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Alcohol hangover: Mechanisms and mediators


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Hangovers are a frequent, though unpleasant, experience among people who drink to intoxication. Despite the prevalence of hangovers, however, this condition is not well understood scientifically. Multiple possible contributors to the hangover state have been investigated, and researchers have produced evidence that alcohol can directly promote hangover symptoms through its effects on urine production, the gastrointestinal tract, blood sugar concentrations, sleep patterns, and biological rhythms. In addition, researchers postulate that effects related to alcohol's absence after a drinking bout (i.e., withdrawal), alcohol metabolism, and other factors (e.g., biologically active, nonalcohol compounds in beverages; the use of other drugs; certain personality traits; and a family history of alcoholism) also may contribute to the hangover condition. Few of the treatments commonly described for hangover have undergone scientific evaluation.
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54 Alcohol Health & Research World
Alcohol Hangover
Mechanisms and Mediators
Robert Swift, M.D., Ph.D.; and Dena Davidson, Ph.D.
Hangovers are a frequent, though unpleasant, experience among people who drink to
intoxication. Despite the prevalence of hangovers, however, this condition is not well
understood scientifically. Multiple possible contributors to the hangover state have been
investigated, and researchers have produced evidence that alcohol can directly promote
hangover symptoms through its effects on urine production, the gastrointestinal tract, blood
sugar concentrations, sleep patterns, and biological rhythms. In addition, researchers
postulate that effects related to alcohols absence after a drinking bout (i.e., withdrawal),
alcohol metabolism, and other factors (e.g., biologically active, nonalcohol compounds in
beverages; the use of other drugs; certain personality traits; and a family history of
alcoholism) also may contribute to the hangover condition. Few of the treatments commonly
described for hangover have undergone scientific evaluation. KEY WORDS: post AOD
intoxication state; symptom; urinalysis; gastrointestinal disorder; hypoglycemia; sleep
disorder; circadian rhythm; ethanol metabolite; disorder of fluid or electrolyte or acid-base
balance; nutrient intake; headache; vomiting; neurotransmitter receptors; congenors;
multiple drug use; personality trait; family AODU (alcohol and other drug use) history;
drug therapy; literature review
My first return of sense or recol-
lection was upon waking in a
strange, dismal-looking room, my
head aching horridly, pains of a
violent nature in every limb, and
deadly sickness at the stomach.
From the latter I was in some
degree relieved by a very copious
vomiting. Getting out of bed, I
looked out of the only window in
the room, but saw nothing but
the backs of old houses, from
which various miserable emblems
of poverty were displayed . . . . At
that moment I do not believe in
the world there existed a more
wretched creature than myself.
I passed some moments in a
state little short of despair . . . .
William Hickey (Spenser 1913)
he British writer William Hickey
wrote these words in the year
1768, vividly describing the
aftermath of a bout of heavy alcohol
drinkingan experience commonly
referred to as a hangover. Similar
descriptions of hangovers appear in the
writings of ancient Egypt and Greece
as well as in the Old Testament. No
doubt, prehistoric people also experi-
enced hangovers soon after they
discovered alcohol.
Despite its long history, however,
hangover has received relatively scant
formal attention from researchers.
Little is known about the physiology
underlying the hangover condition. For
example, it is unclear whether hangover
signs and symptoms are attributable
to alcohols direct effects on the body,
its aftereffects, or a combination of
both. Similarly, investigators are uncer-
tain about the degree to which hangover
affects a persons thinking and mentally
controlled motor functions, a question
with serious implications for activities
ROBERT SWIFT, M.D., PH.D., is associate
professor in the Department of Psychiatry
and Human Behavior at Brown Univer-
sity, Providence, Rhode Island, and
associate chief of staff for research and
education at Providence Veterans
Affairs Medical Center.
ENA DAVIDSON, PH.D., is assistant
professor of psychiatry at Indiana
University of Medicine, Indianapolis,
such as job performance and driving.
In addition, researchers know little
about hangover prevention and treat-
ment. Although folk remedies for
hangovers abound, their efficacy in
reducing the intensity and duration
of a hangover has not received system-
atic study. In fact, some researchers
and clinicians question whether finding
an effective treatment for hangovers
is desirable, given that the hangover
experience may deter some people
from engaging in subsequent episodes
of heavy drinking.
Although gaps clearly remain in
scientific knowledge about hangovers,
research has elucidated several aspects.
This article describes what is known
about the hangover condition, the
possible physiological factors contribut-
ing to it, and treatment options.
What Is a Hangover?
A hangover is characterized by the
constellation of unpleasant physical
and mental symptoms that occur after
a bout of heavy alcohol drinking (see
table 1). Physical symptoms of a
hangover include fatigue, headache,
increased sensitivity to light and
sound, redness of the eyes, muscle
aches, and thirst. Signs of increased
sympathetic nervous system activity
can accompany a hangover, including
increased systolic blood pressure,
rapid heartbeat (i.e., tachycardia),
tremor, and sweating. Mental symp-
toms include dizziness; a sense of the
room spinning (i.e., vertigo); and
possible cognitive and mood distur-
bances, especially depression, anxiety,
and irritability. The particular set of
symptoms experienced and their inten-
sity may vary from person to person
and from occasion to occasion. In
addition, hangover characteristics may
depend on the type of alcoholic beverage
consumed and the amount a person
drinks. Typically, a hangover begins
within several hours after the cessation
of drinking, when a persons blood
alcohol concentration (BAC) is falling.
Symptoms usually peak about the
time BAC is zero and may continue
for up to 24 hours thereafter.
Overlap exists between hangover and
the symptoms of mild alcohol with-
drawal (AW), leading to the assertion
that hangover is a manifestation of
mild withdrawal. Hangovers, how-
ever, may occur after a single bout of
drinking, whereas withdrawal occurs
usually after multiple, repeated bouts.
Other differences between hangover
and AW include a shorter period of
impairment (i.e., hours for hangover
versus several days for withdrawal)
and a lack of hallucinations and seizures
in hangover.
People experiencing a hangover feel
ill and impaired. Although a hangover
may impair task performance and
thereby increase the risk of injury,
equivocal data exist on whether hang-
over actually impairs complex mental
tasks. When subjects with a BAC of
zero were tested following alcohol
intoxication with peak BACs in the
range of 50 to 100 milligrams per
deciliter (mg/dL), most of them did
not show significant impairments in
the performance of simple mental
tasks, such as reaction time (Lemon et
al. 1993). Similarly, several studies
that investigated the hangover effects
on a more complex mental task (i.e.,
simulated automobile driving) did not
report impaired performance (Streufert
et al. 1995; Tornros and Laurell 1991).
