Alcohol & Alcoholism Vol. 43, No. 2, pp. 163–170, 2008 doi: 10.

1093/alcalc/agm160
Advance Access publication 31 January 2008

REVIEW
A REVIEW OF THE LITERATURE ON THE COGNITIVE EFFECTS OF ALCOHOL HANGOVER
RICHARD STEPHENS1,∗ , JONATHAN LING1 , THOMAS M. HEFFERNAN2 , NICK HEATHER2 and KATE JONES3
1 School of Psychology, Keele University, Staffordshire, United Kingdom, ST5 5BG, 2 Division of Psychology, Northumbria University, Newcastle-upon-Tyne,
United Kingdom, NE1 8ST and 3 Biological Monitoring Section, Health and Safety Laboratory, Buxton, United Kingdom, SK17 9JN

(Received 20 July 2007; first review notified 23 August 2007; in revised form 2 October 2007; accepted 4 October 2007;
advance access publication 31 January 2008)

Abstract —Aims: Alcohol misuse is a prime social and health problem in the UK. This paper presents a critical review of literature on
the performance effects in the morning after binge drinking – during the alcohol hangover. Several pathophysiological changes that both
follow and outlast acute intoxication may give rise to alcohol hangover effects. We have identified 27 English language peer-reviewed
studies that investigate aspects of psychological performance during alcohol hangover following controlled alcohol ingestion. However,
the majority of studies had basic methodological shortcomings. Of eight laboratory studies rigorous enough to warrant serious attention,
only two showed effects. We interpret these largely negative findings as evidence of an insensitivity that is intrinsic to laboratory-

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based studies of performance under the influence of alcohol. Several studies have investigated the cognitive consequences of hangover
subsequent to naturalistic consumption, where participants have chosen what and where to drink. Although these studies have tended to
show effects, participants were always informed at the outset that hangover effects were to be assessed, and participants knew which was
the hangover condition. Under these circumstances expectancy effects have possibly contaminated the results significantly. Therefore,
naturalistic alcohol consumption studies (and laboratory studies that did not employ a placebo) can be considered as being suggestive of
hangover effects, but should not be interpreted as providing definitive evidence of such effects. In conclusion, although there is empirical
evidence showing impaired performance as a result of the alcohol hangover, future studies should confirm these findings and overcome
the shortcomings of previous research.

INTRODUCTION
Alcohol misuse appears to be rising to the extent that the UK
Government considers tackling problem drinking as a social
and health priority (Prime Minister’s Strategy Unit, 2004). The
alcohol-related death rate in the UK has increased from 6.9
per 100,000 population in 1991 to 12.9 in 2005 (Office for
National Statistics, 2006). While the dangers of binge drink-
ing have been highlighted (e.g. Pincock, 2003), 35% of all
men (42% of those aged 16–24 years) and 20% of all women
(36% of those aged 16–24 years) still reported exceeding daily
benchmarks on at least 1 day in the previous week to the 2005
Great Britain General Household Survey (Goddard, 2006). A
recent government report estimated the societal costs of heavy
drinking, including costs to the NHS in treating alcohol-related
injuries and illnesses (estimated at £1.7 billion per year), costs
associated with alcohol-related crime and disorder (estimated
at £7.3 billion per year), and costs due to lost productivity
through illness and absence from work (estimated at up to £6.4
billion per year; Prime Minister’s Strategy Unit, 2004). The
latter estimate includes the costs to the economy of alcohol re-
lated deaths. A further, less visible societal cost arises because
of alcohol-related impairment in the morning after an evening’s
binge drinking–due to the so-called alcohol hangover.
Estimating the societal costs of hangover is prone to inac-
curacy when one considers that hangover effects may include
lateness, accident risk, poorly performed work and disputes
(Crofton, 1987) in addition to absenteeism. Even the recent
report by Pittler et al. (2005) cites hangover cost estimates
∗ Author to whom correspondence should be addressed at: School
of Psychology, Keele University, Keele, Staffordshire, ST5 5BG UK.
Tel: (+44) (0)1782 583600; Fax: (+44) (0)1782 583387; e-mail:
r.stephens@psy.keele.ac.uk
(£2 billion) that were made 20 years ago and without refer-
ence to the original author’s caveat concerning the crude na-
ture of the costings (Crofton, 1987). A recent report by the
Prime Minister’s Strategy Unit (2004) estimates that the cost to
the UK economy of alcohol-related absenteeism from work
(due in part to hangover) is between £1.2 and £1.8 billion per
year. However, this estimate does not take into account effects
of depleted worker performance and includes lost days due to
long-term health problems associated with alcohol dependency.
In the grey literature, the BBC (BBC, 2004) cites research car-
ried out by an employment agency estimating that hangovers
cost the UK economy £2.8 billion a year due to the average
of 2.3 sick days per person per year, augmented by a further
2.5 days per year that workers spend, on average, hungover on
the job. Wiese et al. (2000) cited an estimate of hangover costs
to the US economy of $148 billion a year, but this estimate was
criticized by Becker (2001). A fair conclusion would be that
hangover costs are indeterminate but significant.
Several reviews of the hangover state have been undertaken.
Finnigan and Hammersley (1992) report findings from a small
number of hangover and performance studies, although this
review has now become dated. In a brief review of hangover
appearing as an editorial piece, Calder (1997) recounted the
findings of several performance studies but did not conduct
any critical evaluation. Swift and Davidson (1998) gave a de-
tailed account of the mechanisms and mediators of hangover
but did not discuss performance effects. Wiese et al. (2000)
conducted a detailed systematic review of the causes, patho-
physiological characteristics and treatment of alcohol-induced
hangover. They defined hangover as ‘the presence of at least
two symptoms (out of: headache, poor sense of overall well-
being, diarrhoea, anorexia, tremulousness, fatigue, and nausea)
occurring after the consumption and full metabolism of alco-
hol with sufficient severity to disrupt the performance of daily
tasks and responsibilities’ (p. 898). However, the notion that


