Wouldn't it be good to know just what all that alcohol does to a brain?
-- Ed
Difficulty walking, blurred
vision, slurred speech, slowed reaction times, impaired memory: Clearly,
alcohol affects the brain. Some of these impairments are detectable after only
one or two drinks and quickly resolve when drinking stops. On the other hand, a
person who drinks heavily over a long period of time may have brain deficits
that persist well after he or she achieves sobriety. Exactly how alcohol
affects the brain and the likelihood of reversing the impact of heavy drinking
on the brain remain hot topics in alcohol research today.
We do know that heavy
drinking may have extensive and far–reaching effects on the brain, ranging from
simple “slips” in memory to permanent and debilitating conditions that require
lifetime custodial care. And even moderate drinking leads to short–term
impairment, as shown by extensive research on the impact of drinking on
driving.
A number of factors influence
how and to what extent alcohol affects the brain (1), including
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how much and how often a
person drinks;
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the age at which he or she
first began drinking, and how long he or she has been drinking;
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the person’s age, level of
education, gender, genetic background, and family history of alcoholism;
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whether he or she is at risk
as a result of prenatal alcohol exposure; and
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his or her general health
status.
This Alcohol Alert reviews
some common disorders associated with alcohol–related brain damage and the
people at greatest risk for impairment. It looks at traditional as well as
emerging therapies for the treatment and prevention of alcohol–related
disorders and includes a brief look at the high–tech tools that are helping
scientists to better understand the effects of alcohol on the brain.
BLACKOUTS AND MEMORY LAPSES
Alcohol can produce
detectable impairments in memory after only a few drinks and, as the amount of
alcohol increases, so does the degree of impairment. Large quantities of
alcohol, especially when consumed quickly and on an empty stomach, can produce
a blackout, or an interval of time for which the intoxicated person cannot
recall key details of events, or even entire events.
Blackouts are much more
common among social drinkers than previously assumed and should be viewed as a
potential consequence of acute intoxication regardless of age or whether the
drinker is clinically dependent on alcohol (2). White and colleagues (3)
surveyed 772 college undergraduates about their experiences with blackouts and
asked, “Have you ever awoken after a night of drinking not able to remember
things that you did or places that you went?” Of the students who had ever
consumed alcohol, 51 percent reported blacking out at some point in their
lives, and 40 percent reported experiencing a blackout in the year before the
survey. Of those who reported drinking in the 2 weeks before the survey, 9.4
percent said they blacked out during that time. The students reported learning
later that they had participated in a wide range of potentially dangerous
events they could not remember, including vandalism, unprotected sex, and
driving.
| Binge Drinking and Blackouts |
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• Drinkers who
experience blackouts typically drink too much and too quickly, which causes
their blood alcohol levels to rise very rapidly. College students may be at
particular risk for experiencing a blackout, as an alarming number of college
students engage in binge drinking. Binge drinking, for a typical adult, is
defined as consuming five or more drinks in about 2 hours for men, or four or
more drinks for women.
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Equal numbers of men and
women reported experiencing blackouts, despite the fact that the men drank
significantly more often and more heavily than the women. This outcome suggests
that regardless of the amount of alcohol consumption, females—a group
infrequently studied in the literature on blackouts—are at greater risk than
males for experiencing blackouts. A woman’s tendency to black out more easily
probably results from differences in how men and women metabolize alcohol.
Females also may be more susceptible than males to milder forms of
alcohol–induced memory impairments, even when men and women consume comparable
amounts of alcohol (4).
ARE WOMEN MORE VULNERABLE TO
ALCOHOL’S EFFECTS ON THE BRAIN?
Women are more vulnerable
than men to many of the medical consequences of alcohol use. For example,
alcoholic women develop cirrhosis (5), alcohol–induced damage of the heart
muscle (i.e., cardiomyopathy) (6), and nerve damage (i.e., peripheral
neuropathy) (7) after fewer years of heavy drinking than do alcoholic men.
Studies comparing men and women’s sensitivity to alcohol–induced brain damage,
however, have not been as conclusive.
Using imaging with
computerized tomography, two studies (8,9) compared brain shrinkage, a common
indicator of brain damage, in alcoholic men and women and reported that male
and female alcoholics both showed significantly greater brain shrinkage than
control subjects. Studies also showed that both men and women have similar
learning and memory problems as a result of heavy drinking (10). The difference
is that alcoholic women reported that they had been drinking excessively for
only about half as long as the alcoholic men in these studies. This indicates
that women’s brains, like their other organs, are more vulnerable to
alcohol–induced damage than men’s (11).