In contrast, a study of military pilots
completing a simulated flying task
revealed significant decrements in
some performance measures (particu-
larly among older pilots) 8 to 14 hours
after they had consumed enough alco-
hol to be considered legally drunk
(Yesavage and Leirer 1986).
Prevalence of Hangover
Generally, the greater the amount
and duration of alcohol consumption,
the more prevalent is the hangover,
although some people report experi-
encing a hangover after drinking low
levels of alcohol (i.e., one to three
alcoholic drinks), and some heavy
drinkers do not report experiencing
hangovers at all. A survey by Harburg
and colleagues (1993) on the preva-
lence of hangovers found that approx-
imately 75 percent of the subjects
who drank to intoxication reported
experiencing a hangover at least some
of the time. In a study of 2,160 Finnish
men, researchers found an association
between increased weekly alcohol
consumption and the frequency of
hangover: 43.8 percent of the group
of heaviest drinkers (i.e., study subjects
who drank more than 106 grams [g]
of alcohol per week or approximately
9 drinks) reported experiencing a hang-
over monthly or more often, compared
with 6.6 percent of the remaining
study subjects (Kauhanen et al. 1997).
Similarly, in a study of 1,041 drinkers
in New York State, 50 percent of the
subjects who drank two or more drinks
per day reported experiencing hang-
overs in the previous year, whereas
subjects who consumed lower levels
Vol. 22, No. 1, 1998 55
Table 1 Symptoms of Hangover
Class of Symptoms Type
Constitutional Fatigue, weakness, and thirst
Pain Headache and muscle aches
Gastrointestinal Nausea, vomiting, and stomach pain
Sleep and biological rhythms Decreased sleep, decreased REM,
and increased slow-wave sleep
Sensory Vertigo and sensitivity to light and sound
Cognitive Decreased attention and
Mood Depression, anxiety, and irritability
Sympathetic hyperactivity Tremor, sweating, and increased pulse
and systolic blood pressure
REM = rapid eye movements.
Alcohol Hangover
of alcohol reported fewer hangovers
(Smith and Barnes 1983). Other reports,
however, claim that hangovers occur
less often in heavy drinkers. In a study
of 43 alcoholic drinkers admitted for
inpatient treatment, 50 percent of the
subjects reported experiencing no hang-
overs within the previous year and 23
percent reported never experiencing a
hangover (Pristach et al. 1983).
Physiological Factors
Contributing to Hangover
Hangover symptoms have been
attributed to several causes (see table
2), including the direct physiological
effects of alcohol on the brain and
other organs; the effects of the removal
of alcohol from these organs after alco-
hol exposure (i.e., withdrawal); the
physiological effects of compounds
produced as a result of alcohols
metabolism (i.e., metabolites), espe-
cially acetaldehyde; and nonalcohol
factors, such as the toxic effects of
other biologically active chemicals (i.e.,
congeners) in the beverage, behaviors
associated with the alcohol-drinking
bout (e.g., other drug use, restricted
food intake, and disruption of normal
sleep time), and certain personal char-
acteristics (e.g., temperament, person-
ality, and family history of alcoholism).
Although current evidence suggests that
more than one factor most likely con-
tributes to the overall hangover state,
the following sections address each of
the postulated causes in turn.
Direct Alcohol Effects
Alcohol may directly contribute to a
hangover in several ways, including
the following.
Dehydration and Electrolyte Imbal-
Alcohol causes the body to increase
urinary output (i.e., it is a diuretic).
The consumption of 50 g of alcohol in
250 milliliters (mL) of water (i.e. approx-
imately 4 drinks) causes the elimination
of 600 to 1,000 mL (or up to 1 quart)
of water over several hours (Montastruc
1986). Alcohol promotes urine pro-
duction by inhibiting the release of a
hormone (i.e., antidiuretic hormone,
or vasopressin) from the pituitary gland.
In turn, reduced levels of antidiuretic
hormone prevent the kidneys from
reabsorbing (i.e., conserving) water
and thereby increase urine production.
Additional mechanisms must be at
work to increase urine production,
however, because antidiuretic hormone
levels increase as BAC levels decline to
zero during hangover (Eisenhofer et al.
1985). Sweating, vomiting, and diarrhea
also commonly occur during a hang-
over, and these conditions can result in
additional fluid loss and electrolyte
imbalances. Symptoms of mild to mod-
erate dehydration include thirst, weak-
ness, dryness of mucous membranes,
dizziness, and lightheadedness all
commonly observed during a hangover.
Gastrointestinal Disturbances. Alcohol
directly irritates the stomach and
intestines, causing inflammation of
the stomach lining (i.e., gastritis) and
delayed stomach emptying, especially
when beverages with a high alcohol
concentration (i.e., greater than 15
percent) are consumed (Lieber 1995).
High levels of alcohol consumption
also can produce fatty liver, an accu-
mulation of fat compounds called
triglycerides and their components
(i.e., free fatty acids) in liver cells. In
addition, alcohol increases the produc-
tion of gastric acid as well as pancreatic
and intestinal secretions. Any or all of
these factors can result in the upper
abdominal pain, nausea, and vomiting
experienced during a hangover.
Low Blood Sugar. Several alterations
in the metabolic state of the liver and
other organs occur in response to the
presence of alcohol in the body and
can result in low blood sugar levels
(i.e., low glucose levels, or hypoglycemia)
(National Institute on Alcohol Abuse
and Alcoholism 1994). Alcohol metab-
olism leads to fatty liver (described
earlier) and a buildup of an intermediate
metabolic product, lactic acid, in body
fluids (i.e., lactic acidosis). Both of these
effects can inhibit glucose production.
Alcohol-induced hypoglycemia
generally occurs after binge drinking
over several days in alcoholics who have
not been eating. In such a situation,
prolonged alcohol consumption, cou-
pled with poor nutritional intake, not
only decreases glucose production but
also exhausts the reserves of glucose
stored in the liver in the form of glyco-
gen, thereby leading to hypoglycemia.
Because glucose is the primary energy
source of the brain, hypoglycemia can
contribute to hangover symptoms
such as fatigue, weakness, and mood
disturbances. Diabetics are particularly
sensitive to the alcohol-induced alter-
ations in blood glucose. However, it
has not been documented whether
low blood sugar concentrations con-
tribute to hangover symptomatically.
