Can Alcohol Shrink Your Brain?

Can Alcohol Shrink Your Brain
Can Alcohol Shrink Your Brain Share on Pinterest Experts recommend women limit their alcohol intake to one glass a day. Westend61/Getty Images

Experts recommend that women limit alcohol intake to one drink a day and men limit it to two drinks a day. However, researchers say that even a single drink on average per day can decrease brain volume over time. Their study showed that a 50-year-old who drinks a pint of beer or a glass of wine a day effectively ages their brain by 2 years. Experts note, though, that heavier drinking has a more substantial impact on brain size.

A drink a day could shrink your brain away, a new study suggests. Heavy alcohol use has long been associated with changes in the brain. However, researchers from the University of Pennsylvania have found that even light to moderate drinking — as little as a glass of beer or wine daily — is associated with reduced brain size and structure.

  • Such changes could be warning signs of cognitive impairment, the researchers warned.
  • The researchers’ report, based on an analysis of data about drinking and brain health among more than 36,000 people, likened the changes in brain volume among drinkers to aging.
  • For example, a 50-year-old who on average drinks a pint of beer or a glass of wine once a day effectively ages their brain by two years, according to findings published in the journal Nature Communications.

And those who consume an average of 4 drinks daily had brains that were 10 years “older” than those who did not drink. “The fact that we have such a large sample size allows us to find subtle patterns, even between drinking the equivalent of half a beer and one beer a day,” said Gideon Nave, a corresponding author on the study and faculty member at the University of Pennsylvania’s Wharton School.

Does alcohol cause brain shrinkage?

Heavy alcohol consumption has been associated with brain atrophy, neuronal loss, and poorer white matter fiber integrity. However, there is conflicting evidence on whether light-to-moderate alcohol consumption shows similar negative associations with brain structure.

Is alcohol brain shrinkage reversible?

Is Brain Shrinkage Permanent? – Some of the brain damage caused by alcohol can be reversed if a person stops drinking and maintains a period of abstinence. But some of it is permanent and cannot be undone. The most significant permanent damage caused by alcohol is nerve cell loss,

Some nerve cells cannot be replaced once they are lost, including those in the frontal cortex, cerebellum, and other regions deep inside the brain. However, abstinence can help reverse the shrinkage of dendrites. Studies show they will begin to grow again after weeks or months of abstinence. Once this happens, brain function may improve.

Some of the brain damage caused by cirrhosis of the liver can begin to reverse with treatment. Brain damage due to thiamine deficiency in people who misuse alcohol can easily be treated with thiamine supplements, but repeated deficiencies can cause permanent damage.

Does alcohol damage your brain?

Image Diffusion tensor imaging (DTI) of fiber tracks in the brain of a 58-year-old man with alcohol use disorder. DTI maps white-matter pathways in a living brain. Image courtesy of Drs. Adolf Pfefferbaum and Edith V. Sullivan. Alcohol interferes with the brain’s communication pathways and can affect the way the brain looks and works.

Can having just one drink a day shrink your brain new study finds?

Can Alcohol Shrink Your Brain Just two units of alcohol a day are enough to make brains appear two years older. (Image credit: Shutterstock) Drinking even a single pint of beer or glass of wine a day shrinks the brain, and the effect worsens as the daily drinks increase, a new study of middle-age and older adults suggests.

The study, which surveyed over 36,000 U.K. middle-age and older adults, found that, on average, the brains of people who drank two alcoholic units a day — equivalent to a pint (16 ounces) of beer or a 6-ounce glass of wine — had shrunk to appear two years older than the brains of people who consumed none.

And the more drinks that people consumed, the larger the differences in their brains to those who drank none. The brains of people who drank three alcoholic units a day (equivalent to 8.5 ounces of wine) appeared 3.5 years older, and the brains of people who drank four units (just under half a standard bottle of wine) aged by 10 years, according to the study authors.

The research, published March 4 in the journal Nature (opens in new tab), is adds to a growing number (opens in new tab) of (opens in new tab) studies (opens in new tab) that have found any amount of drinking to be unhealthy, and especially damaging to cardiovascular and brain function. Related: Does drinking alcohol warm your body? “There is some evidence that the effect of drinking on the brain is exponential,” Remi Daviet, study first author and an assistant professor of marketing at the University of Wisconsin-Madison, said in a statement (opens in new tab),

“So, one additional drink in a day could have more of an impact than any of the previous drinks that day. That means that cutting back on that final drink of the night might have a big effect in terms of brain aging.” In the study, more than 36,000 U.K.

Participants aged 40 to 69 reported how many alcoholic units they drank, which were compared to MRI scans of their brains. After grouping their subjects by average daily alcohol intake — from none all the way to two beers or glasses of wine or more a day — the researchers saw that those who reported drinking more alcohol had a steeper decline in brain volume than those who didn’t.

They found that the participants who drank even one alcoholic unit (half a pint of beer or a half-glass of wine) per day had noticeable differences to their brains’ structure, particularly in the brain stem, putamen and amygdala — areas of the brain responsible for regulating heart rate, breathing, learning and motor control, and processing emotions, like fear.

  1. The differences held even after the researchers accounted for other factors that might affect brain aging, such as age, genetic ancestry and sex.
  2. In particular, regions of white and gray matter throughout the brain shrank exponentially in volume the more units participants reported drinking.
  3. Named for its pinkish-gray tinge, gray matter is the stuff in the brain responsible for processing information, and white matter is the material that enables communication between gray matter regions.

The shrinking of either region is a bad sign, as it is linked to decreased cognitive ability (opens in new tab), Although the results of the new study may be in line with some past research, the study researchers note that the shrinking of white and gray matter happened even in people who consumed very few units of alcohol.

For example, some earlier (opens in new tab) studies (opens in new tab) suggested (opens in new tab) that a limited amount of drinking could be beneficial to health. The new findings also go against most current scientific and government guidance. “For example, the U.S. National Institute on Alcohol Abuse and Alcoholism recommends that men limit alcohol consumption to two drinks per day, an amount that exceeds the consumption level associated in the study with decreased brain volume,” study co-author Henry Kranzler, a professor of psychiatry and the director of the Center for Studies of Addiction at the University of Pennsylvania School of Medicine, said in the statement.

It’s important to note that the study, and many others like it, can only show a correlation between alcohol intake and brain shrinking, and not necessarily that one causes the other, the researchers said. Another limitation is that people self-reported how much they drank, which can tend to be unreliable.

