Behsv. I&. & Therapy, Vol. 17. pp.

459 lo 466
Pergamon Press Ltd 1979. Prmted m Great Bream

CAN ALCOHOL REDUCE TENSION?

R. J. HODG~N, T. R. STOCKWELL and H. J. RANKIN

Addiction Research Unit, Institute of Psychiatry, 101 Denmark Hill,
London SE5 8AF. England

(Received 24 January 1979)

Summary-The Tension Reduction Hypothesis of alcohol use is examined in the light of recent
criticism. Contrary to the conclusions of Cappell and Herman (1972) it is argued that the hypoth-
esis is supported by evidence from animal research in most cases where an appropriate paradigm
has been employed.

The social drinker, the heavy drinker and the alcoholic often give ‘tension relief’ as
one of their reasons for drinking (e.g. Edwards et al., 1972; Litman et al., 1977; Mulford
and Miller, 1963; Cahalan and Room, 1974) and so it is not surprising that the tension
reduction theory of alcohol consumption (TRT) has been the cornerstone of much
psychological experimentation and treatment (Franks, 1970; Vogel-Sprott, 1967; Masser-
man et al., 1945, 1946; Conger, 1951, 1956, Hedberg and Campbell, 1974; Kraft and
Wijesinghe, 1970). In general discourse ‘tension’ is the label given to a variety of unplea-
sant states such as anxiety, arousal, fear, frustration and stress, which are all difficult
to pin down because they have been defined in many different ways and tend to be
used indiscriminately. If alcoholism can be called a “big fat word” (Christie and Bruun,
1969), because it is ill-defined and used over-inclusively, then arousal and anxiety are
bordering on the obese and one can almost sympathize with the radical behaviourist
who reacts to such ambiguity by ignoring hypothetical constructs or intervening vari-
ables of all kinds. In our view, tension is one of the fattest words in the English language
and so we intend to restrict our attention to just two aversive states, namely fear and
frustration, since they can be defined simply and have been incorporated into an elegant,
comprehensive and useful model (Gray, 1975), which has particular relevance to the
growing field of behavioural pharmacology into which we are about to step.
The tension reduction theory is based on two assumptions. First, that alcohol can
reduce tension (TRH) and second that alcohol is often consumed in order to reduce
tension. It is only recently that both hypotheses have been strongly challenged on the
grounds that “much of the evidence is negative, equivocal and often contradictory”
(Cappell and Herman, 1972; Cappell, 1975). Cappell and Herman comprehensively
reviewed those animal studies which examine the effects of alcohol on conflict and
experimental neurosis, avoidance and escape learning, conditioned suppression and re-
sistance to extinction. They concluded that the tension reduction hypothesis has “a
reasonably good record of confirmation in the literature on conflict and experimental
neurosis but in the other areas surveyed it does not fare very well”. Cappell (1975)
concludes that “When judged solely on its merits as a theory, the TRT is substantially
undermined. In a sense, this failure is perplexing since the rationale underlying the
TRT seems so plausible and so consistent with commonplace experience. But in the
final analysis, the evidence can lead to no other conclusion”. Cappell and Herman’s
review is scholarly, comprehensive, persuasive, and frequently quoted, nevertheless, we
disagree with their conclusions. The sole objective of the present review is to look
again at the animal studies which were discussed by Cappell and Herman, and to
explain why we are forced to disagree and why we conclude that a shot of ethanol
does help the rat to cope with fear and frustration. Our present concern is only with
the series of animal experiments which are relevant to the TRH and not the broader
issue of human alcohol consumption, from social drinking to alcoholism, which is con-
sidered in another publication (Hodgson et al., 1979).