C The Author 2008. Published by Oxford University Press on behalf of the Medical Council on Alcohol. All rights reserved
164 R. STEPHENS et al.
hangover disrupts performance of certain tasks is not as safe
an assumption to make as it might at first appear. Certainly,
Wiese et al. (2000) do not make a convincing case. They re-
viewed several studies claiming to show performance effects
of hangover, but they recounted findings without any critical
evaluation, and they omitted a large number of published peer-
reviewed hangover performance studies.
The present review offers a more critical analysis of all pub-
lished peer-reviewed papers on hangover performance that we
could find. For the purposes of this review, performance effects
are defined primarily as changes in cognitive functioning as-
sessed using cognitive tests. However, more everyday aspects of
performance, such as driving or performance in a management-
style decision-making game are also considered. We began by
searching the PSYCInfo database but this missed a large num-
ber of relevant studies and produced many false positives (e.g.
non-performance based studies). Therefore, while some papers
were identified from database searches, the majority were iden-
tified from references cited in papers already obtained. Some
further papers were identified using citation searching of ob-
tained papers (i.e. searching forwards for papers that cite the
papers we had obtained). This was done using the MIMAS Web
of Knowledge database.
We briefly outline the biological mechanisms that may un-
derlie hangover effects before embarking on a detailed review
of the literature on the performance effects of alcohol hangover.
We set out to include all the peer-reviewed studies published
to date but it is possible that one or two of the less well-cited
studies will have been omitted.
MECHANISMS
Several pathophysiological changes that both follow and outlast
acute alcohol intoxication (i.e. are present after all the acute al-
cohol has been metabolized) may give rise to the alcohol hang-
over. Wiese et al. (2000) note increased levels of acetaldehyde,
hormonal alterations due to deregulated cytokine pathways
and the inhibition of the availability of glucose via a process
mediated by insulin. Calder (1997) lists additional phenom-
ena associated with dehydration, metabolic acidosis, disturbed
prostaglandin synthesis, increased cardiac output and vasodila-
tion. Other potential mechanisms include sleep deprivation and
insufficient eating (Verster et al., 2003). Calder (1997) sug-
gests that the complex organic molecules found in alcoholic
beverages known as congeners may have an important role in
producing hangover effects because some, such as methanol,
are metabolized to the notably toxic substances formaldehyde
and formic acid. Congeners tend to be present in greater con-
centrations in darker drinks (e.g. whisky) compared with clear
drinks (e.g. vodka).
These mechanisms have in common the prediction of the
presence of hangover effects when the blood alcohol level
(BAL) has returned to zero, after having become elevated
during and following the drinking episode. Indeed, a defin-
ing characteristic of alcohol hangover effects is their presence
at zero BAL. This is necessary for research purposes in order
to distinguish between hangover and acute alcohol intoxica-
tion. However, there appears to be inconsistency in the way
that some of these physiological changes would be predicted to
affect cognitive functioning. For example, sleep deprivation is
known to impair executive functioning (e.g. Jones and Harrison,
2001). On the other hand, increased cardiac output is associated
with improved cognitive performance (e.g. Tomporowski and
Ellis, 1986). The wide range of mechanisms and the lack of
a unitary direction of effect make predicting the effects of
hangover complex. Fisk and Scerbo (1987) found that, during
acute alcohol intoxication, controlled processes were affected
more than automatic processes, implicating an effect on exec-
utive function. Such an effect may persist into the hangover
phase. Likewise, Jones and Harrison (2001) found executive
function decrements following modest amounts of experimen-
tally induced sleep loss, one of the mechanisms thought to
underlie hangover. Therefore, executive function, or certainly
higher cognitive functions, should be considered as candidate
functions to be affected by hangover.
Humans have been drinking alcohol, and presumably expe-
riencing hangovers, since the first mead was brewed from fer-
mented honey around 8000 BC (Meyer and Quenzer, 2005).
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Nevertheless, although a number of studies have been car-
ried out addressing hangover effects on cognition and perfor-
mance, we argue in the following sections that their interpre-
