hodgson and his colleagues in London concluded that relevant animal
studies supported the theory (Hodgson, Stockwell and Rankin, 1979). The key word here was
“relevant”. The English group argued that only those procedures that evaluate the effects of alcohol
on fear or frustration (e.g. procedures for studying experimental neurosis, conflict, and passive
avoidance) provide a fair test of the theory. These, they claimed, supported the theory. Negative
results, they contended, came primarily from studies using escape learning and well-learned active
avoidance responses, which they suggested, are not mediated by fear or frustration and therefore
are ill-suited to testing the theory.
In summary, then, the evidence of an anxiolytic or stress-reducing effect of alcohol in animals
is generally positive.

HUMAN STUDIES

One way to view the conflicting results of experimental studies with people is to attribute them
to the heterogeneity of methods and measures used to investigate alcohol’s effects on anxiety. As
part of this methodological diversity, for example, anxiety (or a comparably global concept of
“tension” or “stress”), has been conceptualized in different ways in different studies, including,

‘There is a related, but rarely discussed set of studies that have investigated the effect of induced anxiety (threat of
an electric shock) not on subsequent drinking, but on the effects of intoxication itself. For example, it has been
shown that anxiety may counteract the inhibitory of effect of intoxication on a performance task (Frankenhaeuser,
Dunne, Bjurstrom and Lundberg, 1974). This effect has been referred to as “pulling oneself together.” Frankenhaeuser
and her group in Sweden attribute the effect to the person’s “cognitive evaluation of the situation” (p. 277).
 Alcohol and anxiety 371

among other things, experimentally-induced conflict; aversive stimuli (e.g. fear of an electric shock),
social stressors (e.g. the anticipation of a self-disclosing speech, or a challenging or disagreeable
interaction with a member of the opposite sex); and phobic avoidance.
Anxiety has also been assessed in various ways, including diverse forms of self-report, different
measures of autonomic nervous system arousal, biochemical indices and observational and
behavioral measures. Influenced by Lang and Rachman’s triple response system analyses of anxiety
and its reduction, researchers have increasingly included multiple measure of this construct in their
studies. As I shall note, these different measures do not always change in the same direction. This
desynchrony among the three response systems is not unique to research on alcohol and anxiety.
It has been extensively documented in the assessment and treatment of anxiety disorders (Lang,
1969; Rachman, 1978). Desynchrony does, however, complicate interpretation of studies of
alcohol’s effects still further. It might be that the different factors that influence alcohol’s effects
on anxiety will have partially separate effects on the different response systems that comprise
anxiety.
For the most part, different studies have used different methodologies, making comparison
across studies extremely difficult if not impossible. Even in what at first appears to be a replication
by one group of investigators of another group’s specific experimental procedures for inducing and
measuring anxiety, subtle differences can be detected-the consequences of which are hard to assess
(e.g. Steele and Josephs, 1988).
Nevertheless, I suggest that it is implausible to attribute the conflicting results in the literature
simply to the diversity of experimental procedures that have been used. Rather, the data reflect
what is a complex relationship between alcohol and anxiety. Asking the question “Does alcohol
reduce anxiety?” was conceptually naive. The oftenmade assumption of some invariant and
automatic effect of alcohol on anxiety ignored the multiple bio-psychosocial factors of which this
effect is a function. As I pointed out some years ago, borrowing from Gordon Paul’s (1967)
reframing of the question of the effectiveness of psychological therapies, the more meaningful
question that must be addressed is “At what dose, under which conditions, in whom, and on what
measures does alcohol reduce anxiety?” (Wilson, 1982).
For the past 12 years my students’ and I have pursued a research program guided by this
question, and I draw heavily on our cumulative findings in my following analysis. We have focused
mainly on social anxiety. We chose to investigate social anxiety for two reasons: First, previous
research had indicated that social anxiety or interpersonal evaluation is more likely to elicit
drinking than other sources of anxiety induction (e.g. Higgins and Marlatt, 1975). Second, clinical
experience suggested that interpersonal anxiety and stressful social situations are among the most
common and prominent determinants of alcohol abuse.

VARIABLES THAT DETERMINE ALCOHOL’S EFFECTS ON

ANXIETY DOSE

In his 1969 tome, Bandura concluded that small doses of alcohol have no consistent effect, but
that moderate to large quantities may produce substantial reductions in anxiety. Despite some
contradictory findings, subsequent research has tended to support this conclusion.
In 1980, Abrams, Lipscomb and Wilson reported that alcohol’s effects on social anxiety in young
men were dose dependent, with significantly greater anxiolytic effects at a high dose level of roughly
!g/kg. Both measures of autonomic arousal and observations of subjects’ behavior during an
interaction in which they were asked to make as favorable an impression as possible on a female
confederate of the experimenters, showed this effect. Self-report of anxiety did not, however. Sher
and Walitzer (1986) have subsequently replicated this finding of the dose dependent relationship
between alcohol and heart rate reduction in male social drinkers. They also found a significant but
weaker effect on self-report of anxiety.