459
460 R. J. HODGSON. T. R. ST~CKWELL and H. J. RANKIN

First, there are a number of definitions and distinctions to be considered. The follow-
ing experiments deal with fear or frustration, fear arising from the expected occurrence
of an unpleasant event and frustration from the non-occurrence of an expected pleasant
event. Both are aversive states which tend to be avoided or escaped from, and both
are viewed as tension states by proponents of the tension reduction theory. In order
to understand the apparently contradictory effects of alcohol on avoidance behaviour
a number of distinctions must be noted. The first is between active and passive avoidance,
in the former an animal typically receives a shock if he doesn’t respond (e.g. by jumping
a hurdle) whereas in the latter, he is shocked if he does respond (e.g. by approaching
food). The second distinction is between one-way and two-way active avoidance (Gray,
1975). It is important to note that, in shuttle box avoidance learning (two-way active
avoidance), an animal running to avoid shock (active avoidance) is actually entering
a box which has also been associated with shock and would therefore also tend to
be avoided (passive avoidance). If the distinctions between passive and active avoidance
and between one-way and two-way avoidance are ignored, then a confused picture
emerges. We will argue that passive avoidance is reduced by alcohol consumption, but
that well-learned active avoidance is not. Our aim is not to suggest that alcohol is
always consumed in order to reduce tension or indeed that the TRT is a comprehensive
theory of .alcoholism, but simply to reconsider the animal experimentation designed
to answer the question: “Can alcohol reduce tension?“.

ESCAPE BEHAVIOUR
It would appear that different laws apply to escape and avoidance behaviours since
they involve different response systems. Escape is elicited by an unconditioned stimulus
(UCS) such as an electric shock, whereas passive avoidance is influenced by conditioned
stimuli (Cs’s) rather than shock itself. In the rat, an electric shock (UCS) elicits running,
jumping and squeaking responses, but a conditioned stimulus which has previously been
paired with shock, elicits a freezing response and the rat is usually silent (Myer, 1971).
In human subjects, the cardiac response to shock is acceleration, but to a CS signalling
shock, heart rate decreases (Obrist et al., 1965). The hypothesis that fear and frustration
can be reduced by alcohol does not, therefore, apply to escape behaviour which is
elicited by a painful stimulus (UCS) rather than fear (CR), and so the TRH is not
falsified by the available evidence which does suggest that there is no consistent effect
of alcohol on the speed of escape from shock (Barry and Miller, 1965; Deutsch and
Roll, 1973; Scobie and Bliss, 1974; Skurdal et a/., 1965).

AVOIDANCE BEHAVIOUR
The Miller-Mowrer theory of active avoidance learning assumes that two processes
are involved. First, fear is classically conditioned to the warning signal and the condi-
tioned fear is then reduced by an avoidance response. According to this view, the fre-
quency of avoidance responses should be a function of fear intensity and an anxiolytic
drug should attenuate both fear and avoidance. Now Cappell and Herman find that
the literature on active avoidance learning does not consistently support the hypothesis
that alcohol does act in this way. However, before assuming that the TRH is therefore
wrong, we must consider alternative possibilities. Perhaps the Mowrer theory is not
an adequate explanation of the processes involved in active avoidance learning (Rach-
man, 1976). There is now sufficient evidence, for example, that fear and avoidance do
not necessarily covary, and that the extinction of fear. does not always result in extinction
of avoidance behaviour (Rachman and Hodgson, 1974). For example, Kamin et al.
(1963) measured the intensity of fear which was conditioned to a warning signal by
using the signal as a conditioned suppressor of bar pressing responses. It was found
that early in the acquisition of the avoidance response the signal did inhibit bar pressing
but that, after 27 consecutive avoidance responses, this effect had disappeared. It appears
that when an avoidance response is well established, it is maintained without the pres-
ence of fear and consequent reinforcement by fear reduction. A growing amount of
 Can alcohol reduce tension’? 461

