Literature Review

Stimulant and Sedative Effects of Alcohol

Article· Literature Review (PDF Available)inCurrent Topics in Behavioral Neurosciences 13:489-509 · May 2011with 6,859 Reads
DOI: 10.1007/7854_2011_135 · Source: PubMed
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Abstract
Alcohol produces both stimulant and sedating effects in humans. These two seemingly opposite effects are central to the understanding of much of the literature on alcohol use and misuse. In this chapter we review studies that describe and attempt to measure various aspects of alcohol's subjective, autonomic, motor, cognitive and behavioral effects from the perspective of stimulation and sedation. Although subjective sedative and stimulatory effects can be measured, it is not entirely clear if all motor, cognitive and behavioral effects can be unambiguously assigned to either one or the other category. Increased heart rate and aggression seem strongly associated with stimulation, but motor slowing and cognitive impairment can also show a similar time course to stimulation, making their relation to sedation problematic. There is good agreement that alcohol's ability to induce striatal dopamine release is the mechanism underlying alcohol's stimulatory effects; however, the change in brain function underlying sedation is less well understood. In general, stimulatory effects are thought to be more rewarding than sedative effects, but this may not be true for anxiolytic effects which seem more closely related to sedation than stimulation. The two major theories of how response to alcohol predicts risk for alcoholism both postulate that individuals at high risk for alcohol use disorders have a reduced sedative response to alcohol compared to individuals not at high risk. In addition one theory proposes that alcoholism risk is also associated with a larger stimulatory response to alcohol.
Stimulant and Sedative Effects of Alcohol
Reuben A. Hendler, Vijay A. Ramchandani, Jodi Gilman
and Daniel W. Hommer
Abstract Alcohol produces both stimulant and sedating effects in humans. These
two seemingly opposite effects are central to the understanding of much of the
literature on alcohol use and misuse. In this chapter we review studies that describe
and attempt to measure various aspects of alcohol’s subjective, autonomic, motor,
cognitive and behavioral effects from the perspective of stimulation and sedation.
Although subjective sedative and stimulatory effects can be measured, it is not
entirely clear if all motor, cognitive and behavioral effects can be unambiguously
assigned to either one or the other category. Increased heart rate and aggression
seem strongly associated with stimulation, but motor slowing and cognitive
impairment can also show a similar time course to stimulation, making their
relation to sedation problematic. There is good agreement that alcohol’s ability to
induce striatal dopamine release is the mechanism underlying alcohol’s stimula-
tory effects; however, the change in brain function underlying sedation is less well
understood. In general, stimulatory effects are thought to be more rewarding than
sedative effects, but this may not be true for anxiolytic effects which seem more
closely related to sedation than stimulation. The two major theories of how
response to alcohol predicts risk for alcoholism both postulate that individuals at
high risk for alcohol use disorders have a reduced sedative response to alcohol
compared to individuals not at high risk. In addition one theory proposes that
alcoholism risk is also associated with a larger stimulatory response to alcohol.
Keywords Alcoholism Sedation Stimulation
R. A. Hendler V. A. Ramchandani J. Gilman D. W. Hommer (&)
Laboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse
and Alcoholism, National Institutes of Health, Bethesda, MD 20892, USA
e-mail: dan.hommer@mail.nih.gov
Curr Topics Behav Neurosci (2013) 13: 489–509 489
DOI: 10.1007/7854_2011_135
ÓSpringer-Verlag Berlin Heidelberg 2011
Published Online: 11 May 2011
Contents
1 The Nature of Stimulant and Sedative Effects ................................................................ 490
1.1 Effects on Subjective Experience ............................................................................ 490
1.2 Effects on Autonomic Motor Activity..................................................................... 493
1.3 Effects on Motor and Cognitive Performance......................................................... 494
1.4 Effects on Behavior.................................................................................................. 495
2 Specific Factors in Stimulant and Sedative Effects......................................................... 496
3 Neurobiological Mediation of Alcohol’s Effects ............................................................. 497
3.1 Stimulation................................................................................................................ 497
3.2 Sedation..................................................................................................................... 499
4 Systems-Level Theories of Alcohol’s Biphasic Effects .................................................. 499
5 Clinical Implications: Risk Factors for Alcoholism and Alcohol Use Disorders........... 501
6 Directions for Future Research......................................................................................... 502
References ............................................................................................................................... 503
Everyone knows that if you drink enough alcohol you get high and you get sleepy.
The behavior resulting from the combination of these two states can be quite
amusing; people have been laughing about alcohol’s effects at least since
Shakespeare’s time. In Macbeth (Act 2, Scene 3), Shakespeare has a drunken
porter tell an elaborate (and somewhat annoying) drunk joke at a dramatic high
point in the plot. Scholars argue about why Shakespeare inserted the joke where he
did, but there is no arguing with the porter’s description of the effects of alcohol.