*I wish to acknowledge the contributions of David B. Abrams, as well as the support of my colleague Peter E. Nathan,
and the staff of the Rutgers Alcohol Behavior Research Laboratory.
372 G. TERENCE
WLSON

It has been claimed that a relatively high dose of alcohol (roughly lg/kg) is required to reduce
anxiety (Sher and Levenson, 1982). However, there are too many exceptions to place much
confidence in such a conclusion. For example, Sher and Walitzer (1986), obtained a significant and
large reduction in heart rate in response to social anxiety at as low a dose as 0.425 g/kg.
Nevertheless, the reduction of heart rate arousal in response to a stressor at a relatively high
BAL does seem to be more consistent outcome (Levenson et al., 1980; Niaura et al., 1987; Zeichner
et al., 1983).

Cognitive set
To understand alcohol’s effects on social and emotional behavior we have to go beyond its
pharmacological impact and examine the psychosocial context in which drinking occurs. The
beliefs people hold about alcohol’s effects and the consequences of intoxication have been shown
to influence a range of important psychosocial phenomena (Marlatt and Rohsenow, 1980;
Wilson, 1981). Wilson and Abrams (1977) used the balanced placebo design to investigate the
effects of both alcohol and alcohol expectations in male social drinkers. We found that subjects
who believed that they had consumed alcohol showed less anxiety than subjects who believed that
they were sober, irrespective of the actual consumption of a low dose of alcohol. Once again, we
demonstrated this effect on both heart rate arousal and observational measures of subjects’
behavior during the social interaction, but not self-report of anxiety.
Further evidence of the influential role of expectations of alcohol’s effects on anxiety-related
behavior comes from our analyses of self-disclosure in interpersonal interactions. Caudill, Wilson
and Abrams (1987) have shown that male social drinkers who believed that they were intoxicated,
irrespective of whether or not they had actually consumed alcohol, engaged in significantly greater
self-disclosure than their peers who believed that they were sober.
Other studies, including one of our own (Wilson, Perold and Abrams, 198 1) have called this effect
of alcohol expectations into question, however. For example, Sher and Walitzer found no
significant correlation between subjects’ expectations about alcohol’s relaxing effects and measures
of social anxiety. Nevertheless, expectations about alcohol’s stress-reducing effects are correlated
with drinking behavior in different populations (Goldman et al., 1987).

ENVIRONMENTAL SETTING

The physical and social surroundings in which alcohol is consumed have been shown to influence
the rate and amount of consumption, as well as the effects of intoxication. This relationship bears
on alcohol’s effects on anxiety. Following our earlier finding of the significant influence of subjects’
expectations on the degree of anxiety they experienced, we examined subjects’ expectations of their
partner’s drinking in dyadic social interaction (Wilson et al., 1981). We found that if male social
drinkers believed that the unfamiliar woman, whom they were asked to impress in a social
interaction, had been drinking, they reported less anxiety than if they believed that she was sober.
Ratings of subjects’ behavior by independent observers confirmed these self-reports. Our male
subjects who had been led to believe that their partner had consumed alcohol were not only rated
as less anxious but were also seen as more personally attractive and likable. An analysis of subjects’
self-disclosure revealed the same pattern of results (Caudill et al., 1987).
We concluded that not only individuals’ expectations about their own intoxication, but also their
expectations about a partner’s drinking can significantly influence social anxiety and self-disclosure.
The importance of the context in which drinking occurs has also been shown by other
investigators. For example, the concurrent behavior the person engages in while drinking, appears
to moderate alcohol’s effects on self-reported anxiety, at least under some conditions. If this
concurrent activity is affectively neutral or pleasant, drinking reduces stress; if it is unpleasant it
may increase stress (Langenbucher, 1985; Steele and Josephs, 1988).

INDIVIDUAL DIFFERENCES

It is hardly novel to note that drugs-including alcohol-affect different people in different ways,
and perhaps at different times. What is more novel-and I believe, most significant-has been the
 Alcohol and anxiety 373

increasingly systematic experimental analysis of the role of individual differences in understanding

alcohol’s effects on anxiety. Several lines of evidence now indicate the central importance of
individual differences in moderating alcohol’s effects on anxiety or stress. (These data have a
parallel in animal studies. Vogel and Deturck (1983) noted “Large individual differences in the
response to ethanol during stress. . . Selective breeding of low and high ethanol responders showed
that the stress response alone and the effects of ethanol on the stress response carry a genetic
component” [p. 4371).