For future work, the researchers want to study participants over time to really pin down whether drinking is the cause of the brain shrinkage, as well as look at how other behaviors, such as binge drinking, affect the brain. “This study looked at average consumption, but we’re curious whether drinking one beer a day is better than drinking none during the week and then seven on the weekend,” study co-author Gideon Nave, a neuroscientist at the University of Pennsylvania, said in the statement.

“There’s some evidence that binge drinking is worse for the brain, but we haven’t looked closely at that yet.” The team also noted that the exponential nature of the correlation means that those who drink the most are also likely to benefit the most from drinking less, even if it’s just one less drink per day.

Originally published on Live Science. Stay up to date on the latest science news by signing up for our Essentials newsletter. Ben Turner is a U.K. based staff writer at Live Science. He covers physics and astronomy, among other topics like tech and climate change. He graduated from University College London with a degree in particle physics before training as a journalist.

When he’s not writing, Ben enjoys reading literature, playing the guitar and embarrassing himself with chess.

How bad is 1 beer a day?

Pros and cons of moderate alcohol use – Moderate alcohol consumption may provide some health benefits, such as:

  • Reducing your risk of developing and dying of heart disease
  • Possibly reducing your risk of ischemic stroke (when the arteries to your brain become narrowed or blocked, causing severely reduced blood flow)
  • Possibly reducing your risk of diabetes

However, eating a healthy diet and being physically active have much greater health benefits and have been more extensively studied. Keep in mind that even moderate alcohol use isn’t risk-free. For example, even light drinkers (those who have no more than one drink a day) have a tiny, but real, increased risk of some cancers, such as esophageal cancer.

How much alcohol is bad for your brain?

Your Brain on Alcohol – Your whole body absorbs alcohol, but it really takes its toll on the brain. Alcohol interferes with the brain’s communication pathways. It can also affect how your brain processes information. There are several stages of alcohol intoxication :

  1. Subliminal intoxication. With a blood alcohol content (BAC) between 0.01 – 0.05, this is the first stage of intoxication. You may not look like you have been drinking, but your reaction time, behavior and judgment may be slightly altered. Depending on weight, most men and women enter this stage after one drink.
  2. Euphoria. During the early stages of drinking, your brain releases more dopamine. This chemical is linked with pleasure. During euphoria, you may feel relaxed and confident. But, your reasoning and memory may be slightly impaired. Often referred to as “tipsy,” this stage occurs when your BAC is between 0.03 and 0.12.
  3. Excitement. At this stage, with a BAC from 0.09 to 0.25, you are now legally intoxicated. This level of intoxication affects the occipital lobe, temporal lobe and frontal lobe in your brain. Drinking too much can cause side effects specific to each lobe’s role, including blurred vision, slurred speech and hearing, and lack of control, respectively. The parietal lobe, which processes sensory information, is also affected. You may have a loss of fine motor skills and a slower reaction time. This stage is often marked by mood swings, impaired judgment, and even nausea or vomiting.
  4. Confusion. A BAC of 0.18 to 0.3 often looks like disorientation. Your cerebellum, which helps with coordination, is impacted. As a result, you may need help walking or standing. Blackouts, or the temporary loss of consciousness or short-term memory, are also likely to occur at this stage. This is a result of the hippocampus, the region of the brain that is responsible for making new memories, not working well. You may also have a higher pain threshold, which may increase your risk for injury.
  5. Stupor. If you reach a BAC of 0.25, you may have concerning signs of alcohol poisoning. At this time, all mental, physical and sensory functions are severely impaired. The risk for passing out, suffocation and injury is high.
  6. Coma. At a BAC of 0.35, you are at risk for going into a coma. This occurs due to compromised respiration and circulation, motor responses and reflexes. A person in this stage is at risk of death.
  7. Death. A BAC over 0.45 may cause death due to alcohol poisoning or failure of the brain to control the body’s vital functions.

What are the benefits of alcohol on the brain?

Alcohol on the brain: the pros – Alcohol is one of the most popular psychoactive substances in the world, and it can have a powerful effect on your mood and mental state. Most drinkers would agree that moderate amounts of alcohol make us feel relaxed, happier, less tense, and more sociable.

We can even see the positive outcomes of drinking on brain scans with the noticeable release of endorphins that bind to the opioid receptors in the brain. While there are many social benefits to having a few drinks, there is generally a nagging concern about the physical consequences. Alcohol crosses the blood-brain barrier where it interacts directly and indirectly with a wide range of neurotransmitters, including GABA, serotonin, dopamine, opioid, and many more.

The good news is that moderate alcohol consumption can have benefits on our heart health due to the presence of polyphenols in beer and wine. Unfortunately, moderate consumption of most other alcoholic drinks doesn’t offer the same benefits. Did you know that alcohol consumption is also linked to the reduction in dementia risk in older adults? It even has some data in small amounts of alcohol improving creativity.

See also:  Does Alcohol Cure Hangover?

Does drinking after studying improve memory?

‘ Alcohol blocks the learning of new information and therefore the brain has more resources available to lay down other recently learned information into long-term memory,’ Morgan said.

Is 7 beers a day a lot?

Drinking in Moderation: According to the “Dietary Guidelines for Americans 2020-2025,” U.S. Department of Health and Human Services and U.S. Department of Agriculture, adults of legal drinking age can choose not to drink or to drink in moderation by limiting intake to 2 drinks or less in a day for men and 1 drink or less in a day for women, when alcohol is consumed.

NIAAA defines binge drinking as a pattern of drinking alcohol that brings blood alcohol concentration (BAC) to 0.08 percent – or 0.08 grams of alcohol per deciliter – or higher. For a typical adult, this pattern corresponds to consuming 5 or more drinks (male), or 4 or more drinks (female), in about 2 hours.

The Substance Abuse and Mental Health Services Administration (SAMHSA), which conducts the annual National Survey on Drug Use and Health (NSDUH), defines binge drinking as 5 or more alcoholic drinks for males or 4 or more alcoholic drinks for females on the same occasion (i.e., at the same time or within a couple of hours of each other) on at least 1 day in the past month.

Heavy Alcohol Use:

NIAAA defines heavy drinking as follows:

For men, consuming more than 4 drinks on any day or more than 14 drinks per week For women, consuming more than 3 drinks on any day or more than 7 drinks per week

SAMHSA defines heavy alcohol use as binge drinking on 5 or more days in the past month.