The porter first mentions two of alcohol’s effects not mediated by the central
nervous system, increased urine production and flushing, but he’s really interested
in alcohol’s ability to provoke sleep and lechery (not necessarily in that order). The
joke is that alcohol provokes sexual desire but then takes away the ability to
perform and puts you and your lechery to sleep. How does this happen? What are
the brain mechanisms that allow alcohol to act as both a stimulant and a sedative?
In this chapter we will review some of the literature on the dualistic effects of
alcohol. We will begin by discussing exactly what alcohol’s effects are, focusing
particularly on how alcohol induces stimulation and sedation. Scientists have
assessed alcohol’s effects on subjective experience, autonomic motor activity,
motor and cognitive performance, and behavior. We will discuss the methods
scientists have employed and the conclusions they have reached in studying each
type of effect.
1 The Nature of Stimulant and Sedative Effects
1.1 Effects on Subjective Experience
Though subjective experiences are difficult to assess and quantify, alcohol
researchers do their best using self-report measures. Research on alcohol-induced
subjective effects generally involves having subjects consume alcohol and then
490 R. A. Hendler et al.
rate how they feel using a paper-and-pencil questionnaire. Several such ques-
tionnaires exist, each with its own strengths and weaknesses. The following are
most commonly used.
The Biphasic Alcohol Effects Scales (BAES) was specifically designed to
measure the stimulant and sedative effects of alcohol (Martin et al. 1993). The
BAES assesses subjects’ experience of seven subjective states associated with
stimulation (elated, energized, excited, stimulated, talkative, up, and vigorous) and
seven states associated with sedation (difficulty concentrating, down, heavy head,
inactive, sedated, slow thoughts, and sluggish). Subjects rate their experience of
each state from ‘‘not at all’’ to ‘‘extremely’’ on a scale from 0 to 10. Their ratings
of stimulation and sedation are each summed into numerical scores which can be
compared with a baseline score and analyzed mathematically. Studies have con-
firmed the reliability and validity of the BAES as a measure of alcohol-induced
stimulation and sedation (Martin et al. 1993; Earleywine and Erblich 1996; Rueger
et al. 2009).
The Profile of Mood States (POMS) measures natural mood states (e.g.
‘cheerful’’ and ‘‘grouchy’’), on a five point scale from ‘‘not at all’’ to ‘‘extremely’’
(Speilber 1972). Several studies have shown that the POMS is sensitive to drug or
alcohol-induced changes in mood (Johanson and Uhlenhuth 1980; Johanson and de
Wit 1989; Nagoshi et al. 1991). Though the POMS measures some mood states
probably irrelevant to stimulation and sedation (e.g. ‘‘lonely’’ and ‘‘sympathetic’’),
self-report of ‘‘elation’’ and ‘vigor’’ intuitively reflects stimulation and is asso-
ciated with physiological stimulation (Conrod et al. 2001), preference for alcohol
over placebo in a laboratory setting, and increased drinking behavior outside the
lab (de Wit et al. 1987).
The Addiction Research Center Inventory (ARCI) measures the effects of
specific classes of drugs (Martin et al. 1971), and has been shown to do so sen-
sitively and reliably (Fischman and Foltin 1991). The ARCI consists of several
dozen true/false statements, categorized by class of drugs. Subjects’ answers in
each category are summed to a scale score. The stimulant effects of alcohol can be
measured using the Amphetamine scale, alcohol-induced euphoria can be mea-
sured using the Morphine-Benzedrine Group scale, and sedative effects can be
measured using the Pentobarbital-Chlorpromazine-Alcohol Group scale (King
et al. 2002).
The Drug Effects Questionnaire (DEQ) measures general drug effects and drug
liking, though it does not measure stimulation and sedation directly. Subjects
answer questions like ‘‘Do you feel any drug effects?’’ and ‘‘Would you want more
of what you consumed, right now?’’ Rather than using a numerical scale, subjects
indicate their response by drawing a mark on a 100 mm line, each end of which
represents an extreme answer. The position of the mark is converted to a scaled
score (King et al. 2002).
The Subjective High Assessment Scale (SHAS) was designed to measure
subjective experience of drug or alcohol-induced intoxication (Judd et al. 1977a,b).
The original version required subjects to answer 38 questions about their sub-
jective state on a six point scale. Schuckit et al. have used a revised 13-item
Stimulant and Sedative Effects of Alcohol 491
version in studies to demonstrate differences in subjective effects of alcohol
between individuals with family history of alcoholism and controls (Schuckit et al.
