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The Alcohol Hangover
Jeffrey G. Wiese, MD; Michael G. Shlipak, MD, MPH; and Warren S. Browner, MD, MPH
R-E-M-O-R-S-E!
Those dry Martinis did the work for me:
Last night at twelve I felt immense,
Today I feel like thirty cents.
My eyes are blurred, my coppers hot,
I’ll try to eat, but I cannot.
It is no time for mirth and laughter,
The cold, gray dawn of the morning after.
Purpose: To review the cause, pathophysiologic characteristics, cost, and treatment of alcohol-induced hangover.
Data Sources: A MEDLINE search of English-language
reports (1966 to 1999) and a manual search of bibliographies of relevant papers.
Study Selection: Related experimental, clinical, and
basic research studies.
Data Extraction: Data in relevant articles were reviewed,
and relevant clinical information was extracted.
Data Synthesis: The alcohol hangover is characterized
by headache, tremulousness, nausea, diarrhea, and fatigue combined with decreased occupational, cognitive, or
visual–spatial skill performance. In the United States, related absenteeism and poor job performance cost $148
billion annually (average annual cost per working adult,
$2000). Although hangover is associated with alcoholism,
most of its cost is incurred by the light-to-moderate
drinker. Patients with hangover may pose substantial risk
to themselves and others despite having a normal blood
alcohol level. Hangover may also be an independent risk
factor for cardiac death.
Symptoms of hangover seem to be caused by dehydration, hormonal alterations, dysregulated cytokine pathways, and toxic effects of alcohol. Physiologic characteristics include increased cardiac work with normal peripheral
resistance, diffuse slowing on electroencephalography,
and increased levels of antidiuretic hormone.
Effective interventions include rehydration, prostaglandin inhibitors, and vitamin B6. Screening for hangover
severity and frequency may help early detection of alcohol
dependency and substantially improve quality of life. Recommended interventions include discussion of potential
therapies and reminders of the possibility for cognitive
and visual–spatial impairment. No evidence suggests that
alleviation of hangover symptoms leads to further alcohol
consumption, and the discomfort caused by such symptoms may do so. Therefore, treatment seems warranted.
Conclusions: Hangover, a common disorder, has substantial morbidity and societal cost. Appropriate management may relieve symptoms in many patients.
George Ade, The Sultan of Sulu, 1903 (1)
T
he alcohol hangover has been well-known since
at least Biblical times: “Woe unto them that
rise up early in the morning, that they may follow
strong drink” (Isaiah 5:11) (2). Medical investigation, however, has focused on the acute effects of
alcohol ingestion. More than 4700 articles have
been written about alcohol intoxication since 1965,
but only 108 have addressed alcohol hangover (3–5).
Recent studies suggest that the alcohol hangover
induces cardiovascular and psychomotor morbidity
independent of the quantity of alcohol consumed or
the frequency of ingestion (6 – 8).
Methods
We searched the MEDLINE database (1965 to
1999) for epidemiologic, physiologic, and economic
studies about alcohol hangover, using the terms
hangover, alcohol withdrawal, and alcohol intoxication. Bibliographies of selected articles and personal
communication with selected authors were used to
extend the search. Articles were screened for their
relevance to the specific topic of alcohol hangover
on the basis of the title and abstract. All studies
that specifically referred to the alcohol hangover
were included in the data analysis. A formal metaanalysis was not performed because the few clinical
trials were not similar in design or hypotheses.
Definition
There is no consensus definition of veisalgia (“alcohol hangover,” from the Norwegian kveis, or “uneasiness following debauchery,” and the Greek algia,
or “pain”). Most descriptive (7, 9) and experimental
studies (10 –12) have identified a set of common
symptoms: headache, diarrhea, anorexia, tremulous-
Ann Intern Med. 2000;132:897-902.
For author affiliations and current addresses, see end of text.
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Table 1. Symptoms of Alcohol Hangover*
Symptom
Persons Affected, %
Headache
Poor sense of overall well-being
Diarrhea
Anorexia
Tremulousness
Fatigue
Nausea
66
60
36
21
20
20
9
* Data taken from reference 13.
ness, fatigue, and nausea (Table 1). Objective criteria have focused on decreased occupational, cognitive, or visual–spatial skill performance or on
alterations in hemodynamic and hormonal measurements. Although tachycardia, tremor, orthostasis,
cognitive impairment, and visual–spatial impairment
are frequently observed (12, 14), they do not capture the overall experience for the patient. This
remains subjective, varying from person to person
and from episode to episode (15). To permit a
uniform discussion, we defined hangover as the presence of at least two of the symptoms in Table 1,
occurring after the consumption and full metabolism of alcohol with sufficient severity to disrupt the
performance of daily tasks and responsibilities.