Patterns of Drinking Associated with Alcohol Use Disorder : Binge drinking and heavy alcohol use can increase an individual’s risk of alcohol use disorder. Certain people should avoid alcohol completely, including those who:

Plan to drive or operate machinery, or participate in activities that require skill, coordination, and alertness Take certain over-the-counter or prescription medications Have certain medical conditions Are recovering from alcohol use disorder or are unable to control the amount that they drink Are younger than age 21 Are pregnant or may become pregnant

What causes brain shrinkage?

What Is Cerebral Atrophy? – Cerebral atrophy is the loss of brain cells, called neurons, and their electrochemical connectors, called synapses, This cell loss results in brain shrinkage and, depending on its source and extent, declines in cognitive ability.

Cerebral atrophy occurs naturally in all humans. But cell loss can be accelerated by a variety of causes, including injury, infection, and medical conditions such as dementia, stroke, and Huntington’s disease. These latter cases sometimes culminate in more severe brain damage and are potentially life-threatening.

Brain disease in all forms affects as many as one in six Americans and cerebral atrophy is a major indicator. There is no cure for brain-cell loss but treatments exist to reduce or manage symptoms. If you or a loved one is having issues with cognitive decline, see your Baptist Health medical provider.

What things cause brain shrinkage?

What is cerebral atrophy? – Cerebral atrophy—the loss of nerve cells (neurons) and the connections that help them communicate in the brain’s tissues—occurs in many disorders that affect the brain, such as stroke, Alzheimer’s, disease, traumatic brain injury, multiple sclerosis, or infections.

  1. Atrophy of the brain can affect different areas, depending on the disease involved.
  2. Atrophy can be generalized, which affects cells all over the brain and shrinks it, or focal, which affects cells in some regions of the brain and decreases function those areas control.
  3. If the two lobes in the brain that form the cerebrum, known as the cerebral hemisphere, are affected, conscious thought and voluntary processes may be impaired.

The symptoms of cerebral atrophy vary depending on which area of the brain is affected. Depending on the disease or disorder causing the cerebral atrophy, symptoms can include: Some conditions that cause cerebral atrophy are progressive, while others may be manageable.

What parts of the brain does alcohol shrink?

Marlene Oscar–Berman, Ph.D., and Ksenija Marinkovic, Ph.D. – Marlene Oscar–Berman, Ph.D., is a professor in the Departments of Anatomy and Neurobiology, Psychiatry, and Neurology, Boston University School of Medicine, and a research career scientist at the U.S. Department of Veterans Affairs Healthcare System, Jamaica Plain Division, Boston, Massachusetts. Ksenija Marinkovic, Ph.D., is a research scientist at the Athinoula A. Martinos Center for Biomedical Imaging, instructor in the Radiology Department at Harvard Medical School, and assistant in Neuroscience at the Massachusetts General Hospital, Boston, Massachusetts. This work was supported by National Institute on Alcohol Abuse and Alcoholism grants R37–AA–07112, K05–AA–00219, K01–AA–13402, and by the Medical Research Service of the U.S. Department of Veterans Affairs.

Alcoholism can affect the brain and behavior in a variety of ways, and multiple factors can influence these effects. A person’s susceptibility to alcoholism–related brain damage may be associated with his or her age, gender, drinking history, and nutrition, as well as with the vulnerability of specific brain regions.

Investigators use a variety of methods to study alcoholism–related brain damage, including examining brains of deceased patients as well as neuroimaging, a technique that enables researchers to test and observe the living brain and to evaluate structural damage in the brain. Key words: neurobehavioral theory of AODU (alcohol and other drug use); alcoholic brain syndrome; brain atrophy; neuropsychological assessment; neurotransmission; risk factors; comorbidity; disease susceptibility; neuroimaging; treatment factors; survey of research The brain, like most body organs, is vulnerable to injury from alcohol consumption.

The risk of brain damage and related neurobehavioral deficits varies from person to person. This article reviews the many factors that influence this risk, the techniques used to study the effects of alcoholism 1 on the brain and behavior, and the implications of this research for treatment.

( 1 Alcohol dependence, also known as alcoholism, is characterized by a craving for alcohol, possible physical dependence on alcohol, an inability to control one’s drinking on any given occasion, and an increasing tolerance to alcohol’s effects,) About half of the nearly 20 million alcoholics in the United States seem to be free of cognitive impairments.

In the remaining half, however, neuropsychological difficulties can range from mild to severe. For example, up to 2 million alcoholics develop permanent and debilitating conditions that require lifetime custodial care (Rourke and Löberg 1996). Examples of such conditions include alcohol–induced persisting amnesic disorder (also called Wernicke–Korsakoff syndrome) and dementia, which seriously affects many mental functions in addition to memory (e.g., language, reasoning, and problem–solving abilities) (Rourke and Löberg 1996).

Most alcoholics with neuropsychological impairments show at least some improvement in brain structure and functioning within a year of abstinence, but some people take much longer (Bates et al.2002; Gansler et al.2000; Sullivan et al.2000). Unfortunately, little is known about the rate and extent to which people recover specific structural and functional processes after they stop drinking.

However, research has helped define the various factors that influence a person’s risk for experiencing alcoholism–related brain deficits, as the following sections describe. RISK FACTORS AND COMORBID CONDITIONS THAT INFLUENCE ALCOHOL–RELATED BRAIN DAMAGE Alcoholism’s effects on the brain are diverse and are influenced by a wide range of variables (Parsons 1996).

These include the amount of alcohol consumed, the age at which the person began drinking, and the duration of drinking; the patient’s age, level of education, gender, genetic background, and family history of alcoholism; and neuropsychiatric risk factors such as alcohol exposure before birth and general health status.

Overall physical and mental health is an important factor because comorbid medical, neurological, and psychiatric conditions can interact to aggravate alcoholism’s effects on the brain and behavior. Examples of common comorbid conditions include:

Medical conditions such as malnutrition and diseases of the liver and the cardiovascular system Neurological conditions such as head injury, inflammation of the brain (i.e., encephalopathy), and fetal alcohol syndrome (or fetal alcohol effects) Psychiatric conditions such as depression, anxiety, post–traumatic stress disorder, schizophrenia, and the use of other drugs (Petrakis et al.2002).

These conditions also can contribute to further drinking. MODELS FOR EXPLAINING ALCOHOL–RELATED BRAIN DAMAGE Some of the previously mentioned factors that are thought to influence how alcoholism affects the brain and behavior have been developed into specific models or hypotheses to explain the variability in alcoholism–related brain deficits.