tation is severely limited due to a variety of methodological
considerations.
LABORATORY STUDIES
We identified 27 English language peer-review studies that have
investigated some aspect of psychological performance during
alcohol hangover following controlled alcohol ingestion. Typ-
ically, in a between-subjects design, alcohol is given to one
group and placebo is given to another group. After the pas-
sage of sufficient time for the acute intoxication effects to wear
off (typically 11 hours), one or more cognitive/performance
tests are applied. Decrements in the alcohol group relative
to the placebo group are interpreted as hangover effects. A
similar procedure may be applied in a related design where
an analogous comparison is made but the same participants
are tested twice, once following alcohol and once following
placebo. However, close reading reveals that these relatively
straightforward designs have not been well implemented in
practice in this literature, with the majority of studies having
basic methodological shortcomings.
Several early studies either present no data at all or do
not present inferential statistical analyses of the data, and
it is not possible to estimate statistics, such as effect sizes,
based on the information presented (Carroll et al., 1964;
Ekman et al., 1964; Ideström and Cadenius, 1968; Dowd
et al., 1973). Future studies clearly were able to learn from
these pioneering efforts. Nevertheless, without data or a rig-
orous data analysis it is not possible to draw meaningful con-
clusions from these studies. In an even earlier ground-breaking
study Takala et al. (1958) compared hangover performance in
medical students with non-hangover performance in a group of
psychology and technical students. Unfortunately, in compar-
ing intact groups of participants it is not possible to distinguish
hangover effects from pre-existing participant differences.
Some other studies used a no-alcohol control condition rather
than a placebo (Yesavage and Leirer, 1986; Taylor et al., 1996;
Kruisselbrink et al., 2006). In the laboratory, placebo controlled
trials have become the gold standard for research into effects
of imbibed substances such as alcohol. Results from laboratory
 ALCOHOL HANGOVER EFFECTS ON COGNITION
studies that do not implement a placebo control have little
credibility. Without a placebo, participants would have known
when they were consuming alcohol and so any effects shown
could be expectancy effects, rather than genuine effects arising
from the experimental treatment. In the case of alcohol, which
is renowned amongst the general public for producing perfor-
mance decrements, participants may unwittingly have put in
less effort when completing the performance tests following
alcohol ingestion. Morrow et al. (1990) did employ a placebo
but they used a repeated measures design without properly
controlling for condition order effects. Participants becoming
fatigued during the experiment could explain their findings.
Another common problem is not verifying that BALs have
returned to zero at the time the performance testing is carried
out. As already mentioned, a defining characteristic of alcohol
hangover effects is their presence at zero BAL. Ensuring BAL
genuinely is zero (or so low as to be at the limits of detection) is
necessary for research purposes in order to distinguish between
hangover and acute alcohol intoxication. Lemon et al., (1993)
purport to assess hangover effects without verifying that BAL
is zero. In addition several supposed hangover studies report
carrying out performance testing at elevated BALs. Such stud-
ies are likely to be picking up acute alcohol intoxication effects
and cannot be interpreted as showing genuine hangover effects
(Kelly et al., 1970; Seppela et al., 1976; Collins, 1980; Myrsten
et al., 1980; Kim et al., 2003). Several other studies that are
sometimes cited as assessing hangover effects were actually
concerned with acute alcohol effects on the descending limb
of the blood-alcohol curve. As these studies conducted testing
at raised BALs, they do not elucidate alcohol hangover effects
(Ekman et al., 1963; Jones and Vega, 1972; Peeke et al., 1980;
McCaul et al., 1991; Millar et al., 1999).
Seven laboratory hangover studies are sufficiently rigorous
to warrant serious attention (Collins et al., 1971; Collins and
Chiles, 1980;. Roehrs et al., 1991; Chait and Perry, 1994;
Streufert et al., 1995; Finnigan et al., 1998; Verster et al.,
2003). One further laboratory study that we have criticized for
not verifying zero BAL at testing will also be reviewed fur-
ther. Lemon et al., (1993) found no effects and so this study
is immune from the criticism that, in not verifying zero BAL,
hangover results are contaminated by acute alcohol intoxica-
tion effects. Key aspects of the design, procedure and results of
