U.S. Department of Health

& Human Services 

National Institutes of Health 

National Institute on Alcohol Abuse 

and Alcoholism 

Number 63 October 2004 

ALCOHOL’S DAMAGING


EFFECTS ON 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 (1), 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; and 

• 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 

“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.” 

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. 

women metabolize alcohol. Females also may be more 

susceptible than males to milder forms of alcoholinduced 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 alcoholinduced damage than men’s (11). 

Yet other studies have not shown such definitive findings. In fact, two reports appearing side by side in 

▲ 

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 the American Journal of Psychiatry contradicted each

other on the question of gender-related vulnerability significantly more often and more heavily than the 

women. This outcome suggests that regardless of the to brain shrinkage in alcoholism (12,13). Clearly, more 

amount of alcohol consumption, females—a group research is needed on this topic, especially because alcoholic women have received less research attention than infrequently studied in the literature on blackouts— 

are at greater risk than males for experiencing black- alcoholic men despite good evidence that women may 

outs. A woman’s tendency to black out more easily be particularly vulnerable to alcohol’s effects on many 

probably results from differences in how men and 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. 

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.” 

2

3

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). 

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.

P3

Average EPP for Channel CZ

Control Subject

Alcoholic

-184 -34 116 266 416 566 716 866 1016 1156

Time (ms)

14

12

10

8

6

4

2

0

-2

The P3 component is reduced in alcoholics compared

with control subjects.
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 

related abnormalities. 

lobe 

Hippocampal 

regions lobe 

callosum 

Occipital 

lobe 

Cerebellum 

{ 

Human Brain 

Schematic drawing of the human brain, 

showing regions vulnerable to alcoholismParietal lobe 

Cerebral cortex 

Frontal 

Temporal 

Corpus 

Thalamus 

Hypothalamus 

Patients with Korsakoff ’s psychosis are forgetful and 

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. 

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. 

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). 

“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.” 

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 

4

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. 

• 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. 

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 

Fetal Alcohol Syndrome 

Skin folds at the Small head 

corner of the eye circumference 

Low nasal bridge Small eye 

opening 

Short nose Small midface 

Indistinct philtrum 

(groove between Thin upper lip 

nose and upper lip) 

Children with fetal alcohol syndrome 

(FAS) may have distinct facial features. 

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 

5 
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 brainimaging 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. 

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7

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