Hypotheses Proposed to Explain the Consequences of Alcoholism for the Brain

Hypotheses Emphasizing the Personal Characteristics Associated With Vulnerability
Characteristic Hypothesis
Aging Premature aging hypothesis: Alcoholism accelerates aging. Brains of alcoholics resemble brains of chronologically old nonalcoholics. This may occur at the onset of problem drinking (“accelerated aging”) or later in life when brains are more vulnerable (“increased vulnerability” or “cumulative effects”).
Gender Alcoholism affects women more than men. Although women and men metabolize alcohol differently, it is not yet clear if women’s brains are more vulnerable than men’s brains to the effects of alcoholism.
Family history Alcoholism runs in families; thus, children of alcoholics face increased risk of alcoholism and associated brain changes.
Vitamin deficiency Thiamine deficiency can contribute to damage deep within the brain, leading to severe cognitive deficits.
Hypotheses Emphasizing the Vulnerability of Brain Regions or Systems
Region/System Hypothesis
Entire brain Vulnerable to cerebral atrophy.
Limbic system, thalamus, and hypothalamus Vulnerable to alcohol–induced persisting amnesic disorder (also known as Wernicke–Korsakoff syndrome).
Frontal lobe systems More vulnerable to the effects of alcoholism than other brain regions/systems.
Right hemisphere More vulnerable to the effects of alcoholism than the left hemisphere.*
Neurotransmitter systems (e.g., gamma–aminobutyric acid, glutamate, dopamine, acetylcholine, and serotonin systems) Several neurotransmitter systems are vulnerable to effects of alcoholism.

The right hemisphere is also believed to be more vulnerable to the effects of normal aging than the left hemisphere, which is taken as support for the premature aging hypothesis listed above. NOTE: These hypotheses are not mutually exclusive; some are interrelated.

  1. Supporting data for these models come from neurobehavioral and electrophysiological studies, brain scans, and post mortem neuropathology.
  2. Models Based on Characteristics of Individual Alcoholics Premature Aging Hypothesis.
  3. According to this hypothesis, alcoholism accelerates natural chronological aging, beginning with the onset of problem drinking.

An alternate version suggests that older patients (age 50 and older) are especially susceptible to the cumulative effects of alcoholism, and aging is accelerated only later in life. The preponderance of scientific evidence suggests that although alcoholism–related brain changes may mimic some of the changes seen in older people, alcoholism does not cause premature aging.

Rather, the effects of alcoholism are disproportionately expressed in older alcoholics (Oscar–Berman 2000). Gender, Although it has been hypothesized that women’s brain functioning is more vulnerable to alcoholism than men’s, studies of gender differences have not consistently found this to be true (see Wuethrich 2001 for a review), even though women and men metabolize alcohol differently (i.e., women achieve higher blood alcohol contents than men after consuming the same amount of alcohol).

However, it is not known whether this comparison between men and women holds among older populations (Oscar–Berman 2000). Family History. Family history of alcoholism has been found to be important because it can influence such things as tolerance for alcohol and the amount of consumption needed to feel alcohol’s effects.

  • Also, studies examining brain functioning in people with and without a positive family history of alcoholism have shown that there are clear differences between the groups on measures of brain electrical activity (Porjesz and Begleiter 1998).
  • Vitamin Deficiency,
  • Research on malnutrition, a common consequence of poor dietary habits in some alcoholics, indicates that thiamine deficiency (vitamin B 1 ) can contribute to damage deep within the brain, leading to severe cognitive deficits (Oscar–Berman 2000).

The exact location of the affected parts of the brain and underlying neuropathological mechanisms are still being researched (see the next section). Models Based on Vulnerable Brain Systems The outer, convoluted layer of brain tissue, called the cerebral cortex or the gray matter, controls most complex mental activities (see figure 1).

Figure 1 Schematic drawing of the human brain, showing regions vulnerable to alcoholism–related abnormalities.

Areas of the brain that are especially vulnerable to alcoholism–related damage are the cerebral cortex and subcortical areas such as the limbic system (important for feeling and expressing emotions), the thalamus (important for communication within the brain), the hypothalamus (which releases hormones in response to stress and other stimuli and is involved in basic behavioral and physiological functions), and the basal forebrain (the lower area of the front part of the brain, involved in learning and memory) (Oscar–Berman 2000).

Another brain structure that has recently been implicated is the cerebellum (Sullivan 2000), situated at the base of the brain, which plays a role in posture and motor coordination and in learning simple tasks. Alcohol–Related Brain Atrophy. According to one hypothesis, shrinkage (i.e., atrophy) of the cerebral cortex and white matter, as well as possible atrophy of basal forebrain regions, may result from the neurotoxic effects of alcohol (Lishman 1990).

Furthermore, thiamine deficiency may result in damage to portions of the hypothalamus (perhaps because blood vessels break in that region). According to this hypothesis, alcoholics who are susceptible to alcohol toxicity 2 may develop permanent or transient cognitive deficits associated with brain shrinkage.

  • 2 Some people may have better immunity than others to alcohol’s toxic effects.) Those who are susceptible to thiamine deficiency will develop a mild or transient amnesic disorder, with short–term memory loss as the salient feature.
  • Patients with dual vulnerability, those with a combination of alcohol neurotoxicity and thiamine deficiency, will have widespread damage to large regions of the brain, including structures deep within the brain such as the limbic system.
See also:  Hoe Lang Is Alcohol Aantoonbaar In Bloed?

These people will exhibit severe short–term memory loss and collateral cognitive impairments (Oscar–Berman 2000). Frontal Lobe Vulnerability. Although alcoholics have diffuse damage in the cerebral cortex of both hemispheres of the brain, neuropathological studies performed on the brains of deceased patients as well as findings derived from neuroimaging studies of living brains point to increased susceptibility of frontal brain systems to alcoholism–related damage (Moselhy et al.2001; Oscar–Berman 2000; Sullivan 2000).

The frontal lobes are connected with all other lobes of the brain (i.e., the parietal, temporal, and occipital lobes on both halves of the brain; see figure 1), and they receive and send fibers to numerous subcortical structures. Behavioral neuroscientists have determined that the anterior region of the frontal lobes (i.e., the prefrontal cortex) is important for engaging in ordinary cognitive, emotional, and interpersonal activities.

The prefrontal cortex is considered the brain’s executive—that is, it is necessary for planning and regulating behavior, inhibiting the occurrence of unnecessary or unwanted behaviors, and supporting adaptive “executive control” skills such as goal–directed behaviors, good judgment, and problem–solving abilities.