56 Alcohol Health & Research World
Table 2 Possible Contributing Factors to Hangover
Direct effects of alcohol
Electrolyte imbalance
Gastrointestinal disturbances
Low blood sugar
Sleep and biological rhythm disturbances
Alcohol withdrawal
Alcohol metabolism (i.e., acetaldehyde toxicity)
Nonalcohol effects
Compounds other than alcohol in beverages, especially methanol
Use of other drugs, especially nicotine
Personality type
Family history for alcoholism
Disruption of Sleep and Other
Biological Rhythms.
Although alcohol
has sedative effects that can promote
sleep onset, the fatigue experienced
during a hangover results from alcohols
disruptive effects on sleep. Alcohol-
induced sleep may be of shorter duration
and poorer quality because of rebound
excitation (see the section Effects of
Alcohol Withdrawal) after BACs fall,
leading to insomnia (Walsh et al. 1991).
Furthermore, when drinking behavior
takes place in the evening or at night
(as it often does), it can compete with
sleep time, thereby reducing the length
of time a person sleeps. Alcohol also
disrupts the normal sleep pattern,
decreasing the time spent in the dream-
ing state (i.e., rapid eye movement [REM]
sleep) and increasing the time spent
in deep (i.e., slow-wave) sleep. In
addition, alcohol relaxes the throat
muscles, resulting in increased snoring
and, possibly, periodic cessation of
breathing (i.e., sleep apnea).
Alcohol interferes with other biolog-
ical rhythms as well, and these effects
persist into the hangover period. For
example, alcohol disrupts the normal
24-hour (i.e., circadian) rhythm in body
temperature, inducing a body temper-
ature that is abnormally low during
intoxication and abnormally high during
a hangover. Alcohol intoxication also
interferes with the circadian nighttime
secretion of growth hormone, which
is important in bone growth and
protein synthesis. In contrast, alcohol
induces the release of adrenocortico-
tropic hormone from the pituitary
gland, which in turn stimulates the
release of cortisol, a hormone that plays
a role in carbohydrate metabolism and
stress response; alcohol thereby disrupts
the normal circadian rise and fall of
cortisol levels. Overall, alcohols disrup-
tion of circadian rhythms induces a
jet lag that is hypothesized to account
for some of the deleterious effects of a
hangover (Gauvin et al. 1997).
Alcohol and Headache
In a large epidemiological survey of
headache in Danish 25- to 64-year-olds,
the lifetime prevalence of hangover
headache was 72 percent, making it
the most common type of headache
reported (Rasmussen and Olesen 1992).
Alcohol intoxication results in vasodi-
latation, which may induce headaches.
Alcohol has effects on several neuro-
transmitters and hormones that are
implicated in the pathogenesis of head-
aches, including histamine, serotonin,
and prostaglandins (Parantainen 1983).
However, the etiology of hangover
headache remains unknown.
Effects of Alcohol Withdrawal
The AW syndrome following the
cessation of excessive drinking results
from compensatory changes in the
central nervous system that take place
in response to chronically administered
depressant substances (in this case,
alcohol, or more specifically, ethanol).
These changes include alterations in
two types of receptors embedded in
nerve cell membranes. One receptor
type binds with an important chemi-
cal messenger (i.e., neurotransmitter)
called gamma-aminobutyric acid
(GABA), and the other type binds
with another neurotransmitter, gluta-
mate. Both GABA and glutamate are
critical in regulating nerve cell activity:
GABA is the bodys primary means
of inhibiting nerve cell activity, and
glutamate is the primary means of
exciting it.
Following chronic alcohol exposure,
the body decreases (i.e., downregulates)
the number or sensitivity of GABA
receptors and increases (i.e., upregulates)
the number or sensitivity of glutamate
receptors in an effort to counterbalance
alcohols sedative effects. When alcohol
is removed from the body, however, the
central nervous system and the portion
of the nervous system that coordinates
response to stress (i.e., the sympathetic
nervous system) remain in an unbal-
anced overdrive state (Tsai et al. 1995).
Sympathetic nervous system hyperac-
tivity accounts for the tremors, sweating,
and tachycardia observed in both hang-
over and AW syndrome.
Several lines of evidence suggest that
a hangover is a mild manifestation of
the AW syndrome in non-alcohol-
dependent drinkers. First, the signs
and symptoms of hangover and mild
AW overlap considerably. The revised
Clinical Institute Withdrawal Assess-
ment for Alcohol (CIWA-Ar) scale, an
instrument widely used to assess the
severity of a withdrawal episode in
alcohol-dependent patients, measures
10 withdrawal-associated items: nausea
and vomiting; tremor; sweating; anxi-
ety; agitation; headache; disturbances
in the sense of touch, hearing, and
vision (e.g., hallucinations); and orien-
tation (e.g., awareness of the date and
location) (Sullivan et al. 1989, see also
p. 8 of the article by Saitz for a sample
of the assessment form). Several of
these items also are usually present
during a hangover, including nausea
and vomiting, tremor, sweating, anxiety,
headache, and sensory disturbances.
Second, Begleiter and colleagues
(1974) present evidence that the
hangover condition is actually a state
of central nervous system excitation,
despite the perceived sedation and
malaise. Support for this view comes
from the research of Pinel and Mucha
(1980), which shows that single doses
of alcohol decrease seizure thresholds
in animals several hours later. Their
finding indicates rebound excitation,
a phenomenon noted to occur after
short-term administration of some
sedatives that can quickly clear the
body, including alcohol and certain
benzodiazepine drugs.
Third, the observation that alcohol
readministration alleviates the unpleas-
antness of both AW syndrome and
hangovers suggests that the two expe-
riences share a common process.
Effects of Alcohol Metabolites
Alcohol undergoes a two-step process
in its metabolism (see figure). First, an
enzyme (i.e., alcohol dehydrogenase)
metabolizes alcohol to an intermediate
product, acetaldehyde; then a second
enzyme (aldehyde dehydrogenase
[ALDH]) metabolizes acetaldehyde to
acetate. Acetaldehyde is a chemically
reactive substance that binds to pro-
teins and other biologically important
compounds. At higher concentrations,
it causes toxic effects, such as a rapid
pulse, sweating, skin flushing, nausea,
and vomiting. In most people, ALDH
Vol. 22, No. 1, 1998 57
Alcohol Hangover
metabolizes acetaldehyde quickly and
efficiently, so that this intermediate
metabolite does not accumulate in high
concentrations, although small amounts
are present in the blood during alcohol
intoxication. In some people, however,
genetic variants of the ALDH enzyme
permit acetaldehyde to accumulate.