evidence has exposed weaknesses in the Mowrer theory and a number of alternative
theories have been proposed which all rely on the assumption that avoidance of expected
shock is reinforcing (e.g. Gray, 1971; Seligman and Johnston, 1963 ; Bolles, 1970). Both
Gray and Bolles argue that avoidance learning is reinforced by the achievement of
safety signals, i.e. discriminative stimuli which signal the absence or the reduction in
intensity of aversive stimulation. Since active avoidance responses are not necessarily
motivated by fear and reinforced by fear reduction, then the one-way active avoidance
paradigm cannot be considered to be a good method of testing the TRH. There is
strong evidence that one-way active avoidance is relatively unaffected by moderate doses
of alcohol (Graham and Erickson, 1974; Chittal and Sketh, 1963; Banerjee, 1971)
although very high doses can impair performance (e.g. Graham and Erickson, 1974).
In order to clarify the difference between passive and active avoidance behaviour,
it is useful to make a distinction between a stimulus which warns of future aversive
stimulation, but is not necessarily anxiety arousing and a stimulus which has, through
classical conditioning, acquired anxiety-arousing properties. The former is usually called
a discriminative stimulus (SD) and the latter a conditioned stimulus (CS). In an
approach-avoidance conflict experiment, an animal experiences an increasing number
of fear CS’s as it approaches its goal, whereas, in an active avoidance learning experi-
ment, fear CS’s are not present if the animal successfully avoids when exposed to the
SD or warning signal. A human analogy may further clarify this point. An agoraphobic
walking towards a crowded high street experiences an increase in anxiety conditioned
to internal and external CS’s (passive avoidance), whereas routinely checking door locks
and window catches (active avoidance) before going to bed (SD) is not usually cued
by anxiety. It follows that alcohol should facilitate approach in a conflict (i.e. passive
avoidance) experiment, but would not reduce well established active avoidance behav-
iour. We have already noted that one-way active avoidance is relatively unaffected by
alcohol consumption and there is consistent evidence to support the hypothesis that
alcohol reduces passive avoidance in approach-avoidance conflict experiments (Masser-
man et al., 1945; Masserman and Yum, 1946; Conger, 1951; Barry and Miller, 1962;
Grossman and Miller, 1961; Freed, 1967, 1968, 1971; MacInnes and Uphouse, 1973;
Raynes et al., 1968). The fact that two-way active avoidance also involves passive avoid-
ance, especially during the early trials (Gray, 1975) suggests that using this paradigm
to test the TRH is a particularly hazardous venture. During the early stages, the animal
is running from one danger zone into another (avoidance-avoidance conflict) and it
would be predicted that a reduction in passive avoidance should facilitate active avoid-
ance. A number of studies have confirmed that alcohol has this effect (Crow, 1966:
Holloway, 1972; Chosher., 1974; Izquierdo et al., 1974).
It would appear that the evidence reviewed by Cappell and Herman (1972), which
they consider to be “equivocal, negative and even contradictory”, actually supports the
TRH reasonably consistently. They concluded that studies of experimental conflict (pas-
sive avoidance) are reassuring to advocates of the TRH but they are worried by the
discrepancies between these studies and the active avoidance experiments. They suggest
that: “Perhaps the discrepancy might be resolved by suggesting a drug-situation interac-
tion, since the operations involved in experimental conflict clearly differ from those
in an avoidance paradigm”. But this begs the question: “What is the distinction, in
terms which can be accommodated by the TRH, which makes the difference?” We are
proposing that a well learned active avoidance response is not motivated by fear, whereas
approach-avoidance conflict and shuttlebox avoidance experiments involve the passive
avoidance of fear-arousing CS’s.

CONDITIONED SUPPRESSION
The presentation of a sensory stimulus which has repeatedly signalled the onset of
an electric shock will ‘suppress the rate at which an animal performs a response for
a food or water reward. The ‘conditioned suppression’ paradigm has been employed
to test the fear reducing properties of various drugs on the assumption that the degree
B.R.T.
17/s-0
462 R. J. HODGSON,T. R. ST~CKWELL and H. J. RANKIN

of suppression directly reflects the degree of fear aroused by the aversive conditioned
stimulus. Cappell and Herman quote four ,studies in all of which, contrary to TRH
predictions, alcohol did not lift conditioned suppression (Lauener, 1963; Hendry and
Van Toller, 1964; Goldman and Dotter, 1966; Cicala and Hartley, 1967). However,
in a subsequent paper, Cappell et al. (1972) comment that, in general, there are so
many contradictory findings amongst studies in this field that possibly the conditioned
suppression paradigm is not a suitable model within which to test for the tension reduc-
ing effects of drugs. Observing the effect of a drug on passive avoidance would appear
to be a rather more direct test of its fear reducing properites.