Yet other studies have not
shown such definitive findings. In fact, two reports appearing side by side in
the American Journal of Psychiatry contradicted each other on the
question of gender–related vulnerability to brain shrinkage in alcoholism
(12,13). Clearly, more research is needed on this topic, especially because
alcoholic women have received less research attention than alcoholic men
despite good evidence that women may be particularly vulnerable to alcohol’s
effects on many key organ systems.
BRAIN DAMAGE FROM OTHER
CAUSES
People who have been drinking
large amounts of alcohol for long periods of time run the risk of developing
serious and persistent changes in the brain. Damage may be a result of the
direct effects of alcohol on the brain or may result indirectly, from a poor
general health status or from severe liver disease.
For example, thiamine
deficiency is a common occurrence in people with alcoholism and results from
poor overall nutrition. Thiamine, also known as vitamin B1, is an essential
nutrient required by all tissues, including the brain. Thiamine is found in
foods such as meat and poultry; whole grain cereals; nuts; and dried beans,
peas, and soybeans. Many foods in the United States commonly are fortified with
thiamine, including breads and cereals. As a result, most people consume
sufficient amounts of thiamine in their diets. The typical intake for most
Americans is 2 mg/day; the Recommended Daily Allowance is 1.2 mg/day for men
and 1.1 mg/day for women (14).
Wernicke–Korsakoff
Syndrome
Up to 80 percent of
alcoholics, however, have a deficiency in thiamine (15), and some of these
people will go on to develop serious brain disorders such as Wernicke–Korsakoff
syndrome (WKS) (16). WKS is a disease that consists of two separate syndromes,
a short–lived and severe condition called Wernicke’s encephalopathy and a
long–lasting and debilitating condition known as Korsakoff’s psychosis.
The symptoms of Wernicke’s
encephalopathy include mental confusion, paralysis of the nerves that move the
eyes (i.e., oculomotor disturbances), and difficulty with muscle coordination.
For example, patients with Wernicke’s encephalopathy may be too confused to
find their way out of a room or may not even be able to walk. Many Wernicke’s
encephalopathy patients, however, do not exhibit all three of these signs and
symptoms, and clinicians working with alcoholics must be aware that this
disorder may be present even if the patient shows only one or two of them. In
fact, studies performed after death indicate that many cases of thiamine
deficiency–related encephalopathy may not be diagnosed in life because not all
the "classic" signs and symptoms were present or recognized.
| Human Brain |
|
Schematic drawing of
the human brain, showing regions vulnerable to alcoholism-related
abnormalities.
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Approximately 80 to 90
percent of alcoholics with Wernicke’s encephalopathy also develop Korsakoff’s
psychosis, a chronic and debilitating syndrome characterized by persistent
learning and memory problems. Patients with Korsakoff’s psychosis are forgetful
and quickly frustrated and have difficulty with walking and coordination (17).
Although these patients have problems remembering old information (i.e.,
retrograde amnesia), it is their difficulty in “laying down” new information
(i.e., anterograde amnesia) that is the most striking. For example, these
patients can discuss in detail an event in their lives, but an hour later might
not remember ever having the conversation.
Treatment
The cerebellum, an area of the brain responsible for coordinating movement and
perhaps even some forms of learning, appears to be particularly sensitive to
the effects of thiamine deficiency and is the region most frequently damaged in
association with chronic alcohol consumption. Administering thiamine helps to
improve brain function, especially in patients in the early stages of WKS. When
damage to the brain is more severe, the course of care shifts from treatment to
providing support to the patient and his or her family (18). Custodial care may
be necessary for the 25 percent of patients who have permanent brain damage and
significant loss of cognitive skills (19).
Scientists believe that a
genetic variation could be one explanation for why only some alcoholics with
thiamine deficiency go on to develop severe conditions such as WKS, but
additional studies are necessary to clarify how genetic variants might cause
some people to be more vulnerable to WKS than others.
LIVER DISEASE
Most people realize that
heavy, long–term drinking can damage the liver, the organ chiefly responsible
for breaking down alcohol into harmless byproducts and clearing it from the
body. But people may not be aware that prolonged liver dysfunction, such as
liver cirrhosis resulting from excessive alcohol consumption, can harm the
brain, leading to a serious and potentially fatal brain disorder known as
hepatic encephalopathy (20).
Hepatic encephalopathy can
cause changes in sleep patterns, mood, and personality; psychiatric conditions
such as anxiety and depression; severe cognitive effects such as shortened
attention span; and problems with coordination such as a flapping or shaking of
the hands (called asterixis). In the most serious cases, patients may slip into
a coma (i.e., hepatic coma), which can be fatal.