  1. Disruptions of the normal inhibitory functions of prefrontal networks often have the interesting effect of releasing previously inhibited behaviors.
  2. As a result, a person may behave impulsively and inappropriately, which may contribute to excessive drinking.
  3. There is evidence that the frontal lobes are particularly vulnerable to alcoholism–related damage, and the brain changes in these areas are most prominent as alcoholics age (Oscar–Berman 2000; Pfefferbaum et al.1997; Sullivan 2000) (see figure 2).

Other studies of frontal lobe function in older alcoholics have confirmed reports of a correlation between impaired neuropsychological performance (e.g., executive control skills, as noted above) and decreased blood flow or metabolism (energy use) in the frontal lobes, as seen using neuroimaging techniques (Adams et al.1998).

Figure 2 Brain MRI scans of age–equivalent men with different histories of alcohol use. The image shows clear evidence of brain shrinkage in the alcoholic compared with the control subject. The graph on the right shows that older alcoholics have less cortical tissue than younger alcoholics, and that the prefrontal cortex is especially vulnerable to alcohol’s effects. The location of the temporal, parietal, and occipital regions of the brain can be seen in figure 1. *Z–score is a mathematical measure that is useful for showing the difference between the recorded value and a “normal” value. SOURCE: Pfefferbaum et al.1997.

Vulnerability of the Right Hemisphere, Some investigators have hypothesized that functions controlled by the brain’s right hemisphere are more vulnerable to alcoholism–related damage than those carried out by the left hemisphere (see Oscar–Berman and Schendan 2000 for review).

Each hemisphere of the human brain is important for mediating different functions. The left hemisphere has a dominant role in communication and in understanding the spoken and written word. The right hemisphere is mainly involved in coordinating interactions with the three–dimensional world (e.g., spatial cognition).

Differences between the two cerebral hemispheres can easily be seen in patients with damage to one hemisphere but not the other (from stroke, trauma, or tumor). Patients with left hemispheric damage often have problems with language; patients with right hemispheric damage often have difficulty with maps, designs, music, and other nonlinguistic materials, and they may show emotional apathy.

Alcoholics may seem emotionally “flat” (i.e., they are less reactive to emotionally charged situations), and may have difficulty with the same kinds of tasks that patients with damage to the right hemisphere have difficulty with. New research has shown that alcoholics are impaired in emotional processing, such as interpreting nonverbal emotional cues and recognizing facial expressions of emotion (Kornreich et al.2002; Monnot et al.2002; Oscar–Berman 2000).

Yet, despite the fact that emotional functioning can be similar in some alcoholics and people with right hemisphere damage, research provides only equivocal support for the hypothesis that alcoholism affects the functioning of the right hemisphere more than the left (Oscar–Berman and Schendan 2000).

Impairments in emotional functioning that affect alcoholics may reflect abnormalities in other brain regions which also influence emotional processing, such as the limbic system and the frontal lobes. Disruption of Neurotransmitter Systems. Brain cells (i.e., neurons) communicate using specific chemicals called neurotransmitters.

Neuronal communication takes place at the synapse, where cells make contact. Specialized synaptic receptors on the surface of neurons are sensitive to specific neurotransmitters. Alcohol can change the activity of neurotransmitters and cause neurons to respond (excitation) or to interfere with responding (inhibition) (Weiss and Porrino 2002), and different amounts of alcohol can affect the functioning of different neurotransmitters.

Over periods of days and weeks, receptors adjust to chemical and environmental circumstances, such as the changes that occur with chronic alcohol consumption, and imbalances in the action of neurotransmitters can result in seizures, sedation, depression, agitation, and other mood and behavior disorders.

The major excitatory neurotransmitter in the human brain is the amino acid glutamate. Small amounts of alcohol have been shown to interfere with glutamate action. This interference could affect several brain functions, including memory, and it may account for the short–lived condition referred to as “alcoholic blackout.” Chronic alcohol consumption increases glutamate receptor sites in the hippocampus, an area in the limbic system that is crucial to memory and often involved in epileptic seizures.

During alcohol withdrawal, glutamate receptors that have adapted to the long–term presence of alcohol may become overactive, and this overactivity has been repeatedly linked to neuronal death, which is manifested by conditions such as stroke and seizures. Deficiencies of thiamine caused by malnutrition may contribute to this potentially destructive overactivity (Crews 2000).

How Bad Is Heavy Drinking on the Brain?

Gamma–aminobutyric acid (GABA) is the major inhibitory neurotransmitter. Available evidence suggests that alcohol 3 initially potentiates GABA’s effects (i.e., it increases inhibition, and often the brain becomes mildly sedated). ( 3 The amount of alcohol needed to cause this effect depends on the person.) However, over time, prolonged, excessive alcohol consumption reduces the number of GABA receptors.

When the person stops drinking, decreased inhibition combined with a deficiency of GABA receptors may contribute to overexcitation throughout the brain. This in turn can contribute to withdrawal seizures within a day or two. It should be noted that the balance between the inhibitory action of GABA and the excitatory action of glutamate is a major determinant of the level of activity in certain regions of the brain; the effects of GABA and glutamate on withdrawal and brain function are probably interactive (see Valenzuela 1997 for review).

Alcohol directly stimulates release of the neurotransmitter serotonin, which is important in emotional expression, and of the endorphins, natural substances related to opioids, which may contribute to the “high” of intoxication and the craving to drink.

Alcohol also leads to increases in the release of dopamine (DA), a neurotransmitter that plays a role in motivation and in the rewarding effects of alcohol (Weiss and Porrino 2002). Changes in other neurotransmitters such as acetylcholine have been less consistently defined. Future research should help to clarify the importance of many neurochemical effects of alcohol consumption.

Furthermore, areas amenable to pharmacological treatment could be identified by studying regionally specific brain neurochemistry in vivo using neuroimaging methods such as positron emission tomography (PET) and single photon emission computerized tomography (SPECT) (described below).

  • New information from neuroimaging studies could link cellular changes directly to brain consequences observed clinically.
  • In the absence of a cure for alcoholism, a detailed understanding of the actions of alcohol on nerve cells may help in designing effective therapies.
  • TECHNIQUES FOR STUDYING ALCOHOL–RELATED BRAIN DAMAGE Researchers use multiple methods to understand the etiologies and mechanisms of brain damage across subgroups of alcoholics.

Behavioral neuroscience offers excellent techniques for sensitively assessing distinct cognitive and emotional functions—for example, the measures of brain laterality (e.g., spatial cognition) and frontal system integrity (e.g., executive control skills) mentioned earlier.