Risk factors for alcoholism

Well-controlled research by Levenson and Sher and their associates has shown how two
well-known risk factors for alcoholism may critically influence alcohol’s effects on anxiety. In one
set of studies, male social drinkers selected for characteristics typical of pre-alcoholics (e.g. traits
related to impulsiveness, aggressiveness (and extraversion) have shown greater stress-reduction
from alcohol than their peers who did not have these characteristics (Levenson, Oyama and Meek,
in press; Sher and Levenson, 1982). However, other studies have produced less consistent results,
leading Sher (1987) to conclude that the effect is not robust across studies. The role of these person
variables needs further investigation.
Another risk factors for development alcoholism is being a child of an alcoholic. Levenson et
al. (in press) have recently shown that male and female subjects with an alcoholic parent showed
a greater reduction in physiological measures in response to a stressor. The implications are clear:
Alcohol appears to be a more potent reinforcer-by virtue of its anxiety reducing properties-for
individuals at risk for alcohol abuse than for those not at risk. The differential anxiety reducing
effect of alcohol is a possible mechanism for explaining why these at risk individuals might go on
to develop drinking problems.

Self-awareness
Other person variables have been related to alcohol’s effects on anxiety. According to Hull’s
(1981) self-awareness theory, individuals who are high in dispositional self-awareness or self-
consciousness are especially prone to alcohol’s stress-reducing effects. The theory holds that alcohol
reduces anxiety secondarily as a function of decreasing self-awareness and hence negative (and
anxiety-inducing) self-evaluation. The evidence is mixed. Hull, Young and Jouriles (1986) have
reported that in alcoholics high in dispositional self-consciousness, relapse was significantly
associated with negative self-relevant life events. In alcoholics low in this trait, negative self-relevant
life events were unrelated to relapse. However, laboratory research has generally not indicated a
significant effect of dispositional self-consciousness on alcohol and anxiety (Sher and Walitzer,
1986; Wilson et al., 1987). In one study, it was consistently those individuals who were low
in dispositional self-consciousness who showed the greatest stress-reduction following alcohol
consumption, as discussed next.

Type A behavior pattern

Alcohol’s effects on Type A behavior pattern has been a focus of recent experimental study.
Zeichner, Feurerstein, Schwartzman and Reznick (1983) first showed that alcohol reduced
physiological arousal in response to a stressful quiz in male subjects classified as showing the Type
A behavior pattern, relative to sober Type A’s Niaura, Wilson and Westrick (in press) have
replicated and extended this study with additional controls. Overall, across all subjects, we found
a strong stress reduction effect of alcohol on heart rate, but not self-report. Type A behavior pattern
did have a significant effect on the results. We found that Type A subjects who were low in
dispositional self-consciousness showed the highest systolic blood pressure reactions during a
self-disclosing speech, and were most affected by alcohol. Alcohol completely attenuated this blood
pressure reaction.
Given Hull’s theory we had anticipated a stress reducing effect in subjects high self-
consciousness. Our interpretation of what appears to be the opposite result is that subjects low in
self-consciousness might habitually avoid self-awareness. The forced self-awareness implicit in the
task in this study-giving a self-disclosing speech, about one’s body, which was allegedly
 374 G. TWNCE WILSON

videotaped for later analysis-may have been particularly stressful, and correspondingly responsive
to alcohol’s effects.
Although a second study by Zeichner with college students failed to replicate his earlier results
(Zeichner, Edwards and Cohen, 1986), the results from these studies of Type A behavior pattern
may bear on an explanation of alcohol’s apparently protective effects against coronary artery
disease. Research suggests that autonomic hyperreactivity to psychological stress facilitates the
development of coronary artery disease (CAD). If, as several studies have now shown, alcohol
reduces such autonomic hyperreactivity, this action might mediate some of its protective effects on
the heart. Animal research has also highlighted the possible relationship between alcohol’s effects
on stress and its protective effects against CAD. Brick and his colleagues at Rutgers have shown
that pretreating rats with ethanol significantly attenuates the stress-induced increase in heart
lipoprotein lipase (LPL) which presumably reduces the uptake of triglycerides into the heart (Brick
et al., 1987).