Economic and Epidemiologic Significance
Although hangover might be considered trivial—
just deserts for the overindulgent—it has substantial
economic consequences. A recent British study
noted that alcohol use accounted for 2 billion
pounds ($3.3 billion U.S.) in lost wages each year,
most of which resulted from work missed because of
hangover (16). Alcohol costs in Canada amount to
$7.5 billion each year, and $1.4 billion is lost each
year because of decreased occupational productivity
caused by hangover-like symptoms (17). Studies in
other countries have yielded similar per capita estimates for the annual cost of alcohol ingestion: Australia, $3.8 billion (18); New Zealand, $331 million
(19); and the United States, $148 billion (20).
Greenfield recently estimated the average annual
opportunity cost due to hangover as $2000 per
working adult (20).
In the workplace, the greatest cost incurred by
alcohol is the decreased productivity of affected employees as a result of hangover-related absenteeism
and poor job performance (20, 21). In Finland,
which has a population of 5 million persons, more
than 1 million workdays are lost each year because
of hangover (22). Light-to-moderate users of alcohol (0 to 3 drinks per day for men and 0 to 1 drink
per day for women) (17) account for most of the
lost-work costs because they make up most of the
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work force (23). Fifty-four percent of all alcoholrelated problems in the workplace are caused by
light drinkers, and 87% are caused by light-to-moderate drinkers. The primary morbidity that affects
light-to-moderate drinkers is the hangover, not the
long-term consequences of alcohol abuse, such as
cirrhosis and cardiomyopathy (20). Chronic alcoholism is responsible for only a small proportion of the
total societal cost of alcohol use (24).
Perhaps the most alarming feature of veisalgia is
its high prevalence. In a study of college students,
25% of students reported experiencing a hangover
in the previous week and 29% reported losing
school time for hangover recovery (5). More than
75% of men and women who have consumed alcohol report that they have experienced hangover at
least once (25), and 15% experience hangovers at
least monthly. Ten percent of British men reported
hangover-related problems at work at least monthly
(16). Paradoxically, hangover is much more common in light-to-moderate drinkers (70%) (16) than
in heavier drinkers (13, 17, 26, 27).
Although hangover may be interpreted as merely
uncomfortable, the patient with hangover is at increased risk for injury and poor job performance.
Patients with hangover have diminished visual–spatial
skills and dexterity, even after alcohol can no longer
be detected in the blood. Impairment from hangover has been experimentally demonstrated in pilots
(12, 28), people who drive (29, 30), and skiers (31).
Managerial skills and task completion are also adversely affected (32, 33). Frequent hangovers have
also been shown to be associated with increased
cardiac death in patients not known to have coronary artery disease (relative risk, 2.4 [95% CI, 1.0 to
5.5]); however, after adjustment for risk factors and
alcohol consumption, this association was no longer
statistically significant (relative risk, 1.8 [CI, 0.7 to
4.3]) (6).
Table 2. Comparison of the Signs and Symptoms of
Alcohol Withdrawal and Hangover*
Sign or Symptom
Sign
Electroencephalography
Auditory evoked response
Hypertension
Dehydration or orthostasis
Cognitive impairment
Visual–spatial impairment
Symptom
Headache
Tremulousness
Nausea
Fatigue
Dry mouth
Poor sense of overall well-being
Alcohol
Withdrawal
Increased
Elevated
Common
Uncommon
Common
Common
Slowed
Normal to elevated
Rare
Common
Common
Common
Common
Very common
Uncommon
Common
Uncommon
Common
Common
Occasional
Common
Common
Common
Common
* Data taken from references 13, 22, and 36.