  1. Followup post mortem examinations of brains of well–studied alcoholic patients offer clues about the locus and extent of pathology and about neurotransmitter abnormalities.
  2. Neuroimaging techniques provide a window on the active brain and a glimpse at regions with structural damage.
  3. Behavioral Neuroscience Behavioral neuroscience studies the relationship between the brain and its functions—for example, how the brain controls executive functions and spatial cognition in healthy people, and how diseases like alcoholism can alter the normal course of events.

This is accomplished by using specialized tests designed expressly to measure the functions of interest. Among the tests used by scientists to determine the effects of alcoholism on executive functions controlled by the frontal lobes are those that measure problem–solving abilities, reasoning, and the ability to inhibit responses that are irrelevant or inappropriate (Moselhy et al.2001; Oscar–Berman 2000).

Tests to measure spatial cognition controlled by the right hemisphere include those that measure skills important for recognizing faces, as well as those that rely on skills required for reading maps and negotiating two– and three–dimensional space (visuospatial tasks) (Oscar–Berman and Schendan 2000).

With the advent of sophisticated neuroimaging techniques (described below), scientists can even observe the brain while people perform many tasks sensitive to the workings of certain areas of the brain. Neuropathology Researchers have gained important insights into the anatomical effects of long–term alcohol use from studying the brains of deceased alcoholic patients.

  • These studies have documented alcoholism–related atrophy throughout the brain and particularly in the frontal lobes (Harper 1998).
  • Post mortem studies will continue to help researchers understand the basic mechanisms of alcohol–induced brain damage and regionally specific effects of alcohol at the cellular level.

Neuroimaging Remarkable developments in neuroimaging techniques have made it possible to study anatomical, functional, and biochemical changes in the brain that are caused by chronic alcohol use. Because of their precision and versatility, these techniques are invaluable for studying the extent and the dynamics of brain damage induced by heavy drinking.

  • Because a patient’s brain can be scanned on repeated occasions, clinicians and researchers are able to track a person’s improvement with abstinence and deterioration with continued abuse.
  • Furthermore, brain changes can be correlated with neuropsychological and behavioral measures taken at the same time.

Brain imaging can aid in identifying factors unique to the individual which affect that person’s susceptibility to the effects of heavy drinking and risk for developing dependence, as well as factors that contribute to treatment efficacy. Imaging of Brain Structure.

  1. With neuroimaging techniques such as computerized tomography (CT) and magnetic resonance imaging (MRI), which allow brain structures to be viewed inside the skull, researchers can study brain anatomy in living patients.
  2. CT scans rely on x–ray beams passing through different types of tissue in the body at different angles.

Pictures of the “inner structure” of the brain are based on computerized reconstruction of the paths and relative strength of the x–ray beams. CT scans of alcoholics have revealed diffuse atrophy of brain tissue, with the frontal lobes showing the earliest and most extensive shrinkage (Cala and Mastaglia 1981).

  • MRI techniques have greatly influenced the field of brain imaging because they allow noninvasive measurement of both the anatomy (using structural MRI) and the functioning (using functional magnetic resonance imaging, described below) of the brain with great precision.
  • Structural MRI scans are based on the observation that the protons derived from hydrogen atoms, which are richly represented in the body because of its high water content, can be aligned by a magnetic field like small compass needles.

When pulses are emitted at a particular frequency, the protons briefly switch their alignment and “relax” back into their original state at slightly different times in different types of tissue. The signals they emit are detected by the scanner and converted into highly precise images of the tissue.

  • MRI methods have confirmed and extended findings from post mortem and CT scan studies—namely, that chronic use of alcohol results in brain shrinkage.
  • This shrinkage is most marked in the frontal regions and especially in older alcoholics (Oscar–Berman 2000; Pfefferbaum et al.1997; Sullivan 2000).
  • Other brain regions, including portions of the limbic system and the cerebellum, also are vulnerable to shrinkage.

Imaging of Brain Function: Hemodynamic Methods. Hemodynamic methods create images by tracking changes in blood flow, blood volume, blood oxygenation, and energy metabolism that occur in the brain in response to neural activity. PET and SPECT are used to map increased energy consumption by the specific brain regions that are engaged as a patient performs a task.

  1. One example of this mapping involves glucose, the main energy source for the brain.
  2. When a dose of a radioactively labeled glucose (a form of glucose that is absorbed normally but cannot be fully metabolized, thus remaining “trapped” in a cell) is injected into the bloodstream of a patient performing a memory task, those brain areas that accumulate more glucose will be implicated in memory functions.

Indeed, PET and SPECT studies have confirmed and extended earlier findings that the prefrontal regions are particularly susceptible to decreased metabolism in alcoholic patients (Berglund 1981; Gilman et al.1990). It is important to keep in mind, however, that frontal brain systems are connected to other regions of the brain, and frontal abnormalities may therefore reflect pathology elsewhere (Moselhy et al.2001).

  1. Even though using low doses of radioactive substances that decay quickly minimizes the risks of radiation exposure, newer and safer methods have emerged, such as MRI methods.
  2. MRI is noninvasive, involves no radioactive risks, and provides both anatomical and functional information with high precision.
See also:  Does Alcohol Age Your Skin?

The fMRI method is sensitive to metabolic changes in the parts of the brain that are activated during a particular task. A local increase in metabolic rate results in an increased delivery of blood and increased oxygenation of the region participating in a task.

The blood oxygenation level–dependent (BOLD) effect is the basis of the fMRI signal. Like PET and SPECT, fMRI permits observing the brain “in action,” as a person performs cognitive tasks or experiences emotions. In addition to obtaining structural and functional information about the brain, MRI methodology has been used for other specialized investigations of the effects of alcohol on the brain.

For example, structural MRI can clearly delineate gray matter from white matter but cannot detect damage to individual nerve fibers forming the white matter. By tracking the diffusion of water molecules along neuronal fibers, an MRI technique known as diffusion tensor imaging (DTI) can provide information about orientations and integrity of nerve pathways, confirming earlier findings from post mortem studies which suggested that heavy drinking disrupts the microstructure of nerve fibers.

  • Moreover, the findings correlate with behavioral tests of attention and memory (Pfefferbaum et al.2000).
  • These nerve pathways are critically important because thoughts and goal–oriented behavior depend on the concerted activity of many brain areas.
  • Another type of MRI application, magnetic resonance spectroscopy imaging (MRSI), provides information about the neurochemistry of the living brain.

MRSI can evaluate neuronal health and degeneration and can detect the presence and distribution of alcohol, certain metabolites, and neurotransmitters. Imaging of Brain Function: Electromagnetic Methods. In spite of their excellent spatial resolution—that is, the ability to show precisely where the activation changes are occurring in the brain—hemodynamic methods such as PET, SPECT, and fMRI have limitations in showing the time sequence of these changes.