Those people routinely flush, sweat,
and become ill after consuming small
amounts of alcohol.
Because of the similarity between
the acetaldehyde reaction and a hang-
over, some investigators have suggested
that acetaldehyde causes hangovers.
Although free acetaldehyde is not pre-
sent in the blood after BACs reach
zero, the toxic effects of acetaldehyde
produced during alcohol metabolism
may persist into the hangover period.
Effects of Factors Other
Than Alcohol
Factors other than alcohol also may
contribute to a hangover. These factors
include the following possibilities.
Congeners. Among other reasons,
people consume alcoholic beverages
for their ethanol content. Most alcoholic
beverages contain smaller amounts of
other biologically active compounds,
however, including other alcohols.
These compounds, known as congeners,
contribute to the taste, smell, and
appearance of alcoholic beverages.
Congeners may be produced along
with ethanol during fermentation,
generated during aging or processing
through the degradation of the bever-
ages organic components, or added
to the beverage during the production
process. Investigators now believe
that congeners may contribute to a
beverages intoxicating effects and to
a subsequent hangover. Research
has shown that beverages composed
of more pure ethanol, such as gin
or vodka, induce fewer hangover
effects than do beverages containing
a large number of congeners, such
as whiskey, brandy, or red wine
(Chapman 1970; Pawan 1973). A
hangover also may occur when pure
ethanol is administered, however.
One specific congener implicated
in hangover effects is methanol, which
is an alcohol compound found in
alcoholic beverages along with ethanol.
The two compounds differ slightly in
chemical structure in that methanol
contains one less carbon atom and two
fewer hydrogen atoms than ethanol.
The same enzymes that metabolize
ethanol, alcohol dehydrogenase, and
aldehyde dehydrogenase also metabo-
lize methanol; however, the products
of methanol metabolism (i.e., formalde-
hyde and formic acid) are extremely
toxic and in high concentrations may
cause blindness and death.
Support for methanols contribution
to hangovers comes from several sources.
For example, distilled spirits that are
more frequently associated with the
development of a hangover, such as
brandies and whiskeys, contain the
highest concentrations of methanol.
Moreover, in an experimental study
with four subjects who consumed red
wine containing 100 milligrams per
liter (mg/L) of methanol, Jones (1987)
found that elevated blood levels of
methanol persisted for several hours
after ethanol was metabolized, which
corresponded to the time course of
hangover symptoms. Methanol lingers
after ethanol levels drop, because ethanol
competitively inhibits methanol metab-
olism. The fact that ethanol readmin-
istration fends off hangover effects
may be further evidence of methanols
contribution to the hangover condition,
given ethanols ability to block methanol
metabolism and thereby slow the pro-
duction of formaldehyde and formic acid.
Certain people develop headaches
soon after drinking red wine but not
after drinking white wine or vodka.
Recent research finds that red wine, but
not white wine or vodka, can increase
plasma serotonin and plasma histamine
levels. The specific agents in wine
responsible for these increased levels
are not known. Increased plasma sero-
tonin and histamine can trigger head-
aches in susceptible people (Pattichis
et al. 1995; Jarisch and Wantke 1996).
Use of Other Drugs. The use of other
drugs often accompanies heavy alcohol
consumption. Most heavy drinkers
smoke cigarettes, and some also use
marijuana, cocaine, or other drugs.
Although certain drugs can themselves
produce hangover symptoms and affect
alcohol intoxication, the effects of the
various alcohol and other drug combina-
tions on alcohol hangover are unknown.
Personal Influences. Some evidence
exists that increased hangover symptoms
occur more often in people possessing
certain personality traits, such as neu-
roticism, anger, and defensiveness.
Negative life events and feelings of guilt
about drinking also are associated with
experiencing more hangovers (Harburg
et al. 1993). In addition, Earleywine
a,b) reports greater hangover
symptoms in people who have a higher
personality risk for the development of
alcoholism (as measured by the Mac-
58 Alcohol Health & Research World
Ethanol Acetaldehyde Acetate
The metabolism of beverage alcohol (i.e., ethanol) by the alcohol dehydrogenase
(ADH) pathway.
NOTE: ADH = alcohol dehydrogenase; ALDH = aldehyde dehydrogenase; NAD = nicotinamide adenine
dinucleotide; NADH = reduced NAD.
Andrew Scale [MacAndrew 1965]).
Those studies suggest that people who
have an elevated personality risk for
alcoholism experience more acute
withdrawal and hangover symptoms
and may initiate further drinking in an
effort to find relief.
Research has shown that a history
of alcoholism in a persons family (i.e.,
a positive family history) is associated
with a decreased sensitivity to the intox-
icating effects of alcohol and a greater
risk for developing alcoholism (Schuckit
and Smith 1996). Newlin and Pretorius
(1990) suggested that a positive family
history for alcoholism may be associated
with a tendency for increased hangover
symptoms as well. Their research
compared the self-reported hangover
symptoms in college-age sons of alco-
holic fathers with symptoms in sons
of nonalcoholic fathers and found
that the subjects with a positive fam-
ily history for alcoholism had had
greater hangover symptoms during the
previous year. The amount of drink-
ing was comparable between the two
groups, although the subjects with a
positive family history reported con-
suming significantly more mixed
drinks than the group with a negative
family history.
Treatments for Hangover
Many treatments are described to pre-
vent hangover, shorten its duration,
and reduce the severity of its symptoms,
including innumerable folk remedies
and recommendations. Few treatments
have undergone rigorous investigation,
however. Conservative management
offers the best course of treatment.
Time is the most important compo-
nent, because hangover symptoms
will usually abate over 8 to 24 hours.
Attentiveness to the quantity and
quality of alcohol consumed can have
a significant effect on preventing hang-
over. Hangover symptoms are less
likely to occur if a person drinks only
small, nonintoxicating amounts. Even
among people who drink to intoxication,
those who consume lower amounts of
alcohol appear less likely to develop a
hangover than those who drink higher
amounts. Hangovers have not been
associated with drinking beverages with
a low alcohol content or with drinking
nonalcoholic beverages.
The type of alcohol consumed also
may have a significant effect on reduc-
ing hangover (Chapman 1970; Pawan
1973). Alcoholic beverages that contain
few congeners (e.g., pure ethanol, vodka,
and gin) are associated with a lower
incidence of hangover than are beverages
that contain a number of congeners
(e.g., brandy, whiskey, and red wine).