these eight studies are summarized in Tables 1 and 2.
Each study involved the administration of between 0.7 and
1.6 g/kg of alcohol (median 1 g/kg, roughly equivalent to
9 units, that is 3 pints of typical 5% ABV lager, or one bot-
tle of 13% ABV wine), as pure ethanol or vodka mixed with
orange juice, tonic, lime or lemonade. The placebo was usually
orange juice or another mixer with a small quantity of alco-
hol to provide an appropriate olfactory sensation. The majority
of studies employed all-male samples, the consumption-to-test
interval ranged from 7.5–12 hours (median 10 hours), and ap-
propriate steps were taken to control condition order effects.
Each study verified that BAL was zero at testing (except Lemon
et al., 1993, but see above). A range of cognitive and other per-
formance tests were applied across the memory, attention, pro-
cessing speed, executive function and psychomotor domains,
although attention was tested in more studies than any other
function.
Only two of the studies showed hangover effects. In a
between-subjects design, Verster et al. (2003) showed poorer
165
delayed recall of items from a 15-word list the morning af-
ter 1.4 g/kg of alcohol consumption (mean recall 9.4 items,
SD 3.4) compared with placebo (mean recall 11.5 items, SD
3.5). Four of the eight rigorous laboratory studies assessed di-
vided attention (or dual task performance which amounts to
the same thing) but only Roehrs et al. (1991) showed a signif-
icant hangover decrement, with null effects in the three other
studies (Lemon et al., 1993; Chait and Perry, 1994; Finnigan
et al., 1998). This low ‘hit rate’ of effects across studies ques-
tions the reliability of the finding by Roehrs et al. and this
reliability is further questioned by the small sample size those
investigators employed. Therefore, there are only limited data
to support the hypothesis that hangover produces decrements
in divided attention. Only one of the eight rigorous labora-
tory studies showed a significant hangover decrement in de-
layed recall, although this was the sole study to have assessed
long-term memory (Verster et al., 2003). At this juncture it
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is worth considering the extent to which long-term memory
decrements have been shown in the less rigorous studies. Takala
et al. (1958) noted a poorer rate of improvement due to prac-
tice (later trial performance was compared with earlier trial
performance) on a visual search task after 1.3 g/kg beer, al-
though, as already stated, this result was based on an intact
groups comparison and it is possible that the technical students
in the control group had generally superior visual search ability
relative to the medical students in the hangover group. Ekman
et al. (1964) assessed immediate and 7-minute delayed recog-
nition of letter pairs but neither presented nor analysed the test
scores. A small effect is claimed but it is not clear whether
this is an acute intoxication effect. In a related design, Kim
et al. (2003) showed long-term memory ‘decrements’ follow-
ing 1.5 mg/kg alcohol consumption. However, again it is not
clear whether this is an acute intoxication effect.
We find these mainly null findings surprising and strongly
suspect their explanation lies with study insensitivity rather
than a genuine absence of hangover effects. There are three
reasons for this. First, five of the above studies employed
crossover placebo designs, yet such designs have been argued
to be unsuitable for ingestion studies. A combination of pro-
prioceptive changes due to alcohol ingestion and inferential
reasoning on the part of participants allows some participants
to determine which is the placebo condition and diminishes
study sensitivity (Finnigan and Hammersley, 1992). Second,
all the above studies employ the pharmacological model of
drug action, i.e. the alcohol is administered as a single large
dose under as close to possible double-blinded conditions.
However, this model may not be applicable to study the so-
cial phenomenon of drinking alcohol (Finnigan and Hammer-
sley, 1992). For example, in real life people may control their
drinking rate so that they can continue to function socially and
will often take food with the alcohol. Third, it is possible that
the alcohol doses employed in laboratory studies are insuffi-
cient for a hangover to occur; insufficient; due to research-
ethics-imposed consumption limits. Nevertheless, five of the
identified eight rigorous laboratory studies assessed subjec-
tive hangover symptoms and in all cases hangover symptoms
were detected (Collins and Chiles, 1980; Roehrs et al., 1991;
Streufert et al., 1995; Finnigan et al., 1998; Verster et al., 2003).
It is possible that the alcohol dose required to produce cogni-
tive hangover effects is larger than that for somatic hangover
symptoms.
 166