1996; Eng et al. 2005) as well as genetic influences on subjective responses to
alcohol (Schuckit et al. 2005; Ray and Hutchison 2004). The SHAS measures
subjective intoxication but does not differentiate between stimulation and sedation;
some researchers believe that intoxication measured by the SHAS reflects sedation
more than stimulation (Conrod et al. 2001).
Researchers compare subjects’ experience of alcohol-induced stimulation and
sedation by administering questionnaires at different points along the BAC curve.
Using these self-report measures, researchers have found that people experience
alcohol-induced subjective stimulation and sedation in a reliable pattern, although
with substantial inter-individual variability in the magnitude and duration of the
experience. In general, subjects experience greater stimulation than sedation
during the ascending limb of the BAC curve (when BAC is rising), but when BAC
peaks and begins to decline, sedative effects tend to overwhelm their initial
stimulation (Pohorecky 1977; Babor et al. 1983; Martin et al. 1993; Earleywine
and Erblich 1996).
Though stimulation and sedation seem like opposite states, they may actually
occur simultaneously after alcohol consumption. Self-report measures like the
BAES allow researchers to analyze the time-course of stimulation and sedation
separately. Most subjects predominantly experience stimulant effects at low blood
alcohol concentrations (BACs) soon after consuming alcohol. Subjects rapidly
become increasingly stimulated until their BAC reaches its peak. As BACs
decline, stimulation quickly wanes. In contrast, sedation takes effect slowly and
gradually and predominates at high BACs. Sedation peaks and plateaus after peak
BAC and declines gradually. The time course of stimulation and sedation are
illustrated in Fig. 1.
Individuals differ, however, in when, how much, and under what conditions
they feel stimulant and sedative effects after consuming alcohol (Holdstock and de
Wit 1998). Individual response to alcohol can also change over time; studies have
shown that humans and experimental animals can become more or less sensitive to
stimulant drugs like cocaine and amphetamine over multiple periods of con-
sumption (Robinson and Berridge 2000; Strakowski et al. 1996; Lett 1989; Nestler
and Malenka 2004), and the same may occur with alcohol (Newlin and Thomson
1991,1999).
Stimulant effects are generally experienced as positive and are believed to
motivate drinking behavior (Corbin et al. 2008). Some sedative effects, like
reduced anxiety, are also pleasant, but others, like motor impairment, are widely
considered unpleasant (Morean and Corbin 2010). In general, stimulant effects are
considered more positive than sedative effects. Individuals who experience mostly
stimulant effects tend to experience more alcohol-induced euphoria, like alcohol
more, and prefer alcohol to placebo more than individuals who experience mostly
sedative effects (de Wit et al. 1987).
To complicate matters, however, sedative effects like reduced anxiety can also
motivate drinking behavior. Many people initially drink primarily to experience
492 R. A. Hendler et al.
stimulation and accompanying positive affect but become dependent on alcohol
when they switch to drinking primarily to experience reduced anxiety associated
with sedation (Cooper et al. 1995; Schroder and Perrine 2007).
1.2 Effects on Autonomic Motor Activity
Alcohol-induced increases in heart rate (HR) often accompany subjective stimu-
lation after alcohol consumption, and researchers consider alcohol’s effects on HR
a measure of alcohol-induced stimulation. By measuring heart rate at baseline and
then after alcohol consumption, researchers have found that, like subjective
effects, effects on HR differ in magnitude at different points along the BAC curve
(Conrod et al. 2001,1997a,b). Rapid consumption of alcohol tends to increase
heart rate more during the ascending limb of the BAC curve than during the
descending limb. After more gradual consumption of alcohol, however, HR can
remain elevated during the descending limb (Conrod et al. 1997a,b).
Researchers have found that alcohol-induced increases in HR correlate with
other measures of stimulation. For example, increases in HR correlate with sub-
jective experience of energy and confidence near peak BACs (Conrod et al. 2001)
and, to a lesser extent, with subjective stimulation on the rest of the BAC curve
(Brunelle et al. 2007). Conversely, alcohol-induced increases in HR seem to
Fig. 1 Time course of Stimulation and Sedation Scores, as measured by the Biphasic Alcohol
Effects Scale, following oral administration of a dose of 1 g/l total body water to 44 healthy social
drinkers. Mean change from baseline scores are plotted on the primary y-axis. Mean breath
alcohol concentration (BrAC, thin solid line) is plotted on secondary y-axis. Stimulation scale
scores (dashed line) peak early (around 45 min) and decline to and slightly below baseline values
by 90 min following the oral alcohol dose. Sedation scale scores (dotted line) show a slower
change to a later peak (around 90 min) with a return to baseline by 180 min. The Difference
(thick solid line) is the difference between stimulation and sedation scores and characterizes the
biphasic effects of alcohol. (Ramchandani unpublished)
Stimulant and Sedative Effects of Alcohol 493
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Literature Review