Other interventions may reduce the
intensity of a hangover but have not
been systematically studied. Consump-
tion of fruits, fruit juices, or other
fructose-containing foods is reported
to decrease hangover intensity, for
example (Seppala et al. 1976). Also,
bland foods containing complex car-
bohydrates, such as toast or crackers,
can counter low blood sugar levels in
people subject to hypoglycemia and
can possibly relieve nausea. In addition,
adequate sleep may ease the fatigue
associated with sleep deprivation, and
drinking nonalcoholic beverages during
and after alcohol consumption may
reduce alcohol-induced dehydration.
Certain medications may provide
symptomatic relief for hangover symp-
toms. For example, antacids may alleviate
nausea and gastritis. Aspirin and other
nonsteroidal anti-inflammatory medi-
cations (e.g., ibuprofen or naproxen)
may reduce the headache and muscle
aches associated with a hangover but
should be used cautiously, particularly
if upper abdominal pain or nausea is
present. Anti-inflammatory medications
are themselves gastric irritants and
will compound alcohol-induced gas-
tritis. Although acetaminophen is a
common alternative to aspirin, its use
should be avoided during the hangover
period, because alcohol metabolism
enhances acetaminophens toxicity to
the liver (Girre et al. 1993).
Propranolol, a beta-adrenergic
used to treat high blood
pressure and migraine headaches, re-
duces the sympathetic hyperactivity
of AW; however, a small, double-blind,
placebo-controlled study did not find
propranolol to be effective in reducing
hangover symptoms, including headache
(Bogin et al. 1987). Antagonists at the
serotonin-3 receptor,
such as ondan-
setron and tropisetron, are antiemetics
(i.e., they control nausea and vomiting)
and block certain alcohol effects; how-
ever, a small clinical trial did not show
efficacy in alleviating hangover (Muh-
onen et al. 1997). Caffeine (often taken
as coffee) is commonly used to counter-
act the fatigue and malaise associated
with the hangover condition. Although
this traditional practice lacks scientific
support, William Hickey, quoted at the
beginning of this article, wrote that
very strong coffee proved of infinite
benefit (Spenser 1913).
Readministration of alcoholthe
hair of the dog that bit you remedy
reportedly cures a hangover, but people
experiencing a hangover should avoid
further alcohol use. Additional drink-
ing will only enhance the existing
toxicity of the alcohol consumed during
the previous bout and may increase the
likelihood of even further drinking.
Areas for Future Study
Several topics related to hangovers
warrant research attention. The effect
of congeners, especially methanol, on
the occurrence of hangover needs closer
examination, for example. Such research
could help determine whether it is
ethanol or congeners that produce the
major signs and symptoms of hangover,
and an answer to this key question
would advance our understanding of
hangover pathophysiology.
A particularly intriguing observation
is that people with traits associated with
an increased risk for alcoholism (e.g.,
certain personality factors or a positive
family history for alcoholism) experience
more severe hangovers. Although logic
dictates that enduring more severe or
Vol. 22, No. 1, 1998 59
Alcohol Hangover
An antagonist is an agent that interferes with or
blocks the action of another agent, disease, or
structure. A beta-adrenergic antagonist blocks the
action of certain neurotransmitters governing the
sympathetic nervous system.
Serotonin antagonists block the actions of
serotonin, a neurotransmitter that can affect
mood as well as inhibit gastric secretion and
stimulate smooth muscle, such as that governing
the contractions of the digestive system.
more frequent hangovers would deter,
rather than promote, further alcohol
drinking, mild AW symptoms are also
associated with an increased craving
for alcohol (Littleton and Little 1994).
Future investigations could focus on
whether people can be biologically
predisposed to experience more severe
AW and whether such a tendency in
turn predisposes them to increased
alcohol consumption.
Animal models of hangover have
been developed and may provide in-
sights into the physiological and behav-
ioral changes that occur in the period
immediately after intoxication (Gauvin
et al. 1993, 1997). These animal models
could be used to explore the effects of
early withdrawal and of congeners and to
determine whether hangovers predispose
to or deter further alcohol consumption.
In summary, hangover is a complex
state that probably cannot be under-
stood by a unitary explanation. Under-
standing the hangover condition, how-
ever, will lead to a better comprehension
of the physiological effects of alcohol
and the adaptive responses that alco-
hol engenders.
C. Excitability cycle of somatosensory evoked
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60 Alcohol Health & Research World
... concentration, cognitive deficit) symptoms [5,10]. ...
... The most common symptoms of HS were: Fatigue (67%), thirst (57%), and headache (32%) [6]. The symptoms of a HS appear 6-8 hours after the end of alcoholic excess and can be observed for 20 hours against the background of the absence of alcohol in the blood [10]. The existing gender and age specificity of HS is in the greater severity of symptoms in women [5], as well as its progression with increasing age [3]. ...
... It is known that low sensitivity to the acute effects of alcohol is a predictor of the development of alcohol dependence [25]. It was also found that resistance to HS is associated with the so-called festival style of alcohol consumption (drinking large doses of alcohol for a short period of time) [10]. The constellation of these factors suggests that persons resistant to the development of HS have a higher risk of developing alcohol dependence. ...
... Other factors including dehydration, immune dysregulation, hypoglycaemia, the presence of additional biologically active compounds in alcoholic drinks (i.e. congeners) and an individual's genetic factors are all thought to play a role in the manifestation of hangover symptomatology [3][4][5][6]. ...