Table 1. Summary of design and procedural aspects of the eight rigorous laboratory-based hangover studies

Collins et al. Collins and Chiles Roehrs et al. Lemon et al. (1993) Chait and Perry Streufert et al. (1995) Finnigan et al. (1998) Verster et al. (2003)
(1971) (1980) (1991) (1994)

Country USA USA USA Australia USA USA Scotland Netherlands

Funder FAA Army and – NIH, NIAAA Federal Office of NIDA, USPHS NIDA AERC –
Navy Road Safety, Canberra
Design Independent Related Related Independent Related Related Related Independent
Participants 20 college 11 healthy pilots 5 healthy males 64 healthy males 14 healthy volunteers 21 healthy 40 male healthy heavy 48 healthy moderate
students professionals social drinkers, drinkers
non-smokers
Male:female ratio 20/0 7/4 5/0 64/0 10/4 21/0 40/0 24/24
Age Range 21–30 Mean 39.6 (SD not Range 21–34 Mean 24.6 (SD 6.6) Mean 24.5 (SD Under 46 (Mean not Mean 25.6 (SD Mean 21.9 (SD 17.1)
stated) 21–34) stated) 18–41)
Alcohol 1.6 (2 ml/kg) 1.3 0.8 0.5–1.0 (max 7–8 Males: 1.2 Females: 1.0 0.7 (100 mg/100 ml 1.4
consumed (g/kg) units) 1.0 blood)
Alcoholic drink Vodka and OJ Bourbon and 7-Up Vodka and tonic Ethanol and OJ Ethanol, tonic and Ethanol, tonic and Vodka, water and Ethanol and OJ
or vodka and 7-Up lime peppermint extract diabetic OJ
Placebo drink OJ with few drops Rum extract and Tonic with three 0.5 ml ethanol floated 1% ethanol, tonic and Tonic and peppermint Diabetic OJ, rim OJ and Grand Marnier
R. STEPHENS et al.

rum extract colouring drops of ethanol on OJ lime extract sprayed with swabbed with vodka essence consumed with
floated atomized 10% ethanol and lozenges nose clip
Restricted before – Coffee/ caffeine Caffeine – Eating, smoking, Drugs, alcohol Eating and drinking Eat, smoke, coffee,
morning test coffee anything but water excessive water
session
Consumption to 10 (max) 7.5 9 11 10 12 10 10
test interval (h)
BAL zero at test Yes (at 8 and 10 h Very low (under Yes Not stated Yes (but 2 participants Yes Yes Yes
post-drink) 0.007%) 10 mg/dl)

OJ = orange juice.