Anxiety disorders
The research 1 have discussed thus far has involved the experimental induction of some form
of anxiety or stress. Another way to examine alcohol’s presumed anxiolytic influence is to study
its effects on individuals with high, naturally occurring anxiety-such as patients with anxiety
disorders. The link between alcohol and clinical anxiety disorders has only recently begun to attract
attention. On the one hand, a significant number of alcoholics have anxiety disorders (Smail et al.,
1984; Stockwell et al., 1984; Thyer et al., 1986). In many of these alcoholics, the anxiety disorder
(typically agoraphobia or social phobia) seems to have preceded the onset of alcoholism. Although
the precise sequencing of the development of the anxiety disorder and the alcoholism is not always
clear (Bowen et al., 1984), alcohol abuse has been interpreted as a form of self-medication to reduce
anxiety symptoms (Quitkin, Rifkin, Kaplan and Klein, 1972).
On the other hand, many anxiety disorder patients report alcohol abuse (Thyer et al., 1986).
DSM-III-R, for example, tells us that alcohol abuse is especially likely in women with agoraphobia
and men with social phobia. In an illustrative study, Bibb and Chambless (1986) reported that from
10 to 20% of outpatient agoraphobics were alcoholic according to DSM-III criteria (and as the
authors note, this is probably a conservative figure). Fully 91% of the patients with a history of
alcoholism and 43% of those without such a history drank to reduce phobic anxiety and control
disturbing cognitions. I might note in passing that Westphal, the German neurologist, who first
used the term agoraphobia to describe three male patients who feared public places, also prescribed
three means of easing the phobia-a trusted companion, a walking stick and alcohol. Alcohol abuse
among patients with PTSD appears to be high (Goodwin, 1986).
Experimental research has complicated this picture-a recurring theme in this area! Two studies
have shown that alcohol did not reduce either phobic anxiety or avoidance behavior in simple
phobics (Cameron, Liepman, Curtis and Thyer, 1987; Thyer and Curtis, 1984). A third found that
alcohol reduced subjective fear but not avoidance behavior in simple phobics (Rimm et al., 1981)
while still a fourth experiment showed that alcohol did reduce avoidance behavior (Lindman, 1980).
Importantly, Cameron et al. (1987) found that alcohol retarded the rate of in uko desensitization
treatment of simple phobia. They contrast this finding with a similar study of diazepam, which
increased approach to a phobic object. This is one of what appear to be several differences in
anxiolytic effects between alcohol and benzodiazepines, as emphasized by Cappell and Greeley
(1987). If alcohol reduces anxiety, it seems to be by mechanisms dissimilar from those of the
benzodiazepines. (Alcohol is less likely to work than Valium or librium, loses its effectiveness more
quickly, and may be experienced as more aversive).
It is possible that direct experimental tests of alcohol’s effects on patients with anxiety disorders
other than simple phobia will similarly reveal negative or conflicting findings. The other possibility
is that there are important pathophysiological differences among the various anxiety disorders
which interact differentially with alcohol. Research in this area may help us understand both the
nature of the differences among the anxiety disorders as well as the mechanisms of alcohol’s actions.
Several current theories interpret alcohol’s anxiolytic properties in terms of its effects on cognitive
processes (e.g. attention allocation, self-evaluation, and attributional processes). To speculate, it
might be that alcohol is self-medicating only in those cases where the anxiety has a significant
 Alcohol and anxiety 375

cognitive component. Simple phobias can be seen as primarily non-cognitive in nature. The
documented absence of anxiety reducing effects of alcohol in simple phobics fits this analysis.
Agoraphobia may be the anxiety disorder that is most responsive to alcohol. The anticipatory
anxiety-the fear-that is characteristic of this disorder is readily conceptualized in cognitive terms.
Moreover, agoraphobics appear to have a distinctive, anxiety-inducing attributional style (Fisher
and Wilson, 1985; Goldstein and Chambless, 1982). Are these the elements of the anxiety disorder
that are influenced by alcohol, and does this lead to anxiety reduction? It can certainly be argued
that there are important cognitive components of social phobia, generalized anxiety disorder, and
panic disorder. Experimental analyses of alcohol use by anxiety disorder patients are needed to
answer these questions.