Full-text available
Aims To compare quantitatively the efficacy and tolerability of pharmacologically active interventions in the treatment and prevention of alcohol-induced hangover. Methods Systematic review of placebo-controlled randomised trials in healthy adults that evaluated any pharmacologically active intervention in the treatment or prevention of hangover. We searched Medline, Embase, PsycINFO and CENTRAL from database inception until 1st August 2021. The primary efficacy outcome was any continuous measure of overall hangover symptoms and the primary tolerability outcome the number of people dropping out due to adverse events (AEs). Quality was assessed using the Grading of Recommendations Assessment Development and Evaluation (GRADE) framework. Results 21 studies were included reporting on 386 participants. No two studies reported on the same intervention; as such, meta-analysis could not be undertaken. Methodological concerns and imprecision resulted in all studied efficacy outcomes being rated as very low quality. When compared with placebo, individual studies reported a statistically significant reduction in the mean percentage overall hangover symptom score for clove extract (42.5% vs. 19.0%, p<0.001), tolfenamic acid (84.0% vs. 50.0%, p<0.001), pyritinol (34.1% vs. 16.2%, p<0.01), Hovenia dulcis fruit extract (p=0.029), L-cysteine (p=0.043), red ginseng (21.1% vs. 14.0%, p<0.05) and Korean pear juice (41.5% vs 33.3%, p<0.05). All studied tolerability outcomes were of low or very low quality with no studies reporting any drop-outs due to AEs. Conclusions Only very low quality evidence of efficacy is available to recommend any pharmacologically active intervention for the treatment or prevention of alcohol-induced hangover. Of the limited interventions studied, all had favourable tolerability profiles and very low quality evidence suggests clove extract, tolfenamic acid, and pyritinol may most warrant further study
... За останні роки помітно збільшилася частота токсичних уражень печінки, які в структурі її гострих та хронічних захворювань становлять від 0,7 до 20%. [1][2][3]. При цьому, частим буває явище медикаментозної інтоксикації, що розвивається внаслідок прийому великих доз препаратів. Зокрема, це стосується отруєння ацетилсаліциловою кислотою, яке ще відоме як саліцилізм і нерідко призводить до захворюваності і смертності [4][5][6][7]. ...
Full-text available
According to the results of the study, it has been established that chronic acetylsalicylic acid poisoning results in severe liver disorders presented by both venous and portal blood overloaded with a reflex throughput decrease of the arterial part of the bloodstream. Prolonged venous stasis and reflex vasoconstriction of arteries lead to ischemia of the liver tissue with the development and progression of dystrophic changes in hepatocytes. With an increase in the duration of observation, there is an expansion of cell zones with signs of granular dystrophy, which pass into fields with dystrophy of hepatic cells, damage of intercellular boundaries, homogenization of cytoplasm and degradation of nuclei of hepatocytes. It was manifested quantitatively by an increase in the cross-section of hepatocytes and their nuclei with an appropriate dynamics of nuclear-cytoplasmic relations.
... Alcohol gets eliminated through its metabolic degradation products via multiple enzymatic and non-enzymatic pathways and affects specific organs or systems such as the brain, gastrointestinal tract, liver and immune system ( Figure 1) resulting in characteristic symptoms like typical hangover, which may cause electrolyte imbalance, hypoglycemia, dehydration or gastrointestinal disturbances [8,9]. ...
Full-text available
The present study objective was to design and develop novel health-supplement formula from plant extracts and was to evaluate the formula for high episodic alcohol toxicities, and associated disorders against alcohol intoxicated and oxidative damaged Human Hepatoma HepG2 cell line. The CC50 of the supplement was determined based on MTT assay. To get the safe dose concentration, an acute toxicity study was performed on Wistar rats as per OECD guidelines 423. The phyto-constituents of the supplement e.g. curcuminoids, piperine, β-caryophyllene, punicalagin, ellagic acid and isoquecetins from respective plant extracts were also analyzed and confirmed via HPLC and GC-FID profiling, which recovered more than 70% HepG2 cells with >75% cell viability. Normalization of oxidative stressed cells were confirmed via biochemical parameter studies. The same was verified via ROS inhibiting properties of the formula to reinforce the claim. In this study, any abnormal clinical symptom was not observed in treated animals at 2000mg/kg BW, hence it was considered as a safe dose for oral consumption. The present studies conclude that this health supplement contains herbal ingredients has a preventing role against alcohol-induced adverse effects and associated disorders.
... Alcohol gets eliminated through its metabolic degradation products via multiple enzymatic and non-enzymatic pathways and affects specific organs or systems such as the brain, gastrointestinal tract, liver and immune system ( Figure 1) resulting in characteristic symptoms like typical hangover, which may cause electrolyte imbalance, hypoglycemia, dehydration or gastrointestinal disturbances [8,9]. ...
Full-text available
The phyto-constituents of the supplement e.g. curcuminoids, piperine, β-caryophyllene, punicalagin, ellagic acid and isoquecetins from respective plant extracts were also analyzed and confirmed via HPLC and GC-FID profiling, which recovered more than 70% HepG2 cells with >75% cell viability. Normalization of oxidative stressed cells were confirmed via biochemical parameter studies. The same was verified via ROS inhibiting properties of the formula to reinforce the claim. In this study, any abnormal clinical symptom was not observed in treated animals at 2000mg/kg BW, hence it was considered as a safe dose for oral consumption. The present studies conclude that this health supplement contains herbal ingredients has a preventing role against alcohol-induced adverse effects and associated disorders. Keywords: Alcoholism; Alcohol disorder; Alcohol toxicity; Antihangover; Nutraceuticals
... Absenteeism and loss of productivity due to illnesses after alcohol consumption can result in significant economic loss (Foster and Vaughan, 2005;Piasecki et al., 2005;Prat et al., 2008). The hangover phenomenon is not well understood scientifically, but some studies have reported that a hangover may be due to a combination of ethanol's main metabolic product, acetaldehyde; congeners, including methanol; and dehydration (Calder, 1997;Swift and Davidson, 1998;Wiese et al., 2000). Although many researchers have made an effort to develop functional nutraceuticals using traditional medicines to alleviate a hangover, there are no clinically effective products on the market (Pittler et al., 2005;Verster and Penning, 2013). ...
Full-text available
Water soluble propolis was prepared using β–cyclodextrin, and its effect on an ethanol-induced hangover was examined in Sprague–Dawley (SD) rats fed with ethanol. When SD rats were administrated with propolis 30 min after ethanol feeding, ethanol content in the rat serum decreased 2.1 times 1 h after ethanol feeding. Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) activity in rat liver increased 3.0 and 4.4 times, respectively, 1 h after ethanol feeding and administration of propolis 30 min after ethanol feeding. There were no differences in the expression of ADH and ALDH genes regardless of propolis administration. These results indicated that a decrease in ethanol content in the serum was not due to an increase in the expression of ADH or ALDH genes but rather, an increase in activities of ADH and ALDH.
... The next two articles discuss the "causes" of alcohol hangover, and articles review the current knowledge on the pathology of the alcohol hangover. Whereas previous reviews on the causes of the alcohol hangover relied heavily on research data from the 1970s by the Finnish group Ylikhari et al., [17][18][19], the articles in this book provide major advances in the understanding of the pathology of the alcohol hangover. Article six reviews the role of alcohol metabolism in the pathology of the alcohol hangover [20], and article seven presents new data on the inflammatory response to alcohol consumption and its contribution to the alcohol hangover [21]. ...