  • Activation maps can reveal brain areas involved in a particular task, but they cannot show exactly when these areas made their respective contributions.
  • This is because they measure hemodynamic changes (blood flow and oxygenation), indicating the neuronal activation only indirectly and with a lag of more than a second.

Yet, it is important to understand the order and timing of thoughts, feelings, and behaviors, as well as the contributions of different brain areas. The only methods capable of online detection of the electrical currents in neuronal activity are electromagnetic methods such electroencephalography (EEG), event–related brain potentials (ERP), 4 and magnetoencephalography (MEG).

  • 4 The ERP method is considered derived from electroencephalography.) EEG reflects electrical activity measured by small electrodes attached to the scalp.
  • Event–related potentials are obtained by averaging EEG voltage changes that are time–locked to the presentation of a stimulus such as a tone, image, or word.

MEG uses sensors in a machine that resembles a large hair dryer to measure magnetic fields generated by brain electrical activity. These techniques are harmless and give us insight into the dynamic moment–to–moment changes in electrical activity of the brain.

  1. They show when the critical changes are occurring, but their spatial resolution is ambiguous and limited.
  2. ERP and MEG have confirmed that alcohol exerts deleterious effects on multiple levels of the nervous system.
  3. These effects include impairment of the lower–level brain stem functions resulting in behavioral symptoms such as dizziness, involuntary eye movement (i.e., nystagmus), and insecure gait, as well as impairment of higher order functioning such as problem solving, memory, and emotion.

ERP and MEG are remarkably sensitive to many alcohol–related phenomena and can detect changes in the brain that are associated with alcoholism, withdrawal, and abstinence. That is, these methods show different activity patterns between healthy and alcohol–dependent individuals, those in withdrawal, and those with a positive family history of alcoholism.

  1. As shown in figure 3, when brain electrical activity is measured in response to target stimuli (which require the subject to respond in some way) and nontarget stimuli (to be ignored by the subject), the brains of alcoholics are less responsive than the brains of nonalcoholic control subjects.
  2. Some of the ERP abnormalities observed in alcoholics do not change with abstinence, and similar abnormalities have been reported in patients who do not drink but come from families with a history of alcoholism.

The possibility that such abnormalities may be genetic markers for the predisposition for alcoholism is under intensive scrutiny in studies combining genetic and electromagnetic measures in people with or without a family history of alcoholism (Porjesz and Begleiter 1998).

Figure 3 Brain electrical activity measured as event–related potentials (ERPs) in response to target stimuli (which require the subject to respond in some way) and nontarget stimuli (to be ignored by the subject). The brains of alcoholics are less responsive than the brains of nonalcoholic control subjects. The heights of the peaks are measured in terms of the strength of the electrical signal (volts) recorded from the scalp over time (in thousandths of a second, or mS). SOURCE: Porjesz and Begleiter 1995.

IMPLICATIONS FOR TREATMENT Because alcoholism is associated with diverse changes to the brain and behavior, clinicians must consider a variety of treatment methods to promote cessation of drinking and recovery of impaired functioning. With an optimal combination of neuropsychological observations and structural and functional brain imaging results, treatment professionals may be able to develop a number of predictors of abstinence and relapse outcomes, with the purpose of tailoring treatment methods to each individual patient.

Neuroimaging methods have already provided significant insight into the nature of brain damage caused by heavy alcohol use, and the integration of results from different methods of neuroimaging will spur further advances in the diagnosis and treatment of alcoholism–related damage. Clinicians also can use brain imaging techniques to monitor the course of treatment because these techniques can reveal structural, functional, and biochemical changes in living patients across time as a result of abstinence, therapeutic interventions, withdrawal, or relapse.

For example, functional imaging studies might be used to evaluate the effectiveness of drugs such as naltrexone on withdrawal–induced craving. (Naltrexone is an anticraving medicine that suppresses GABA activity.) Additionally, neuroimaging research already has shown that abstinence of less than a month can result in an increase in cerebral metabolism, particularly in the frontal lobes, and that continued abstinence can lead to at least partial reversal in loss of brain tissue (Sullivan 2000).

  • Neuroimaging indicators also can be useful in prognosis, permitting identification and timely treatment of patients at high risk for relapse.
  • SUMMARY Alcoholics are not all alike; they experience different subsets of symptoms, and the disease has different origins for different people.
  • Therefore, to understand the effects of alcoholism, it is important to consider the influence of a wide range of variables.

Researchers have not yet found conclusive evidence for the idea that any one variable can consistently and completely account for the brain deficits found in alcoholics. The most plausible conclusion is that neurobehavioral deficits in some alcoholics result from the combination of prolonged ingestion of alcohol, which impairs the way the brain normally works, and individual vulnerability to some forms of brain damage.

  1. Characterizing what makes alcoholics “vulnerable” remains the subject of active research.
  2. In the search for answers, it is necessary to use as many kinds of tools as possible, keeping in mind that specific deficits may be observed only with certain methods, specific paradigms, and particular types of people with distinct risk factors.

Neuroscience provides sensitive techniques for assessing changes in mental abilities and observing brain structure and function over time. When techniques are combined, it will be possible to identify the pattern, timing, and distribution of the brain regions and behaviors most affected by alcohol use and abuse.

Electromagnetic methods (ERP and MEG) specify the timing of alcohol–induced abnormalities, but the underlying neural substrate (i.e., the anatomical distribution of the participating brain areas) cannot be unequivocally evaluated based on these methods alone. Conversely, the hemodynamic methods (fMRI, PET, and SPECT) have good spatial resolution but offer little information about the sequence of events.

Drawing on the respective advantages of these complementary methods, an integrated multimodal approach can reveal where in the brain the critical changes are occurring, as well as the timing and sequence in which they happen (Dale and Halgren 2001). Such confluence of information can provide evidence linking structural damage, functional alterations, and the specific behavioral and neuropsychological effects of alcoholism.

  1. These measures also can determine the degree to which abstinence and treatment result in the reversal of atrophy and dysfunction.
  2. REFERENCES ADAMS, K.M.; GILMAN, S.; JOHNSON–GREENE, D.; et al.
  3. Significance of family history status in relation to neuropsychological test performance and cerebral glucose metabolism studied with positron emission tomography in older alcoholic patients.