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Hangover
Table 3. Effects of Alcohol Intoxication and Subsequent Hangover on Serum Hormone Concentrations
Hormone and Electrolytes Affected (Reference)
Antidiuretic hormone (46)
Aldosterone (47, 48)
Renin (47, 48)
Insulin response to glucose (49)
Glucagon (50)
Cortisol (51)
Thyroid-stimulating hormone (44, 52)
Growth hormone (52)
Acid– base states (53, 54)
Electrolytes (54)
Testosterone (51)
Follicle-stimulating hormone or luteinizing hormone (52)
Prolactin secretion in response to thyroid-stimulating hormone (52)
Acute Alcohol Intoxication
Hangover
Effect Proportional to
Hangover Severity
Decreased
Decreased
Decreased
Increased
Increased
Unchanged or decreased
Unchanged
Unchanged
Metabolic acidosis
Unchanged
Unchanged
Unchanged
Increased
Increased
Increased
Increased
Unknown
Unknown
Increased
Unchanged
Decreased
Metabolic acidosis
Unchanged
Unchanged
Unchanged
Inhibited
Yes
No
No
No
Unknown
No
No
No
Yes
No
No
No
Unknown
The ways in which hangover affects total alcohol
consumption are not clearly understood. Many persons believe that hangover is a punishment for alcohol consumption and therefore prevents subsequent alcohol use (34). Hangover has never been
shown to effectively deter alcohol consumption,
however, and no evidence shows that alleviation of
hangover symptoms would result in further consumption (34). In contrast, the discomfort of hangover symptoms may prompt further alcohol intake
(for example, the “eye opener”). One study of 178
persons found that “those who experience greater
hangover may choose to drink more alcohol in order to relieve these adverse effects” (35). Therefore,
successful treatment of hangover could mitigate total alcohol consumption.
Physiologic and Clinical
Manifestations of Hangover
Part of the mystery of hangover is the set of illdefined physiologic characteristics that underlie the
syndrome. One theory is that hangover is the first
stage of alcohol withdrawal. However, the hormonal
and hemodynamic changes seen in hangover are
distinct from those seen in alcohol withdrawal
(Table 2).
Although larger doses of alcohol lead to more
severe symptoms, hangover is not solely doserelated (37). Acetaldehyde, the dehydrogenated
product of alcohol metabolism (38), might be responsible for hangover symptoms (10). Congeners,
the byproducts of individual alcohol preparations
(which are found primarily in brandy, wine, tequila,
whiskey, and other dark liquors), increase the frequency and severity of hangover (24, 39, 40). Clear
liquors, such as rum, vodka, and gin, tend to cause
hangover less frequently, which may explain why
patients with chronic alcoholism use these liquors
disproportionately. In an experimental setting, 33%
of patients who consumed 1.5 g/kg of body weight
of bourbon (which has high congeners) but only 3%
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of those who consumed the same dose of vodka
(which has low congeners) experienced severe hangover (41).
The constellation of hangover symptoms (nausea,
headache, diarrhea) resembles that seen in conditions related to dysregulated cytokine pathways (for
example, in viral infections and after administration
of interferon-␣). Alcohol alters cytokine production
through a thromboxane pathway. Levels of thromboxane B2 are elevated during experimentally induced alcohol hangover (42), and the administration
of tolfenamic acid, a prostaglandin inhibitor, at the
time of alcohol consumption has a small prophylactic effect in reducing hangover severity (9).
Several hormonal alterations have been observed
in patients with hangover (43– 45) (Table 3). Hangover severity is proportional to antidiuretic hormone
concentration (46). Alcohol inhibits the effect of
antidiuretic hormone on the kidneys, thereby inducing diuresis that is out of proportion to the volume
of fluid ingested. As blood alcohol concentration
decreases and dehydration persists, the serum level
of antidiuretic hormone increases, maintaining water retention in dehydrated patients with hangover.
In our clinical experience, hydration attenuates but
does not completely relieve hangover symptoms. Serum aldosterone and renin levels also increase with
hangover, but unlike antidiuretic hormone, they do
not correlate well with hangover severity (47, 48).
The effect of alcohol consumption and hangover
on glucose metabolism is incompletely understood.
Alcohol seems to inhibit the availability of glucose
through an insulin-mediated mechanism (49). Glucagon is increased in acute alcohol intoxication, but
its effect during hangover is unknown (50). Cortisol
release is also suppressed during acute alcohol intoxication, but this effect does not persist in hangover (51). Levels of thyroid (44, 52) and growth
hormone (52) do not change during acute alcohol
intoxication or hangover. Both acute intoxication
and hangover cause metabolic acidosis (53, 54).
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Hemodynamic changes seen in the patient with
hangover include increases in heart rate, left ventricular performance (as measured by ejection fraction), and blood pressure (14, 55). The peripheral
vasodilatation seen with acute alcohol ingestion is
not observed in hangover (14). The increased cardiac work with normal peripheral resistance that
occurs in hangover may explain the associated increased cardiac mortality rates (6).