New imaging techniques have
enabled researchers to study specific brain regions in patients with alcoholic
liver disease, giving them a better understanding of how hepatic encephalopathy
develops. These studies have confirmed that at least two toxic substances,
ammonia and manganese, have a role in the development of hepatic
encephalopathy. Alcohol–damaged liver cells allow excess amounts of these
harmful byproducts to enter the brain, thus harming brain cells.
Treatment
Physicians typically use the following strategies to prevent or
treat the development of hepatic encephalopathy.
-
Treatment that lowers blood
ammonia concentrations, such as administering L–ornithine L–aspartate.
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Techniques such as
liver–assist devices, or “artificial livers,” that clear the patients’ blood of
harmful toxins. In initial studies, patients using these devices showed lower
amounts of ammonia circulating in their blood, and their encephalopathy became
less severe (21).
-
Liver transplantation, an
approach that is widely used in alcoholic cirrhotic patients with severe (i.e.,
end–stage) chronic liver failure. In general, implantation of a new liver
results in significant improvements in cognitive function in these patients
(22) and lowers their levels of ammonia and manganese (23).
ALCOHOL AND THE DEVELOPING
BRAIN
Drinking during pregnancy can
lead to a range of physical, learning, and behavioral effects in the developing
brain, the most serious of which is a collection of symptoms known as fetal
alcohol syndrome (FAS). Children with FAS may have distinct facial features
(see illustration). FAS infants also are markedly smaller than average. Their
brains may have less volume (i.e., microencephaly). And they may have fewer
numbers of brain cells (i.e., neurons) or fewer neurons that are able to
function correctly, leading to long–term problems in learning and behavior.
| Fetal Alcohol Syndrome |
|
Children with fetal
alcohol syndrome (FAS) may have distinct facial features.
|
Treatment
Scientists are investigating the use of complex motor training and medications
to prevent or reverse the alcohol–related brain damage found in people
prenatally exposed to alcohol (24). In a study using rats, Klintsova and
colleagues (25) used an obstacle course to teach complex motor skills, and this
skills training led to a re–organization in the adult rats’ brains (i.e.,
cerebellum), enabling them to overcome the effects of the prenatal alcohol
exposure. These findings have important therapeutic implications, suggesting
that complex rehabilitative motor training can improve motor performance of
children, or even adults, with FAS.
Scientists also are looking
at the possibility of developing medications that can help alleviate or prevent
brain damage, such as that associated with FAS. Studies using animals have
yielded encouraging results for treatments using antioxidant therapy and
vitamin E. Other preventive therapies showing promise in animal studies include
1–octanol, which ironically is an alcohol itself. Treatment with l–octanol
significantly reduced the severity of alcohol’s effects on developing mouse
embryos (26). Two molecules associated with normal development (i.e., NAP and
SAL) have been found to protect nerve cells against a variety of toxins in much
the same way that octanol does (27). And a compound (MK–801) that blocks a key
brain chemical associated with alcohol withdrawal (i.e., glutamate) also is
being studied. MK–801 reversed a specific learning impairment that resulted
from early postnatal alcohol exposure (28).
Though these compounds were
effective in animals, the positive results cited here may or may not translate
to humans. Not drinking during pregnancy is the best form of prevention; FAS
remains the leading preventable birth defect in the United States
today.
GROWING NEW BRAIN
CELLS
For decades scientists
believed that the number of nerve cells in the adult brain was fixed early in
life. If brain damage occurred, then, the best way to treat it was by
strengthening the existing neurons, as new ones could not be added. In the
1960s, however, researchers found that new neurons are indeed generated in
adulthood—a process called neurogenesis (29). These new cells originate from
stem cells, which are cells that can divide indefinitely, renew themselves, and
give rise to a variety of cell types. The discovery of brain stem cells and
adult neurogenesis provides a new way of approaching the problem of
alcohol–related changes in the brain and may lead to a clearer understanding of
how best to treat and cure alcoholism (30).
For example, studies with
animals show that high doses of alcohol lead to a disruption in the growth of
new brain cells; scientists believe it may be this lack of new growth that
results in the long–term deficits found in key areas of the brain (such as
hippocampal structure and function) (31,32). Understanding how alcohol
interacts with brain stem cells and what happens to these cells in alcoholics
is the first step in establishing whether the use of stem cell therapies is an
option for treatment (33).
SUMMARY
Alcoholics are not all alike.
They experience different degrees of impairment, and the disease has different
origins for different people. Consequently, researchers have not found
conclusive evidence that any one variable is solely responsible for the brain
deficits found in alcoholics. Characterizing what makes some alcoholics
vulnerable to brain damage whereas others are not remains the subject of active
research (34).