Alcoholics and problem drinkers

If the tension reduction theory has merit, we should, at the very least, find that alcohol has an
anxiolytic effect in the people most critically affected by alcohol-alcoholics. Ironically, it was the
emergence of inpatient behavioral research on actual drinking by alcoholics that helped to call the
tension reduction theory into question. Studies of the chronic administration of alcohol to
alcoholics gave rise to the rapidly accepted notion that intoxication had a “paradoxical”,
tension-inducing effect on alcoholics. As they continued to drink, the alcoholic subjects in these
studies were said to increasingly report dysphoria or negative affect.
In retrospect, these studies were, for the most part, inadequately designed to test the anxiety
reduction theory. Their results, which were uncritically interpreted, confused rather than clarified
the issues. In a comprehensive and incisive analysis of this literature (all 15 chronic administration
and 13 acute administration studies in alcoholics from 1964 to 1984), Langenbucher has
underscored the irrelevance of many of these studies to the theory, and has concluded that the
better controlled studies tended to support, rather than disconfirm, the tension reduction theory.
However, because of various methodological limitations, this body of research does not un-
equivocally confirm the theory.

Tolerance and drinking patterns

Not surprisingly, tolerance seems to play a role in mediating alcohol’s effects on anxiety. Wilson
et al. (1980) found that intoxicated male social drinkers who were high in tolerance showed less
anxiety reduction, as indexed by heart rate to a psychosocial challenge, than comparable, low
tolerant subjects. Tolerance here was defined in terms of degree of body sway when intoxicated.
We concluded that to the extent that alcohol reduces anxiety, it works less well for the drinker
who is more tolerant. As a result, the highly tolerant drinker who has learned to drink in response
to stressful experiences must consume more alcohol to achieve the desired effect. Increasing
consumption may lead, in turn, to even greater tolerance, thereby further increasing the dose
required to reduce or control anxiety. In short, tolerance and the anxiolytic effects of alcohol may
interact to produce continued drinking.
In a recent study of female social drinkers, Wilson, Brick, Adler, Cocco and Breslin (in press)
obtained comparable results. High tolerant female social drinkers, when intoxicated, showed more
anxiety (defined by increased heart rate and systolic blood pressure) than their low tolerant peers.
In neither of these studies was tolerance a function of drinking pattern. In commenting on our
findings, Sher (1987) has suggested that what was analyzed was constitutional sensitivity to alcohol
rather than the effect of experiential factors.
Few data are available on the impact of different drinking patterns on the relationship between
alcohol and anxiety. Smith, Parker and Noble (1975) reported that subjects with more experience
with alcohol showed less anxiety during a social interaction, after drinking, than did comparable
subjects with less drinking experience. However, Wilson et al. (1980) found that heavier, more
experienced drinkers did not differ from more moderate drinkers.

Gender
Potential gender differences in alcohol use and abuse must always be considered. Alcohol’s effects
on anxiety, and anxiety-related phenomena, may be a good case in point. In 1976, Polivy,
376 G. TERENCE
WILSOS

Schueneman and Carlson reported that women who has been led to believe that they were
intoxicated showed increased social anxiety. Abrams and Wilson (1979) replicated this finding, as
did Sutker, Allain, Brantley and Randall (1982), which stands in contrast to findings with men.
Also in opposition to findings with male subjects, women who believe that they have consumed
alcohol display less self-disclosure than their sober peers, irrespective of whether or not they have
drunk alcohol (Caudill, Wilson and Abrams, 1987). Perhaps not surprisingly, Rohsenow (1983)
found that women generally report expectations of less relaxation and tension reduction from a
few drinks than men. A dose-response relationship between increasing BAL and anxiety reduction
or dampening holds for men (Wilson et al., 1980) but not, apparently, for women (Wilson et al.,
in press). Men show self-handicapping effects of consuming alcohol, but not women (Bordini and
Tucker et al., 1986). In research by Konovsky and Wilsnack, intoxicated women, but not men,
report lowered self-esteem (Konovsky and Wilsnack, 1982).
Lest we too quickly conclude that there really is a gender difference in alcohol’s effects on anxiety,
however, consider the results of two recent studies. In one, Levenson et al. (in press) found that
alcohol reduced physiological measures of stress equally in both men and women. Neither did
gender interact with risk status (either personality type or having and alcoholic parent). These
investigators concluded that “there is much more that is similar than is different” between the sexes.
Importantly, Levenson et al. were careful to control for extent of drinking experience, and included
both sexes in the same study. Whether or not the differences obtained in other studies can be
attributed to uncontrolled sampling differences remains to be seen. In a second study, Steele and
Josephs (1988) similarly reported no difference between men and women in alcohol’s effects on
self-report of anxiety in response to a social stressor.
I have focused on experimental, primarily laboratory studies in evaluating alcohol’s effects on
anxiety. An alternative, sociological approach was adopted by Linsky, Straus and Colby (1986).
They examined the theory that sociostructural factors that produce stress for members of a society
increase the rate of alcohol abuse. To do this, they defined two types of social stress and related
these to alcohol-related problems (e.g. cirrhosis, and diagnosed alcoholism) and per capita alcohol
consumption in all 50 states. Social stress was conceptualized either in terms of negative life events
(e.g. divorce, plant closings and the like), or as chronic stressful conditions.
The results showed that both stressful events and stressful life conditions were strongly and
consistently correlated with all indices of alcoholism. For example, their measures accounted for
47% of the variance of alcohol consumption. Aside from providing a different type of support for
the anxiolytic effects of drinking, this study also found that this association held at least as strongly
for women as for men.

