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Alcohol Dependence: Diagnosis, Clinical Aspects, and Biopsychosocial Causes

By Joseph R. Volpicelli, M.D., Ph.D. 

Substance Abuse Library 1997 by Treatment Research Center, University of Pennsylvania.

Alcohol drinking has decreased in recent years. Still, two- thirds of all adults drink alcohol and one-third of all high school seniors report that they drink alcohol. The average alcohol consumption for Americans over the age of 14 is 3 gallons of pure alcohol per person per year. The lifetime prevalence of alcoholism is about thirteen percent in the United States. There are significant sex differences: about five times as many men as women are alcohol-dependent . About one in five of the people who use alcohol for recreational purposes become alcohol-dependent for some part of their lives. Later, we will discuss why certain people may be at special risk to become dependent on alcohol.

Alcohol-related deaths account for about five percent of all deaths in the U.S.--this ranks alcohol-related death between the 3rd (cerebrovascular diseases) and 4th (injuries) major causes of death (Stinson, 1992). It is impossible to calculate the high cost of human suffering, but we can calculate the cost of alcohol dependence with medical complications, lost work productivity and legal costs. On this basis alone, it is estimated that alcohol dependence costs society about 116 billion dollars per year (National Council on Alcoholism, 1986). About 40 percent of all hospital admissions are alcohol-related. Alcohol-dependent people use health services at twice the rate of the general population. Alcohol dependence is the leading cause of lost productivity resulting from missed work days, as well as, home and industrial accidents. Legal costs from drunk driving and the prosecution of rapes and homicides also contributes to the high cost of alcohol dependence.


When does someone cross that boundary between recreational alcohol use and dependence? Three main symptom clusters have been used to help draw this distinction.

Loss of Control. Some people have defined addiction by focusing on the degree of control over alcohol. In the past, addiction experts called this psychological dependence. For example, a business executive may plan to have 1 or 2 beers after work, but he ends up having 5 or 6. Loss of control also becomes evident when a person makes repeated, but unsuccessful, attempts to cut down or stop drug use. Finally, loss of control is marked by compulsive thoughts and actions. Much of the day is spent either thinking about getting high again or recovering from a previous high.

Maladaptive Consequence. A second measure of alcohol dependence is the presence of negative psychological, social, and medical consequences. As discussed above alcohol dependence is the leading cause of missed days at work. Alcohol dependence is also associated with severe medical problems which we will discuss in more detail below. People who continue to use alcohol despite adverse effects on their health, occupational or social functioning show symptoms of alcohol dependence.

Biological Adaptation. Finally, some substance abuse experts define dependence solely with physiological adaptation to alcohol. In the past this has been referred to as physical dependence. Physical dependence is shown by either tolerance or withdrawal. Tolerance is defined as a decrease in the response to alcohol as use continues over time. Thus, it takes a progressively larger amounts of alcohol to produce the same effect. Chronic alcohol users may also experience withdrawal symptoms such as rapid heart rates or excessive sweating when they stop or decrease alcohol drinking. People who show either physical tolerance or symptoms of withdrawal are said to be physically adapted to the drug.



The behavioral effects of alcohol intoxication depend on two factors: one's beliefs and expectations about alcohol and the amount of alcohol consumed. These factors interact in complex ways to influence behavior.

For example, many people think that alcohol can increase sexual arousal. Contrary to these expectations, sexual arousal decreases as blood alcohol level increases. However, sexual arousal increases for people who believe they have consumed alcohol, but have really been given a non-alcohol substitute.

The dose of alcohol also interacts with alcohol's psychological effects. Alcohol is a CNS depressant. At low doses, however, it selectively depresses inhibitory centers. This means that alcohol may decrease behavioral inhibitions at low doses, and paradoxically increase aggressive or social behaviors. For example, some people will have a drink or two before a social function to decrease their social inhibitions. Other people are more likely to express their feelings including anger when intoxicated. About one half of all suicides and homicides occur during alcohol intoxication. Also, thirty-five percent of all rapes are related to alcohol drinking, particularly date rapes.

At higher concentrations (BAC > 100 mg %), alcohol depresses both the excitatory and inhibitory centers. That is it suppresses everything, from rational thinking to motor coordination. Alcohol drinking is responsible for about 50 percent of fatal car accidents and accounts for 25,000 traffic fatalities each year. At still higher concentrations (BAC > 500 mg %), alcohol suppresses consciousness leading to blackouts. Finally, alcohol can suppress respiratory centers and, particularly when combined with other sedatives (e.g.Valium), can lead to death.