Patients with hangover have a diffuse slowing on
electroencephalography (36), which persists up to 16
hours after blood alcohol level becomes undetectable. Decreased auditory evoked responses and psychomotor deficits have also been noted (22). These
findings suggest that hangover, which manifests as
“diffuse cortical depression,” may be a different
physiologic process than “alcohol withdrawal,”
which is characterized by general hyperexcitability
of the brain (22, 56).
Hangover Assessment and Treatment
The absence of a standard instrument for hangover assessment makes comparison of treatments
difficult (15). Among patients with experimentally
induced hangover, an alcohol dose of 1.5 to 1.75
g/kg (five to seven standard cocktails), administered
orally over 4 to 6 hours, is almost always followed
by hangover symptoms (36, 37, 42, 48, 49, 52).
Other factors that increase the severity of hangover
include lack of food consumption, decreased quality
and quantity of sleep, increased physical activity
while intoxicated, dehydration, and poor physical
health (28, 30, 38).
Despite the ease in inducing hangover, only a few
trials have studied treatment of hangover symptoms.
Bogin and coworkers (10) compared propranolol
with placebo but found no effect. In their crossover
study, 10 healthy college students drank enough alcohol to reach a blood alcohol level of at least 0.1
g/dL. On the night the alcohol was consumed, 5 of
the students received a long-acting oral preparation
of 160 mg of propranolol; the remaining students
received placebo. The study was repeated on a second occasion with a switch in treatment assignment.
The morning after each night of alcohol consumption, researchers assessed the vital signs of each
participant and calculated a score on a hangover
severity scale. Objective analysis of hand tremor,
blood pressure, and cardiac rate and rhythm showed
no significant differences. On a scale of 1 to 5, the
mean (⫾SD) severity of hangover was 2.9 ⫾ 1.1 in
participants who received propranolol and 2.8 ⫾ 0.9
in those who received placebo (CI for the mean
difference, ⫺0.84 to 1.04). The authors concluded
that propranolol does not produce a clinically im900
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portant benefit in the symptoms of hangover. However, the study’s power was only 50% for the hypothesized primary finding, at a two-sided ␣ value
of 0.05 (10).
Two trials have investigated the effect of simple
carbohydrates on hangover severity. Seppala and
colleagues (29) assigned 40 healthy men to receive
one of six treatments. Participants received 1.75
g/kg of alcohol from 6:00 p.m. to 9:00 p.m. and an
oral glucose or fructose solution (0.5 g/kg or 1 g/kg).
The participants in the two control groups received
alcohol or glucose but not both. All patients subjectively assessed their hangover severity and underwent psychomotor tests that determined reaction
time, coordination, and attention span. Administration of glucose at the time of alcohol ingestion
reduced mistakes by 50% on the choice reaction
test (which was given 15 hours later) but slightly
increased mistakes on the coordination test. Hangover severity was not affected. The study was limited
by the small number of participants (n ⫽ 5) in each
treatment group. Moreover, the statistical analysis
did not account for multiple comparisons. Ylikahri
and coworkers (37) used a similar design to study
109 healthy men (1.75 g/kg of alcohol administered
orally over 3 hours, followed by 1 g/kg of oral
glucose or fructose). Patients who received glucose
or fructose had lower serum levels of free fatty
acids and ketones but no change in subjective or
objective hangover symptoms.
In a nonblinded study sponsored by its manufacturer, an herbal preparation called Liv.52 (Himalaya
Drug Co., Bombay, India) decreased hangover
symptoms more than placebo (11). Among patients
who took Liv.52 at the time of alcohol consumption,
the ratio of blood and urine alcohol levels to acetaldehyde increased; this was the postulated mechanism for the observed decrease in hangover symptoms. The investigators hypothesized that Liv.52
blocked the conversion of ethanol to acetaldehyde,
which they believed to be the cause of hangover
symptoms.
Tolfenamic acid, a prostaglandin inhibitor, was
associated with a small improvement in hangover
symptoms when administered prophylactically on
the night of alcohol consumption. Thirty healthy
volunteers participated in a double-blind crossover
study, in which they received 200 mg of tolfenamic
acid or placebo before sleep. The following morning, participants who received tolfenamic acid reported less headache, nausea or vomiting, irritation,
and thirst. Levels of prostaglandin E2 and thromboxane B2 were lower in the tolfenamic acid group,
and the investigators suggested that these cytokines
may be associated with hangover symptoms (9).
Other nonsteroidal agents are frequently used to
treat hangover symptoms but have not been studied.