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 ALCOHOL HANGOVER EFFECTS ON COGNITION 167
Table 2. Summary of cognitive domains and tests used in the eight rigorous laboratory-based hangover studies (underlined tests showed hangover decrements)

Collins et al. Collins and Chiles Roehrs et al. Lemon et al. Chait and Perry Streufert et al. Finnigan et al. Verster et al.
(1971) (1980) (1991) (1993) (1994) (1995) (1998) (2003)

Memory – – – – Word recall task – Probed- (short 15 word list

term) memory learning
recall task (immediate
recall; 60 min
delayed recall
and
recognition)
Attention – Choice RT, meter Divided Divided attention, Visual divided – Sustained Mackworth
monitoring, attention simple RT, attention, attention, dual clock test
pattern ID, Mackworth backwards task (tracking (vigilance)
clock test digit span and RT)
(vigilance)
Processing – Mental arithmetic – – Baddeley logical – – –
speed reasoning,
digit symbol
Executive – Problem solving – – Time production Management – –

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function simulation
(developing
country/floods)
Psycho- Tracking Tracking – – Standing – – –
motor steadiness

While some aspects of the design of laboratory studies
can easily be addressed to improve sensitivity, research ethics
limitations on alcohol dose and the limitations of the pharmaco-
logical model of drug action applied to alcohol ingestion studies
have led some investigators to look beyond the laboratory.
NATURALISTIC ALCOHOL CONSUMPTION
Using an alternative approach, three studies have investigated
the cognitive consequences of hangover subsequent to more
naturalistic consumption, i.e. after participants have been al-
lowed to drink what and sometimes where they choose. One
of these showed decrements on several tests of attention –
but, as zero BAL at testing was not confirmed, these could be
due to acute alcohol intoxication rather than hangover effects
(Anderson and Dawson, 1999). McKinney and Coyle (2004)
used a related design with n = 48 and found impairments for
free recall of a word list, delayed recognition of words in the list,
and both simple and complex reaction times. Testing was car-
ried out at least 7 hours after reported consumption of an aver-
age of 1.6 g/kg of alcohol and BAL was zero at testing for all ex-
cept two participants whose readings were very low. Finnigan
et al. (2005) used a between-subjects design with n = 25 in
the hangover group but showed no cognitive effects at zero
BAL the morning after reported consumption of an average of
1.7 g/kg of alcohol. We estimate the power of these studies to be
0.94 and 0.47, respectively, for the detection of medium-sized
effects using two-tailed hypotheses (Cohen, 1988). Therefore
the absence of effects in the latter study, in common with the
laboratory studies, is likely to be due to poor study sensitivity
because of low statistical power.
Two further naturalistic consumption studies have assessed
different aspects of driving ability during hangover. Laurell and
Törnros (1983) showed impaired cone avoidance while driving
a real car. Törnros and Laurell (1991) showed no difference in
the ability to go as fast as possible without losing control on
a driving simulator. These studies were otherwise comparable
on amount of alcohol consumed, each ensured BAL was zero
at testing and each used a related design with comparable n.
Key aspects of the design, procedure and results of the five
naturalistic drinking hangover studies conducted to date are
summarized in Tables 3 and 4.
In keeping with the laboratory studies reported earlier, natu-
ralistic consumption studies indicate that hangover affects as-
pects of long-term memory and attention, as well as psychomo-
tor tasks. Although the quantity of alcohol reportedly consumed
in these naturalistic studies appears to be similar to that adminis-
tered in the laboratory studies, consumption data reported in the
naturalistic studies are averages. Therefore, some participants
would have drunk substantially more in the naturalistic studies
than would ethically be allowed in the laboratory. While this un-
doubtedly contributes to the sensitivity of naturalistic studies,
there is a substantial problem in the interpretation of these re-
sults. In these studies participants were always informed at the
outset that hangover effects were to be assessed and they knew
which was the hangover condition. Under these circumstances
expectancy effects are likely to have significantly contaminated
the results. Therefore, while naturalistic alcohol consumption
studies can be considered as being suggestive of hangover ef-
fects they should not, on their own, be interpreted as providing
definitive evidence of hangover effects.
REVISITING LABORATORY STUDIES LACKING A
PLACEBO CONTROL
Earlier we argued that findings from laboratory studies that did
not employ a placebo control were likely to be biased as any
effects found were likely to be contaminated by expectancy ef-
fects, rather than genuine effects arising from the experimental
treatment. However, we went on to review naturalistic alcohol
consumption studies on the grounds that these studies do not
employ the pharmacological model of drug action and so may
have greater sensitivity relative to laboratory studies employing
168 R. STEPHENS et al.
Table 3. Summary of design and procedural aspects of the five naturalistic alcohol consumption hangover studies

