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Alcohol & The Brain
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, including:
• How much and how often a person drinks
• The age at which he or she first began drinking, and how long he or she
has been drinking
• The person’s age, level of education, gender, genetic background, and
family history of alcoholism
• Whether he or she is at risk as a result of prenatal alcohol exposure
• 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 & 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.
White and colleagues 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
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.
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.
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,
alcohol–induced damage of the heart muscle (i.e., cardiomyopathy), and
nerve damage (i.e., peripheral neuropathy) 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 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.
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.
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.
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.
Wernicke–Korsakoff Syndrome
Up to 80 percent of alcoholics, however, have a deficiency in thiamine,
and some of these people will go on to develop serious brain disorders
such as Wernicke–Korsakoff syndrome (WKS). 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.
Regions Vulnerable to Alcohol
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.
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.
Custodial care may be necessary for the 25 percent of patients who have
permanent brain damage and significant loss of cognitive skills.
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.
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.
• 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.
• 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 and lowers their levels of ammonia
and manganese.
Alcohol & 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. In a study using rats, Klintsova
and colleagues 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.
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. 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.
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.
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.
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). 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.
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.
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. 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.
From National Institute on Alcohol
Abuse
and Alcoholism (NIAAA)
http://www.niaaa.nih.gov