EXTINCTION AND THE PARTIAL REINFORCEMENT

EXTINCTION EFFECT
Extinction of approach behaviour is generally considered to be a function of frustrative
non-reward (Amsel, 1962). If alcohol reduces frustration then the administration of alco-
hol during extinction should interfere with the extinction process. Cappell and Herman
note that: “The best designed and executed experiment in this area was clearly in support
of the hypothesis” (i.e. Barry, Wagner and Miller, 1962).
It has often been demonstrated that speed of extinction is a function of the reinforce-
ment schedule during acquisition. Continuous reinforcement (CR) is associated with
quick extinction, whereas partial reinforcement (PR) during acquisition, results in behav-
iqur which is more difficult to extinguish. Explanations of this robust phenomenon,
known as the partial reinforcement extinction efSect (PREE), have in common the concept
of frustration or some analogous notion (Capaldi, 1967; Amsel, 1958, 1962; Gray, 1975).
It is argued that at the start of a rewarded trial during PR acquisition, animals will
be experiencing frustration which carries over from previous trials (Capaldi, 1967) or
conditioned frustration which has been acquired during previous trials (Amsel, 1962).
Gray (1975) argues that both processes are probably operating. During partial reinforce-
ment trials animals therefore learn that frustration or conditioned frustration can be
followed by a reward so that frustration during the extinction phase will be less likely
to inhibit behaviour. In other words, animals do not stop responding when experiencing
frustration during the extinction phase if they have experienced frustration during the
acquisition phase. Now, if alcohol reduces frustration and/or conditioned frustration,
it might be expected that alcohol given to animals during a PR acquisition phase will
reduce or eliminate the PREE.
Cappell and Herman (1972) cite one study which challenges this prediction (Taylor
et al., 1968) but again, the PREE paradigm is rather complicated and this single piece
of evidence does not permit a decision one way or the other. Amylobarbitone is a
drug with very similar properties to alcohol, including cross tolerance, and there is
now sufficient evidence from a number of different laboratories that amylobarbitone
given during PR acquisition will considerably reduce the PREE (Ison and Pennes, 1969;
Gray, 1969; Gray and Dudderidge, 1971; Capaldi and Spalding, 1971). Gray (1975)
discusses this topic in considerable detail and concludes that alcohol and amylobarbitone
will only disrupt PREE if the experimental procedure involves many trials, long inter-
trial intervals and small rewards, and since the Taylor et al. experiment mentioned
above does not fulfil these conditions, it would not be a crucial test of the TRH. We
can only conclude that the effect of alcohol on the PREE has not been adequately
tested, although a drug with very similar properties does reduce the PREE as predicted
by the tension reduction hypothesis.
We will turn now to the more recent pioneering work of Gray and his colleagues
on hippocampal theta rhythms which is suggestive but requires further elaboration
before it can be considered to be conclusive evidence (Gray and Ball, 1970; Gray,
1970, 1976).
 Can alcohol reduce tension? 463