Full-text available
The alcohol hangover is defined as the combination of negative mental and physical symptoms, which can be experienced after a single episode of alcohol consumption, starting when blood alcohol concentration (BAC) approaches zero. Here, we present the book “The alcohol hangover: causes, consequences, and treatment”, written to celebrate the 10th anniversary of the Alcohol Hangover Research Group (AHRG), summarizing recent advances in the field of alcohol hangover research.
Alcohol hangover refers to the combination of negative mental and physical symptoms that can be experienced after an episode of alcohol consumption, typically emerging as blood alcohol concentration (BAC) approaches zero. Hangover has been associated with heavy drinking and may be relevant in the transition to alcohol use disorder (AUD). Our aim was to examine hangover prevalence and associated symptoms following intravenous alcohol self-administration (IV-ASA), and to identify possible predictors of hangover in non-dependent drinkers. Ninety-five non-dependent drinkers completed an IV-ASA session. Pharmacodynamic measures of alcohol consumption included peak and average breath alcohol concentrations. Subjective measures of alcohol response included the Drug Effects Questionnaire and Biphasic Effects of Alcohol Scale. The Alcohol Hangover Scale assessed hangover symptoms from the end of the session until the following morning. 78% of participants endorsed at least one hangover symptom following IV-ASA. There was no association between hangover scores and IV-ASA measures of alcohol consumption. Additional mediation and moderation analysis revealed that self-reported intoxication was a significant mediator of the relationship between recent drinking and hangover symptoms. Hangover symptoms may be an early marker of the relationship between subjective response to alcohol and heavy drinking for those with no prior history of AUD. In particular, the effects of hangover go beyond exposure to alcohol and an individual’s subjective response to this exposure is associated with their experience of hangover. Future studies should further characterize the determinants of hangover across different populations of drinkers to better understand the risk for AUD and inform prevention methods.
Objectives: Our aim was to determine whether alcohol hangover is associated with eating unhealthy foods (hot chips, soft drink) or healthy foods (fruit, vegetables). Design: Daily diary study across 13 days (micro-longitudinal design). Methods: We examined a sample of 605 young adults (71% women; ages 17-25; mean age 19.91 [SD 1.86] years) who completed daily diaries in the university community and reported drinking alcohol at least twice during the 13-day study period. Each day, participants reported on their hangover severity, their consumption of fruit, vegetables, hot chips (French fries), and soft drink, and their alcohol consumption from the previous day. Linear mixed models were used to examine within-person associations between hangover severity and food consumption, by gender. Exploratory models also controlled for previous day alcohol consumption to acknowledge potential variability in hangover susceptibility. Results: On days when participants reported higher severity of hangovers, they reported consuming more hot chips (β = .09, p = .001), more soft drink (β = .08, p = .001) and less fruit (β = -.06, p = .05). In our exploratory model controlling for previous day alcohol consumption, the predictive effect of hangover severity on hot chips remained (β = .08, p = .009) and significant interaction effects were observed between gender and previous day alcohol consumption on fruit (β = -.03, p = .003) and vegetable (β = -.03, p = .03) servings. Conclusions: Higher hangover severity may lead to greater intake of some unhealthy foods such as hot chips, an effect that may not be reduceable to those associated with alcohol consumption per se. Interventions that target excessive drinking primarily, but also emphasize the importance of a healthy diet, should be considered for this population.
Full-text available
Hangovers resulting from alcohol intoxication can lead to adverse effects ranging from generalized discomfort and work-related absenteeism to emergency department visits from patients seeking symptomatic care. The purpose of this study was to evaluate the efficacy of a low dose (600–1800 mg) of N-Acetylcysteine (NAC) vs placebo on mitigating hangover symptoms. This was a randomized, double-blinded, placebo controlled crossover study involving 49 volunteers who consumed beer to obtain a breath alcohol content (BrAC) of 0.1 g/210L. The participants met on two separate occasions at which time they were given either NAC or placebo capsules. Opposing treatments were administered during the second encounter. The morning after the participant’s intoxication and treatment, a Hangover Symptom Scale Questionnaire was administered to determine subjective changes in hangover symptoms. Data was analyzed by self-control, comparing the participant’s hangover symptom severity when using NAC compared to placebo. No significant difference was found in the general distribution of total hangover scores ( P = .45) (NAC = 10; Placebo = 13). There was also no significant difference found in the general distribution of specific hangover symptoms. However, a significant difference was found in the general distribution of total hangover difference scores based on gender ( P = .04) (Female − 3.5; Male 2), specifically for nausea ( P = .05) and weakness ( P = .03). Although no difference was found in the general hangover scale scores, the study was suggestive of gender specific susceptibility with female participants having improved hangover symptoms after NAC use.
Background: Between 1978 and 1988, 453 sons (age range, 18 to 29 years) of alcoholic and control subjects were evaluated for their level of reaction (LR) to alcohol. This article presents the results of the 8.2-year follow-up of 450 of these men. The three goals were (1) to attempt to replicate results of the follow-up of the first 223 subjects, (2) to evaluate the potential impact of the quantity and frequency of drinking at the time of the original study on the relationship between LR and alcoholic outcome (ALC), and, most importantly, (3) to test if the relationship between family history (FH) and ALC might be mediated by LR in a subset of the sample. Methods: Face-to-face structured follow-up interviews were carried out with the subjects and separately with an additional informant, and blood samples, as well as urine specimens, were obtained for determination of state markers of heavy drinking and drug toxicology screens. Results: First, the rate of development of DSM-ÍIÍ-R abuse and dependence on alcohol was 14.1% and 28.6%, respectively, for family history positive (FHP) subjects, compared with 6.6% and 10.8%, respectively, for family history negative (FHN) men. Second, neither consideration of the quantity nor the frequency of drinking at the time of the original study, nor their combination, effectively diminished the relationships between LR and ALC. Third, among men who drank and demonstrated the 15% highest and lowest scores on LR at about the age of 20 years (ie, 30% of the relevant population), the correlation between FH and ALC was greatly reduced when LR was considered, but the correlation between LR and ALC was not greatly diminished when the impact of FH was evaluated. Conclusions: In this sample of moderately functional white men, the development of alcoholism occurred in relationship to an FH of alcoholism, but alcohol abuse or dependence was unrelated to prior psychiatric disorders. For this group, LR at the age of 20 years was associated with future alcoholism in a manner that was independent of the drinking practices at the time of the original study. At least among those men with clearly high and low LR scores, these data are consistent with the conclusion that LR might be a mediator of the alcoholism risk.