THEORETICAL MECHANISMS IN ALCOHOL’S EFFECTS ON ANXIETY

Peripheral versus central mediation
As I have already noted, animal research points towards a central mechanism of alcohol’s effects
on anxiety. Sher (1987), in his incisive review of the human literature, observes that alcohol’s
stress-reducing effects have been most consistently seen in cardiovascular functioning, raising the
possibility that the effect is relatively specific to this system. If this were so, it would suggest
peripheral mediation (e.g. blocking of beta-adrenergic receptors on the heart). However, given the
data showing effects on other physiological systems (e.g. electrodermal reactivity) and self-report,
Sher concludes that alcohol produces a generalized, centrally mediated reduction in anxiety. A
recent, detailed physiological analysis of alcohol’s effects on response to a mental stressor supports
this conclusion. Eisenhofer, Lambie and Johnson (1986) found that the effects of alcohol on heart
rate to a stressor were not secondary to the action of alcohol on adrenoceptor responsiveness. The
relationship between alcohol-induced reduction in heart rate and adrenalin responses was
significant, which led these investigators to conclude that “the reduced heart rate response [to the
stressor] was secondary to attenuated sympathetic nervous activation of the heart” (p. 100).

Psychosocial theories
Two-factor learning theory. Conger’s (1956) original formulation of the TRT was in terms of
conditioning principles-essentially Mowrer’s well-known two-factor theory of avoidance behav-
 Alcohol and anxiety 377

ior. The depressant pharmacological effects of alcohol were assumed to reduce an underlying drive
state of anxiety. Since this drive state was thought to be causally related to escape/avoidance
behavior, the latter would then be altered. It is this formulation of the tension reduction theory
that can be criticized, just as two-factor theory has proved to be inadequate in accounting for the
maintenance and modification of anxiety disorders. Sher (1987) has pointed out that Conger
himself envisaged a more complex determination of alcohol’s effects on anxiety than many
subsequent investigators assumed. For example, Conger predicted that alcohol could increase as
well as decrease tension, depending on the relative strengths of the two competing drives-the
approach-avoidance conflict. The notion here was that alcohol might reduce the negative drive
state (anxiety) sufficiently for the organism to get close enough to a desired goal for an appetitive
drive to be aroused. This would increase the conflict and hence increase anxiety. However, this
analysis of competing response tendencies has not facilitated differentiation of alcohol’s anxiolytic
or anxiogenic effects in humans.
The stress resonse dampening model also allows for alcohol to both increase and decrease
anxiety. As Sher (1987) observes, real or imagined negative consequences of intoxication (e.g.
impaired cognitive or behavioral performance in a social interaction) might increase anxiety.
(Certainly one sees this clinically in some anxiety patients. They report drinking to reduce anxiety,
but, at the same time, become worried about losing control and doing or saying something foolish).
However, even here, the prediction of the stress dampening model remains that a “sufficient dose
of alcohol” should dampen this anxiety response.
Cognitive theories. Several reformulations of the putative anxiolytic effects of intoxication are,
in one way or another, predicted upon alcohol’s primary impact on cognitive mediating processes.
Anxiety is altered, secondarily, as a result of this cognitive change. Among these cognitive theories
are Bandura’s (1986) cognitive-social learning theory, Berglas’s (1987) self-handicapping theory,
Hull’s (1981) self-awareness theory, Marlatt’s (1984) expectancy model, and Steele’s attention
allocation model (Steele and Josephs, 1988). A full analysis of these mini-theories is beyond the
scope of the present discussion. Nevertheless, I do want to comment on Hull’s and Steele’s models,
both to illustate the sort of thinking behind these cognitive approaches, and because of the novel
research they have generated.
Hull’s self-awareness model holds that people may use alcohol to minimize their awareness of
negative, self-relevant information. The more self-aware the person, the more aversive is negative
self-relevant feedback, and hence the more likely alcohol will be consumed to inhibit self-awareness
and bring psychological relief. One of the contributions of Hull’s model is that it has helped to
forge closer links between experimental-social psychology and alcohol research. It also enjoys some
empirical support. Studies by Hull and his associates have shown that alcohol decreases
self-awareness, and that failure feedback affects highly self-aware individuals more powerfully than
low self-aware controls (Hull, 1987). For example, among treated alcoholics, those who were high
in dispositional self-consciousness, and who encountered negative life events during follow-up, were
more likely to return to drinking than their counterparts with low self-consciousness (Hull, Young
and Jouriles, 1986). Replication of the role of self-consciousness as a risk factor for relapse would
have important implications.
There are problems with this model, however. First, as already noted, high dispositional
self-awareness has been unrelated to alcohol’s anxiolytic effects in my own laboratory research and
that of Sher’s (Niaura et al., 1987; Sher and Walitzer, 1986). Second, several studies have shown
that alcohol does not reduce self-awareness, at least as it is operationalized as the use of first person
pronouns (Frankenstein and Wilson, 1985). Third, alcohol reduces self-critical self-evaluation in
the face of negative interpersonal feedback in the absence of effects on self-awareness (Yankofsky,
Wilson, Adler, Hay and Vrana, 1986). This suggests that alcohol does not decrease the awareness
or amount of negative self-relevant feedback, but rather distorts the meaning the intoxicated person
attributes to such information. Finally, Niaura et al. (in press) found that in male Type A subjects,
intoxication significantly attenuated blood pressure reactivity while leaving use of first pronouns
(during the stressful self-disclosing speech) unaffected.
Steele and Josephs (1988) have proposed a model in which alcohol’s effect on psychological stress
is indirect, mediated through its known impairment of information processing capacity. Alcohol’s
narrowing of perception to immediate cues and its reduction of cognitive abstracting capacity
 378 G. TERENCEWILSON