HIPPOCAMPAL THETA RHYTHMS

Gray (1976) has summarized the results of a series of experiments which suggest
that hippocampal theta rhythms are neurophysiological correlates of anxiety and frust-
ration. In rodents, this rhythm is a regular high voltage slow wave which lies in the
frequency band 6 to 10 Hz. More specifically, Gray and Ball (1970) demonstrated that
frustrative non-reward is associated with an average hippocampal theta rhythm fre-
quency of 7.7 Hz. We have already noted that frustrative non-reward is involved in
extinction and that the occurrence of frustrative non-reward during partial reinforcement
results in later resistance to extinction. One might predict therefore that electrical induc-
tion of the 7.7 Hz hippocampal theta rhythm during extinction would speed up extinction
but that eliciting this rhythm randomly on 50% of trials during a continuous reinforce-
ment acquisition phase would enhance the PREE. Both of these predictions have been
confirmed (Gray, 1976). So, frustrative non-reward is associated with a 7.7. Hz hippocam-
pal theta rhythm and electrical induction of this frequency in the hippocampus mimics
the behavioural effects of frustrative non-reward. This is the first strand of evidence
which links hippocampal theta thythms with anxiety and frustration.
Other evidence is based on the finding that the threshold electrical activity needed
to induce hippocampal theta rhythms is minimal for a frequency of 7.7 Hz, but only
for certain rats. Gray and his colleagues tested groups of Maudsley reactive and Mauds-
ley non-reactive rats which have been selectively bred to produce a group of ‘anxious’
and a group of ‘non-anxious’ rats differing on a number of measures of ‘anxiety’-for
example, the speed with which they learn passive avoidance. The clear finding was
that, at least for male rats, only the highly reactive showed a lower threshold at 7.7 Hz.
Putting all the evidence together Gray concludes that 7.7 Hz hippocampal theta
rhythms are associated with anxiety and frustration and that this particular frequency
is differentially sensitive to electrical induction only in the reactive (i.e. anxious) rats.
Now if alcohol is an anxiety reducing drug it should eliminate the differential sensi-
tivity of the 7.7 Hz hippocampal theta rhythm. Figure 1 shows that this is exactly what
happens not only with alcohol but also with amytal, Librium and cannabis (THC).
It appears that alcohol inhibits one of the neurophysiological correlates of anxiety and
frustration. This evidence, together with our own reinterpretation of the data presented
by Cappell and Herman (1972) certainly does not allow us to reject the hypothesis that
alcohol can reduce and prevent fear and frustration.
In summary, a reconsideration of the literature on experimental conflict, avoidance
behaviour, conditioned suppression, extinction and partial reinforcement has forced us
to conclude that alcohol can inhibit fear and frustration. From a theoretical point of
view, the least equivocal test of the TRH should be the approach-avoidance conjlict
paradigm and the evidence strongly confirms the hypothesis that, in this type of experi-
ment, passive avoidance tends to be reduced after alcohol consumption. One-way active
avoidance learning is relatively unaffected and two-way active avoidance appears to be
facilitated by alcohol, but both of these predictions are in line with the tension reduction
hypothesis. Furthermore, the best controlled experimental test of the hypothesis that
alcohol inhibits extinction supports the TRH. The use of the conditioned suppression
paradigm is beset with difficulties. Although alcohol failed to lift conditioned suppression
in four studies, the main opponents of the TRH themselves question the utility and
relevance of the procedure in this context. There is no adequate test of the hypothesis
that alcohol reduces the partial reinforcement extinction effect, although amylobarbitone
certainly does reduce the PREE and, finally, recent work on the neurophysiological
correlates of anxiety support the Tension Reduction Hypothesis.
Although the evidence from animal experimentation does support the hypothesis that
alcohol can reduce fear and frustration, we will not attempt to elaborate upon the
relevance of the TRH to social drinking, heavy drinking and alcoholism, since the argu-
ments for and against are discussed elsewhere (Hodgson, Stockwell and Rankin, 1979).
There is no doubt that the effect of alcohol is a complex function of personality, dose
464 R. .I. HODGSON. T. R. ST~CKWELL and H. J. RANKIN

0-0 Control
- Control - Drug

‘\ - Drug

Amytol 15 mg/kg Chlordlazepoxlde 5mg/kg

’ 1 I 1 I I I
60
59 69 77 91 100 59 69 77 91 100
Dwng frequency (Hz) Drwnq frequency (Hz)

- Control
- Drug

04 Control
\ - Drug

1
80
59 69 77 91 100 59 69 77 91 100
Dwng frequency (Hz) Dwng frequency (Hz)

Fig. 1. Effects of four drugs which impair behavioural inhibition on the theta-driving curve.
Reproduced with permission from Theoretical and Experimental Bases of the Behaviour Therapies,
Edited by M. P. FELDMAN and A. BROADHURST, Copyright 0 1976. John Wiley, London, 1976.

and situational variables and that many factors influence drinking behaviour, including
ethnic group and other sociological factors, social approval, modelling, price and avail-
ability, nevertheless, we cannot ignore the prevalent belief that alcohol can reduce fear
and frustration especially since the evidence from animal research provides it with a
solid base.

Acknowledgements-We would like to thank Dr. Jeffrey Gray of the Department of Experimental Psychology,
Oxford University and also Dr. Griffith Edwards and Dr. R. Kumar, Institute of Psychiatry, London, for
their very useful comments on the first draft of this paper.

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