Blood samples were obtained from 44 alcoholics during withdrawal and analysed for plasma vasopressin, osmolality and ethanol. Control samples were obtained from 23 normal subjects and 28 abstinent alcoholics. Urine samples were also collected and analysed for vasopressin, sodium, creatinine and osmolality. Alcoholics showing symptoms of withdrawal had elevated plasma and urine vasopressin concentrations compared to control subjects and withdrawing alcoholics without symptoms. No significant difference in plasma osmolality was evident. Raised plasma vasopressin concentrations during alcohol withdrawal may be due to dehydration, nausea or liver disease, or may be a direct consequence of alterations in central nervous system function associated with the alcohol withdrawal syndrome. Whether increased plasma vasopressin concentratons contribute to water retention and overhydration during alcohol withdrawal remains to be determined.
We investigated alcohol-induced hangovers among college men at high and low risk for alcoholism. Thirteen sons of alcoholics reported significantly (p < 0.001) greater hangover symptoms in the past year than 25 sons of nonalcoholics. The two groups reported comparable quantity-frequency of recent drinking. To the extent that hangover represents an acute withdrawal syndrome to alcohol, this raises the question of whether sons of alcoholics are “dependence-prone.”
Abstract Thirty healthy male volunteers drank ethyl alcohol (1.75 g/kg) from 6 p. m. to 9 p. m., which resulted in hangover the next morning, and 10 subjects served as controls. The twenty subjects, who drank alcohol, received glucose or fructose during the same evening (1.0 g/kg) or on the following morning (0.5 g/kg). In the hangover phase psychomotor performance was recorded by a choice reaction test, two coordination tests and an attention test. The intensity of the hangover was graded subjectively and objectively. Blood ethanol, acetaldehyde and glucose concentrations were analysed. The testing procedure was repeated at 8, 10 and 12 a. m. Ethanol, administered alone, increased significantly the number of mistakes on the choice reaction test in hangover phase, but this effect was abolished by the simultaneous administration of sugar. On the other hand, after the combined administration of ethanol and sugars the number of mistakes and mistake percentage on one coordination test were increased. The etiology on the impaired psychomotor skill during the hangover period is probably not directly related to the pathophysiology of the hangover, as there was no correlation between the impairment of the psychomotor performance and the intensity of the hangover of the subjects.
We have confirmed our earlier finding that most red wines are able to bring about 5-hydroxytryptamine (5-HT, serotonin) release from platelets in vitro. Platelets from individual subjects manifested varying degrees of releasing ability but responded to different wines with a similar rank ordering. There was a high correlation (r = 0.87) between the effect of red wine and that of reserpine in different individuals. Some types of red wine caused a consistently higher release of 5-HT than others in all subjects; one red wine in particular resulted in neglible release. When several brands of this ·low-releasing” red wine were further examined, they all showed a lower activity than all the brands of a ‘high-releasing’ red wine type. This variation in releasing power was not related to intensity of red colour. Partial purification of red wine was achieved by column chromatography and showed releasing activity to be associated with a low molecular weight orange fraction. Preliminary studies, using solid phase extraction methods, showed that the active components lie mainly in a subgroup of the flavonoid fraction. If any of the adverse effects of red wine, such as headache induction, derive from this 5-HT releasing ability, then it may be possible to prepare red wines free from the chemical substances responsible.
The effects of alcohol on the formation of prostaglandins (PGs) and the blockade of some actions of alcohol by PG-inhibitors suggest that PGs may be involved in the action of ethyl alcohol. Regulation of lipid peroxidation and synthesis and release of precursor fatty acids may affect the overall formation of PGs. The effect of alcohol may be qualitative for several reasons: (i) the possible preferred formation of 1-series of PGs would mean an important qualitative change in PG-impact in some tissues; (ii) inhibition of PG-metabolism in the lung might affect mostly the plasma levels of PGE; (iii) a selective blockade of certain PG-effects and a potentiation of some others gives rise to qualitative changes in the actions of PGs.PGs may be involved in several acute or short-term reactions caused by alcohol. Chlorpropamide-alcohol flush, alcohol intolerance and hangover are effectively alleviated by a prophylactic use of PG-inhibitors. Speculatively PGs might also be involved in migraine attacks provoked by alcohol and in antabuse in reaction. The roles of PGs in the regulation of vascular tone, water and electrolyte balance as well as in certain secretory and metabolic processes may be important in the generation of alcohol related reactions.
We assessed the lifetime prevalences of headache disorders in a cross-sectional epidemiologic survey of a representative 25- to 64-year-old general population. We classified the headaches on the basis of a clinical interview and a physical and neurologic examination using the operational diagnostic criteria of the International Headache Society. Lifetime prevalence of idiopathic stabbing headache was 2%, of external compression headache 4%, and of cold stimulus headache 15%. Benign cough headache, benign exertional headache, and headache associated with sexual activity each occurred in 1%. Lifetime prevalence of hangover headache was 72%, of fever headache 63%, and of headache associated with disorders of nose or sinuses 15%. Headaches associated with severe structural lesions were rare. External compression headache, fever headache, headache associated with metabolic disorders, and headache associated with disorders of nose or sinuses all showed significant female preponderance. The symptomatic headaches and headaches unassociated with structural lesions were more prevalent among migraineurs. In subjects with tension-type headache, only hangover headache was overrepresented. There was no association between the headache disorders and abnormal routine blood chemistry or arterial hypertension. In women with migraine, however, diastolic blood pressure was significantly higher than in women without migraine.
The sedative effect of 0.7 g/kg of 100% ethanol, ingested at 9:30 PM, was investigated to examine the combined effects of ethanol and circadian sleepiness/alertness levels. Fourteen healthy young adults participated in a placebo-controlled, double-blind crossover design. Each subject, on two separate occasions (placebo or ethanol), completed multiple sleep latency testing and the repeated test of sustained wakefulness as objective measures of physiological sleep tendency, and completed the Stanford Sleepiness Scale as a measure of subjective sleepiness. The results indicate that a moderate dose of ethanol significantly increases physiological sleepiness during early morning hours even in individuals that are relatively alert at these times. Therefore, the marked reduction in alertness and related performance deficits that normally occur at night are worsened by ethanol ingestion. Sleepiness, due to any cause, and ethanol may well be a dangerous combination.