restricts attention to the most immediate, salient aspects of experience. Given this assumption, the
concurrent activity in which the intoxicated person engages will help determine alcohol’s effects.
In the face of a stressful event, intoxication without a neutral or pleasant distracting activity would
not reduce anxiety and might even result in an increase in anxiety because of narrowing of attention
on the imminent stressor. Intoxication with a pleasant activity is said to reduce anxiety by blocking
out of awareness distress-eliciting thoughts.
The appeal of this model is that it bids fair to explain how alcohol can either decrease or increase
anxiety. Studies by Steele have provided support for the model’s predictions, although the data
have been limited to self-report of anxiety. These data are inconsistent with the stress dampening
model, Hull’s model, and other versions of the anxiety reduction theory. Steele and Josephs (1988)
consider and dismiss alternative interpretations of their data, including the possibility that alcohol’s
anxiogenic effects were caused by the anticipation of impaired ability to give a satisfactory speech.
(This possible cause of anxiogenic effects has been raised by Cappell and Greeley [1987] and Sher
[1987]).
The model also explains an otherwise puzzling finding with alcoholics. Langenbucher found that
in a small group of alcoholics who were drinking in a convivial bar-setting, alcohol consumption
reduced tension or anxiety. However, when the group process was disrupted and social stress
induced, alcohol consumption is associated with increased tension. This pattern is what Steele’s
model would predict.
What is perplexing is that the model seems unable to account for the anxiety reduction that has
been documented in studies by Levenson and Sher (1982) Niaura et al. (in press), Wilson et al.
(1980) among others. In these studies of alcohol consumption, the concurrent behavior-
anticipating a self-disclosing speech or a reliably anxiety-inducing heterosocial interaction-was
both aversive and salient, the two conditions for an anxiogenic effect according to Steele’s model.
Yet physiological arousal-and sometimes self-report-were significantly reduced. No increase in
anxiety was observed on any measure.
Whatever the fate of this attention allocation model, (and there are procedural differences
among the studies in question that remain to be sorted out), alcohol’s effects on anxiety seem
determined by multiple cognitive processes. Aside from the role of attention, or perceptual
narrowing to immediately salient cues, the way in which those cues are processed will influence
secondary affective reactions. For example, Yankofsky et al. (1986) have shown that intoxicated
male social drinkers, despite being fully aware that their female partner was giving them the cold
shoulder during an interpersonal interaction, nevertheless did not evaluate themselves self-critically.
Their possibly less fortunate, sober counterparts, however, reported significant negative self-
evaluation in the face of this unnerving feedback. This would seem to be a case where awareness
of the feedback was discounted or distorted in a self-serving fashion. Whatever these higher-order
cognitive processes-and we are currently exploring the role of attributions in this context-they
can critically influence alcohol’s effects on anxiety.
To summarize, the good news is that innovative mini-theories, linking the alcohol field to
mainstream experimental psychology, are proliferating, and that, for the most part, they are
encouraging increasingly better controlled research. The bad news is that the new findings have
at times only added to our perplexity. We are still very far from an adequate theory of alcohol’s
effects on anxiety.