Alcoholism: Clinical and Experimental Research 22(1): 105–110, 1998. American Psychiatric Association (APA). Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Washington, DC: APA, 1994. BATES, M.E.; BOWDEN, S.C.; and BARRY, D. Neurocognitive impairment associated with alcohol use disorders: Implications for treatment.

  • Experimental and Clinical Psychopharmacology 10(3):193–212, 2002.
  • BERGLUND, M.
  • Cerebral blood flow in chronic alcoholics.
  • Alcoholism: Clinical and Experimental Research 5:295–303, 1981.
  • CALA, L.A., and MASTAGLIA, F.L.
  • Computerized tomography in chronic alcoholics.
  • Alcoholism: Clinical and Experimental Research 5(2):283–294, 1981.

CREWS, F.T. Neurotoxicity of alcohol: Excitotoxicity, oxidative stress, neurotrophic factors, apoptosis, and cell adhesion molecules. In: Noronha, A.; Eckardt, M.J.; and Warren, K., eds. Review of NIAAA’s Neuroscience and Behavioral Research Portfolio. National Institute on Alcohol Abuse and Alcoholism (NIAAA) Research Monograph No.34.

Bethesda, MD: NIAAA, 2000. pp.189–206. DALE, A.M., and HALGREN, E. Spatiotemporal mapping of brain activity by integration of multiple imaging modalities. Current Opinion in Neurobiology 11(2):202–208, 2001. GANSLER, D.A.; HARRIS, G.J.; OSCAR–BERMAN, M.; et al. Hypoperfusion of inferior frontal brain regions in abstinent alcoholics: A pilot SPECT study.

Journal of Studies on Alcohol 61:32–37, 2000. GILMAN, S.; ADAMS, K.; KOEPPE, R.A.; et al. Cerebellar and frontal hypometabolism in alcoholic cerebellar degeneration studied with positron emission tomography. Annals of Neurology 28:775–785, 1990. HARPER, C.

  1. The neuropathology of alcohol–specific brain damage, or does alcohol damage the brain? Journal of Neuropathology and Experimental Neurology 57(2):101–110, 1998.
  2. ORNREICH, C.; PHILIPPOT, P.; FOISY, M.L.; et al.
  3. Impaired emotional facial expression recognition is associated with interpersonal problems in alcoholism.

Alcohol and Alcoholism 37:394–400, 2002. LISHMAN, W.A. Alcohol and the brain. British Journal of Psychiatry 156:635–644, 1990. MONNOT, M.; LOVALLO, W.R.; NIXON, S.J.; and ROSS, E. Neurological basis of deficits in affective prosody comprehension among alcoholics and fetal alcohol–exposed adults.

  • Journal of Neuropsychiatry and Clinical Neuroscience 14:321–328, 2002.
  • MOSELHY, H.F.; GEORGIOU, G.; and KAHN, A.
  • Frontal lobe changes in alcoholism: A review of the literature.
  • Alcohol and Alcoholism 36:357–368, 2001.
  • OSCAR–BERMAN, M.
  • Neuropsychological vulnerabilities in chronic alcoholism.
  • In: Noronha, A.; Eckardt, M.J.; and Warren, K.; eds.

Review of NIAAA’s Neuroscience and Behavioral Research Portfolio. National Institute on Alcohol Abuse and Alcoholism (NIAAA) Research Monograph No.34. Bethesda, MD: NIAAA, 2000. pp.437–471. OSCAR–BERMAN, M., and SCHENDAN, H.E. Asymmetries of brain function in alcoholism: Relationship to aging.

  • In: Connor, L.T., and Obler, L.K., eds.
  • Neurobehavior of Language and Cognition: Studies of Normal Aging and Brain Damage,
  • New York: Kluwer Academic Publishers, 2000.
  • Pp.213–240.
  • PARSONS, O.A.
  • Alcohol abuse and alcoholism.
  • In: Nixon, S.J., ed.
  • Neuropsychology for Clinical Practice,
  • Washington, DC: American Psychological Press, 1996.

pp.175–201. PETRAKIS, I.L.; GONZALEZ, G.; ROSENHECK, R.; and KRYSTAL, J.H. Comorbidity of alcoholism and psychiatric disorders. Alcohol Research & Health 26:81–89, 2002. PFEFFERBAUM, A.; SULLIVAN, E.V.; MATHALON, D.H.; and LIM, K.O. Frontal lobe volume loss observed with magnetic resonance imaging in older chronic alcoholics.

  • Alcoholism: Clinical and Experimental Research 21:521–529, 1997.
  • PFEFFERBAUM, A.; SULLIVAN, E.V.; HEDEHUS, M.; et al.
  • In vivo detection and functional correlates of white matter microstructural disruption in chronic alcoholism.
  • Alcoholism: Clinical and Experimental Research 24:1214–1221, 2000.
  • PORJESZ, B., and BEGLEITER, H.

Event–related potentials and cognitive function in alcoholism. Alcohol Health & Research World 19(2):108–112, 1995. PORJESZ, B., and BEGLEITER, H. Genetic basis of event–related potentials and their relationship to alcoholism and alcohol use. Journal of Clinical Neurophysiology 15:44–57, 1998.

ROURKE, S.B., and LÖBERG, T. The neurobehavioral correlates of alcoholism. In: Nixon, S.J., ed. Neuropsychological Assessment of Neuropsychiatric Disorders, 2d ed. New York: Oxford University Press, 1996. pp.423–485. SULLIVAN, E.V. Neuropsychological vulnerability to alcoholism: Evidence from neuroimaging studies.

In: Noronha, A.; Eckardt, M.J.; and Warren, K., eds. Review of NIAAA’s Neuroscience and Behavioral Research Portfolio, National Institute on Alcohol Abuse and Alcoholism (NIAAA) Research Monograph No.34. Bethesda, MD: NIAAA, 2000. pp.473–508. SULLIVAN, E.V.; ROSENBLOOM, M.J.; LIM, K.O.; and PFEFFERBAUM, A.

Longitudinal changes in cognition, gait, and balance in abstinent and relapsed alcoholic men: Relationships to changes in brain structure. Neuropsychology 14:178–188, 2000. VALENZUELA, C.F. Alcohol and neurotransmitter interactions. Alcohol Health & Research World 21: 144–148, 1997. WEISS, F., and PORRINO, L.J.

Behavioral neurobiology of alcohol addiction: Recent advances and challenges. Journal of Neuroscience 22:3332–3337, 2002. WUETHRICH, F.B. Neurobiology: Does alcohol damage female brains more? Neurobiology 291(55):2077–2078, 2001. : Alcoholism and the Brain: An Overview

Adblock
detector