Laurell and Törnros (1983) Törnros and Laurell (1991) Anderson and McKinney and Coyle Finnigan et al. (2005)
Dawson (1999) (2004)

Country Sweden Sweden South Africa Northern Ireland Scotland

Funder None stated None stated None stated None stated AERC
Design Related Related Mixed Related Independent
Participants 22 healthy volunteers 24 healthy volunteers 16 hangover versus 48 students 25 hangover versus 33
(majority were students) 10 controls control versus 13 acute
(students) + hangover
(volunteers)
Male:female ratio 16/6 23/1 8/8 vs. 5/5 15/33 36/35
Age Range 19–38 Range 22–46 Mean 21.7 (SD 1.1) Mean 23.4 (SD 5.3) Mean 24.3 (SD ns)
Alcohol consumed 0.6 approx. (based on mean 0.7 approx. (based on 1.0 (minimum) 1.6 (mean) 1.75 (mean)
(g/kg) peak BAL 147 mg%) man peak BAL 176 mg%)
Alcoholic drink Beer, wine, spirits Beer, wine, spirits Not reported Not reported Not reported
Control condition Abstention ‘Non-alcoholic drinks’ Abstention Abstention Abstention
Restricted before None stated None stated None stated Caffeinated drinks None stated
morning test session
Consumption to test 8+ 14 (at 2 pm) 12–16 7+ Not stated

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interval (h)
BAL zero at test Yes Yes (at 2 pm) Not stated Yes (low readings of Yes
5 ml/100 ml for
two participants)

Table 4. Summary of cognitive domains and tests used in the five naturalistic alcohol consumption hangover studies (underlined tests showed hangover
decrements)

Laurell and Törnros and Laurell (1991) Anderson and Dawson (1999) McKinney and Coyle (2004) Finnigan et al. (2005)
Törnros (1983)

Memory – – – Word recall, delayed word Probe (short-term)

recognition memory recall
Attention – – Digit symbol modalities test, Reaction time (simple and Dual task tracking/ RT,
PASAT, Letter cancellation, 5-choice), selective Vigilance (repeating
star cancellation, symbol attention, divided attention, three-digit numbers)
cancellation spatial attention, sustained
attention,
Processing speed – – – 5-Choice reaction time –
Executive function – – – Stroop –
Psychomotor Car driving (cone Driving simulator – cover – – –
avoidance) 20 km as fast as possible