CONCLUSION

Does alcohol reduce anxiety as we have believed for so long? The answer seems to be
sometimes-at least in some people. Alcohol simply does not have a robust, overriding effect on
anxiety as has often been assumed. As Goodwin (1986) has put it, “If a drug company tried to
get FDA approval to market alcohol for anxiety, it would probably be turned down” (p. 57).
Similarly, Cappell and Greeley (1987) recently stated that “even if alcohol is a tension reducing
agent, it is a relatively ineffective one, primarily because it has other actions which negate its ability
to reduce tension, especially at higher doses” (p. 48). (They base this last comment-about the
negative effects at high BALs-mainly on animal research).
 Alcohol and anxiety 379

If we accept as valid this conclusion, derived as it is from experimental research, we must wonder
why the belief in alcohol’s anxiety reducing effects is so ingrained and widespread? There are several
possibilities. To begin with, we should remind ourselves that persistent belief in notions that fly
in the face of non-supportive or even contradictory empirical evidence is not uncommon.
Learning theory offers some leads in understanding the resistance to extinction of our belief in
alcohol’s anxiolytic effects. Alcohol does reduce anxiety on occasion. This partial reinforcement
effect probably helps maintain our conviction. Also, at least for alcohol abusers, drinking might
function as a partial avoidance response. Whatever the immediate effects of drinking, even if they
are not especially anxiety reducing, they might serve to avoid what is feared to be a worse
alternative. Relatively speaking, anxiety is reduced, as Hodgson, Stockwell and Rankin (1979)
have argued.
It is widely believed that anxiety (or stress) typically triggers problem drinking and that it
precipitates relapse. Analyses of the proximal determinants of relapse among alcoholics are
consistent in showing that negative affect is a prime contributor (e.g. Annis and Davis, in press).
It is believed that anxiety triggers drinking because intoxication relieves that unpleasant affect. But
rather than serving as a drive, the reduction of which reinforces drinking, anxiety (and negative
affect, more generally) may function as a source of cues that directly elicit classically conditioned
responses that are the basis of learned tolerance, craving, and withdrawal reactions. These
classically conditioned compensatory responses (CCRs), to use Siegel’s (1983) model, then lead
to drinking.
The cognitive psychology of human inference suggests other reasons. The times alcohol reduces
anxiety might be particularly striking, so as to make a disproportionate and enduring impression
on both the participants and actors in this interaction. Failure for anxiety reduction to occur tends
to be forgotten. Primed as we are, culturally, about the anxiolytic effects of alcohol, the forces of
confirmatory bias come into play. We might see it when we believe it (Nishbett and Ross, 1980).
It might be that alcohol reduces unpleasant feelings or enhances a sense of well-being when we
are not reacting to stress, as Lagenbucher’s (1985) findings with alcoholics show. Lukas and
Mendelson (in press) have shown that a low alcohol dose (only a couple of drinks), has effects on
the hypothalamic-pituitary-adrenal axis (increased ACTH secretion and altered EEG responses)
during the ascending limb of the blood alcohol curve that may be the biological basis of subjective
reports of euphoria that were closely associated with the biological changes. When we are stressed
and looking for relief, we might turn to alcohol for its euphoria-inducing effects, not realizing that
the psychological and physiological contexts are different.
The really important conclusion from the wealth of experimentation the anxiety reducing theory
has generated is the absence of an automatic and consistent effect of alcohol on anxiety. Rather,
alcohol’s effects on anxiety, as on so many other psychosocial phenomena, including subsequent
drinking by non-abusing and abusing drinkers, are conditional on a wide range of biological,
psychological, and social influences.
It is misleading to look for simple, invariant effects. Alcohol’s reinforcing effects cannot be
explained in terms of direct, pharmacological action. As important as the pharmacology of alcohol
is, it seems clear that the pharmacological impact of alcohol can be altered or masked by a variety
of psychosocial influences. No single perspective will suffice in understanding the workings of
alcohol on behavior. In this sense, then, the continuing investigation of the relationship between
alcohol and anxiety is a microcosm of our attempts to analyze alcohol use and abuse in general.
Acknowledgements-This paper is based on the Distinguished Scientist Award address, Section III, Division 12 of the
American Psychological Association, New York City, August 31, 1987. Preparation of this paper was made possible
by grant 00259-17 from the National Institute on Alcohol Abuse and Alcoholism, and support from the Health and
Behavior Research Network of the John D. and Catherine T. MacArthur Foundation.

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