The good news is that most
alcoholics with cognitive impairment show at least some improvement in brain
structure and functioning within a year of abstinence, though some people take
much longer (35–37). Clinicians must consider a variety of treatment methods to
help people stop drinking and to recover from alcohol–related brain
impairments, and tailor these treatments to the individual patient.
Advanced technology will have
an important role in developing these therapies. Clinicians can use
brain–imaging techniques to monitor the course and success of treatment,
because imaging can reveal structural, functional, and biochemical changes in
living patients over time. Promising new medications also are in the early
stages of development, as researchers strive to design therapies that can help
prevent alcohol’s harmful effects and promote the growth of new brain cells to
take the place of those that have been damaged by alcohol.
|
SIDEBAR
Using High–Tech Tools to Assess Alcoholic Brain Damage
Researchers studying the effects of alcohol use on the brain are
aided by advanced technology such as magnetic resonance imaging (MRI),
diffusion tensor imaging (DTI), positron emission tomography (PET), and
electrophysiological brain mapping. These tools are providing valuable insight
into how alcohol affects the brain’s structure and function.
Long–term heavy drinking may
lead to shrinking of the brain and deficiencies in the fibers (white matter)
that carry information between brain cells (gray matter). MRI and DTI are being
used together to assess the brains of patients when they first stop chronic
heavy drinking and again after long periods of sobriety, to monitor for
possible relapse to drinking (38).
Memory formation and
retrieval are highly influenced by factors such as attention and motivation
(39). Studies using MRI are helping scientists to determine how memory and
attention improve with long-time abstinence from alcohol, as well as what
changes take place when a patient begins drinking again. The goal of these
studies is to determine which alcohol–induced effects on the brain are
permanent and which ones can be reversed with abstinence.
PET imaging is allowing
researchers to visualize, in the living brain, the damage that results from
heavy alcohol consumption (40). This “snapshot” of the brain’s function enables
scientists to analyze alcohol’s effects on various nerve cell communication
systems (i.e., neurotransmitter systems) as well as on brain cell metabolism
and blood flow within the brain. These studies have detected deficits in
alcoholics, particularly in the frontal lobes, which are responsible for
numerous functions associated with learning and memory, as well as in the
cerebellum, which controls movement and coordination. PET also is a promising
tool for monitoring the effects of alcoholism treatment and abstinence on
damaged portions of the brain and may help in developing new medications to
correct the chemical deficits found in the brains of people with alcohol
dependence.
Another high–tech tool,
electroencephalography (EEG), records the brain’s electrical signals (41).
Small electrodes are placed on the scalp to detect this electrical activity,
which then is magnified and graphed as brain waves (i.e., neural oscillations).
These brain waves show real–time activity as it happens in the brain.
Many male alcoholics have a
distinctive electrophysiological profile—that is, a low amplitude of their P3
components (see figure). P3 amplitudes in women alcoholics also are reduced,
although to a lesser extent than in men. For many years it was assumed that the
P3 deficit observed in alcoholics was the result of alcohol’s damage to the
brain. Then it was determined that while many of the clinical symptoms and
electrophysiological measures associated with alcoholism return to normal after
abstinence, the P3 amplitude abnormality persists (42)
.
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The P3 component is reduced in
alcoholics compared with control subjects.
|
This continued deficit in
long–term abstinent alcoholics suggests that P3 deficits may be a marker of
risk for alcohol dependence, rather than a result of alcohol use. In fact, a
number of studies have since reported low P3 amplitudes in young people who
have not started drinking alcohol but who are at high risk for developing
alcoholism, such as young sons of alcoholic fathers (43,44). Markers such as
the P3 can help identify people who may be at greatest risk for developing
problems with alcohol.
END OF SIDEBAR
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| Resources |
Source material for this
Alcohol Alert originally appeared in the journal Alcohol Research &
Health, “Alcoholic Brain Damage” (Vol. 27, No. 2, 2003).
Alcohol Research &
Health is the quarterly, peer–reviewed journal published by the National
Institute on Alcohol Abuse and Alcoholism. Each issue of AR&H provides
in–depth focus on a single topic in the field of alcohol research.
Back issues of Alcohol
Research & Health and additional resources can be downloaded from
NIAAA’s Web site, www.niaaa.nih.gov.
Subscriptions are available from the Superintendent of Documents for $25. Write
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All material
contained in the Alcohol Alert is in the public domain and may be used
or reproduced without permission from NIAAA. Citation of the source is
appreciated. Copies of the Alcohol Alert are available free of charge
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P.O. Box 10686, Rockville, MD 20849–0686.
Prepared: October 2004