such models. Nonetheless, these naturalistic consumption stud-
ies also did not control expectancy effects. In the interests of
balance the findings of the non-placebo controlled laboratory
studies are considered in this section as further examples of sug-
gestive hangover effects, albeit effects which may be primarily
due to expectancy processes.
Yesavage and Leirer (1986) found evidence of poorer per-
formance piloting a flight simulator in 10 male navy pilots 14
hours following administration of approximately 1 g/kg of al-
cohol served as ethanol added to a soft drink. Blood alcohol
was zero. Taylor et al. (1996) did not show any decrements on a
flight simulator in 23 male and female pilots 8 hours following
ingestion of 0.6 g/kg of alcohol served as ethanol and diet soda.
Individual blood alcohol levels were not reported, but the mean
BAL had dropped to zero 1 hour prior to testing. Kruisselbrink
et al. (2006) showed an increase in choice reaction time errors
in 12 female students 8.5 hours following consumption of ap-
proximately 1.2 g/kg of alcohol served as beer, compared with
after abstaining. Blood alcohol was zero.
In summary, these studies have shown decrements in ability
to pilot a simulated aircraft and in attentional processing (choice
reaction time) at alcohol doses ranging from 1 to 1.2 g/kg. The
study employing a much smaller quantity of alcohol (0.6 g/kg)
did not show any effect – probably due to the low alcohol dose.
However, it must be remembered that these studies did not
control expectancy effects pertinent to alcohol consumption,
and this is likely to have biased these participants’ performance
to a sub-optimal level.
DISCUSSION
In the Introduction we highlighted executive function as likely
to be susceptible to hangover effects, based on analogy with re-
search into acute alcohol and sleep deprivation. However, only
one study has assessed executive functioning during hangover
and no effect was observed. This may be due to insensitivity as-
sociated with the manner of assessment – using a management
simulation game rather than using well-validated neuropsycho-
logical testing. Future research should employ well-validated
executive function tests.
Encouragingly, there is some consistency in the kinds of
cognitive effect shown across the laboratory and naturalis-
tic alcohol consumption studies. Verster et al. (2003) and
McKinney and Coyle (2004) showed hangover-related memory
 ALCOHOL HANGOVER EFFECTS ON COGNITION
decrements. The latter study also shares the finding of attention
decrements with the laboratory-based studies of Roehrs et al.
(1991) and Kruisselbrink et al. (2006). A convergent finding
from differing methodologies is known as triangulation and is
considered to be a sign of validity in psychological research
(e.g. Howitt and Cramer, 2005). As more studies are carried
out, there may be a continued trend of convergent findings,
which could lead future reviewers to be able to reach more
definitive conclusions. Nevertheless, we have identified some
serious problems with the two methodological approaches used
to study hangover effects.
Rigorous laboratory-based studies, where participants are
blinded to alcohol consumption, have tended not to show ef-
fects of hangover on performance. This insensitivity may arise
partly because the pharmacological model of drug action, where
a certain drug dose is predicted to affect aspects of behaviour,
may be of little relevance to normal drinking (Finnigan and
Hammersley, 1992). This is because the typical laboratory-
based controlled intake study ignores potentially important ev-
eryday aspects of drinking that are usually set by the drinker –
for example, the number and types of drink consumed, the pace
of consumption, whether food is also consumed, and the social
setting. On the other hand, naturalistic alcohol consumption
studies, which allow for all these factors, have tended to show
effects of hangover on performance. However, as participants
were unblinded in these studies, the significant results are likely
to be contaminated by expectancy effects.
Finnigan and Hammersley (1992) reviewed all the acute al-
cohol studies published from 1980 to 1991 and this remains
the most-up-to-date, comprehensive review published. They
concluded that the research is ‘ambitious rather than rigorous’
(p. 74) and ‘while ample evidence exists that alcohol is capable
of impairing performance. . . it is premature to conclude that it
invariably does so’ (p. 74). The criticisms they raise with respect
to acute alcohol studies may also be applied to the hangover
studies reviewed here. In both literatures there are studies with
flaws in basic experimental design, such as very small sam-
ple size and ineffective control of expectancy, for example by
not including a placebo. Additionally, in both literatures the
majority of publications describe laboratory-controlled alcohol
consumption studies employing the pharmacological model of
drug action. As outlined in the previous paragraph, this model
may be of little relevance to normal drinking. Finnigan and
Hammersley (1992) argued that: ‘Natural intoxication may lead
to more impairment, less impairment or different impairments’
(p. 78). This is likely to be true for hangover effects as well as
for acute intoxication.
CONCLUSION
One could say that the literature on performance effects of
the alcohol hangover resembles a Catch 22. Each of the two
methodological approaches employed in this literature has
its own interpretative problems. Controlled-intake laboratory-
based studies appear to lose a significant quantity of variability
attributable to user-controlled aspects of social drinking. On the
other hand, data from naturalistic alcohol consumption studies
are likely to be contaminated by expectancy effects. Currently
there is little definitive empirical evidence determining what,
if any, effects on performance arise as a result of the alcohol
169
hangover. In this respect, the hangover and performance litera-
ture resembles the acute alcohol intoxication and performance
literature, which has also yielded largely inconclusive data.
Future research must overcome the shortcomings of previous
research identified in this review if a full understanding of the
performance effects of the alcohol hangover is to be gained.
For naturalistic drinking studies, the main issue is control-
ling expectancy effects. A novel approach would be for future
studies to exploit the predictability with which social drinking
occurs, e.g. on Friday evenings. Such regularity could be used
to assess hangover effects in individuals believing that they are
taking part in research with other aims, by simply inviting them
to attend for testing on mornings likely to follow an evening
spent drinking, and on mornings likely to follow an evening
of abstinence. Not all participants would have hangovers but
those that do would arrive in the laboratory in a frame of mind
similar to any hungover person arriving at work or college –
Downloaded from http://alcalc.oxfordjournals.org by Marisa Levy on March 28, 2010
aiming to have a reasonable go under the circumstances. This
scenario is potentially very useful for understanding hangover
effects and could contribute a further strand to a convergent
alcohol hangover and performance literature.
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