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Prophylactic vitamin B6 (pyritinol) reduced the
number of hangover symptoms by approximately
50% in one study (57). Seventeen men and women
attended two parties and were asked to drink the
alcoholic beverage of their choice until intoxicated.
Fifty percent of participants received 1200 mg of
vitamin B6 (400 mg at the beginning of the party,
400 mg 3 hours later, and 400 mg at the party’s
conclusion), and 50% received placebo. At the second party, participants received the alternate tablet.
A survey instrument of 20 symptoms was used to
assess hangover severity. On a scale of 1 to 10, the
mean symptom score (⫾SD) was 3.2 ⫾ 2.8 with pyritinol and 6.8 ⫾ 3.8 with placebo (P ⬍ 0.01). The
mechanism of this effect is unknown.
Therapeutic administration of 1 g of chlormethiazole (a psychotropic sedative) reduced symptoms of
hangover when compared with placebo. However, it
also diminished cognitive performance and had important side effects, such as sedation (58).
Implications for the Clinician: Interventions
in Patients with Hangover
Despite the hazards of hangover, the question
remains whether treatment of hangover symptoms
improves physical health. Although the physiologic
and symptomatic impairments seem to be correlated, symptomatic therapy may not improve physiologic outcomes. If a successful treatment were
found, patients might experience less discomfort
with hangover but retain its visual–spatial, cognitive,
and cardiovascular detriments.
However, interviewing patients about their hangover experiences may have clinical relevance. First,
hangover is common and underdiagnosed and can
have serious physical, psychiatric, and occupational
consequences. Therefore, it is a potentially modifiable cause of morbidity and offers an opportunity
for substantial symptom relief (59). Particular attention should be paid to patients with cardiac risk
factors or coronary artery disease, who may be particularly at risk because of the physiologic stress
induced by veisalgia.
Standard alcohol screening, which focuses on detecting alcohol dependency, rarely addresses the frequency and severity of hangovers. Screening for
hangover severity and frequency may be used to
augment current strategies for early detection of
alcohol dependency (3). For example, sons of alcoholic parents, who are at greater risk for alcoholism,
have more frequent hangovers (60). The Short
Michigan Alcoholism Screening Test has adopted
this consideration, noting “hangover severity” as
one of the predictive criteria for alcoholism. Newlin
and Pretorious (60) have noted that patients with
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frequent hangovers seem to be at risk for further
alcohol dependence. Finally, depression and other
psychological disorders are more common in patients
with hangover (61).
For the patient with occasional hangovers, recommended interventions include the discussion of
potential therapies for alcohol hangover (adequate
hydration) and a reminder that 1.5 g/kg of alcohol
(approximately 5 to 6 drinks for an 80-kg man and
3 to 5 drinks for a 60-kg woman) will almost always
lead to hangover. Patients should also be educated
about the physiologic effects of hangover. Most patients understand the impairment inherent in acute
alcohol intoxication, but few appreciate the cognitive and visual–spatial impairment that may accompany alcohol hangover (7, 12). Patients who work
with heavy equipment or are involved in transportation should be warned of the potential hazards.
Hangover’s historical past may predict its future.
Homer provided one of the first descriptions of the
disorder. A companion of Odysseus, Elpenor, awoke
from a drunken sleep, sprang up, and jumped off a
roof, falling to his death (62, 63). Of interest, Elpenor “returned from the dead, begging Odysseus to
bury his body,” a sentiment we have often heard
echoed by patients with hangover. The most extreme form of hangover, a psychiatric dissociation
characterized by irrational behavior, has since become known as the Elpenor syndrome.
As a condition warranting physician recognition
and treatment, veisalgia, with its cardiac, neurologic,
and psychiatric effects, is far more than a mere
nuisance. Perhaps the spirit of Elpenor will inspire
physicians to prevent and treat hangover, thereby
preventing patients from falling to their deaths.
From Veterans Affairs Medical Center and the University of
California, San Francisco, San Francisco, California.
Requests for Single Reprints: Jeffrey Wiese, MD, General Internal
Medicine Section (111), Veterans Affairs Medical Center, 4150
Clement Street, San Francisco, CA 94121.
Requests To Purchase Bulk Reprints (minimum, 100 copies): Barbara Hudson, Reprints Coordinator; phone, 215-351-2657;
e-mail, [email protected].
Current Author Addresses: Drs. Weise, Shlipak, and Browner:
General Internal Medicine Section (111), Veterans Affairs Medical Center, 4150 Clement Street, San Francisco, CA 94121.
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