Chronic Alcohol Dependence

There are several medical and psychiatric complications from alcohol dependence. Clinical effects of alcohol dependence are summarized below.

Gastrointestinal. Alcohol dependence is the most common cause of cirrhosis of the liver, the eighth leading cause of death in the United States. Alcohol is also associated with other gastrointestinal disorders such as ulcers, gastritis, and pancreatic cancer.

Cardiovascular. Alcohol causes several cardiovascular complications and is responsible for about 15% of all cases of hypertension and most of the cases of cardiomyopathy.

Neurological. Chronic alcohol dependence can produce severe damage to the peripheral and central nervous system. Peripheral neuropathy is often responsible for the ataxia seen in chronic alcoholics. Other neurological complications caused by chronic alcohol abuse include the following: Wernicke's disease (ocular disturbance, ataxia and confusion) associated with thiamine deficiency, Korsakoff's psychosis, a permanent inability to learn new information and finally, structural changes in the brain associated with severe cognitive impairment (dementia).

Immunologic. Alcohol drinking suppresses neutrophil function and cell-mediated immunity. This predisposes alcoholics to serious infections including fatal cases of pneumonia and tuberculosis. Suppression of cell-mediated immunity may be responsible for the higher incidence of several types of cancers seen in alcoholics.

Endocrine. Male alcoholics have increased estrogen and decreased testosterone. This leads to impotence, testicular atrophy and gynecomastia.

Obstetric. An often overlooked complication of alcohol drinking is the adverse effects of alcohol during pregnancy that can cause mental retardation, facial deformity, other neurological problems (fetal alcohol syndrome).

Psychiatric. Chronic alcohol dependence is often associated with emotional problems. Many alcoholics have co-existing anxiety disorders (about 25%), depression (20%-40%), and occasionally hallucinations (alcohol hallucinosis). It is not clear if psychiatric disorders predispose to alcohol dependence (self- medication hypothesis) or result from chronic abuse of alcohol. Alcohol-dependent patients are often suicidal, and about one-quarter of all suicides are committed by alcoholics, generally white males over 35 years old.


Just as alcohol intake depresses the nervous system, alcohol withdrawal produces overexcitation of the nervous system. Many alcoholics begin to experience tremors called "the shakes" about 24 hours after their last drink. Without a drink, they begin to experience rapid heart rates, sweating, decreased appetite, and difficulty sleeping. For some individuals, symptoms of withdrawal can become quite severe. One to three days after their last drink, alcoholics can have a generalized seizure (rum fits). About three to five days after their last drink, these patients can suffer from disorientation, high fevers, and visual hallucinations. This syndrome is call delirium tremens (DTs). During the DTs people are very susceptible to suggestion. For example, one patient became convinced that a pink elephant was dancing on an imaginary string between his therapist's fingers. Individuals in DTs can also be paranoid. The DTs are a serious medical emergency. Before aggressive modern medical treatment, fifteen percent of patients with DTs died. Now with adequate medication and nutritional support, fatalities from DT's are rare.

Following this initial withdrawal phase, many people go through protracted alcohol withdrawal. This can last anywhere from one to four weeks. People in the protracted withdrawal phase remain anxious and have difficulty eating and sleeping. In serious cases, alcohol hallucinosis occurs.




All the psychological theories of drug dependence assume that alcohol satisfies some important need. Psychoanalytic theories focus on unconscious needs while behavioral theories focus on the role of tension reduction to account for alcohol abuse.

Psychoanalytic. One early psychoanalytic theory suggested that children who are fixated at the oral stage are more prone to abuse alcohol later in life. Psychoanalysts theorize that oral fixation results when children are either frustrated in their oral dependent needs (unloving mother) or too easily satisfied by oral stimulation (overprotective mother). When stressed as adults, oral-dependent people are more likely to turn to alcohol to cope.

Adams (1978) suggests that it is not deprived infants who develop oral traits but rather children (particularly boys) with overprotective mothers. Later in life such men will have a strong need to remain dependent on either their mother or another woman. When their needs become frustrated, they become angry. Unable to deal with anger assertively, these people find that alcohol provides an effective way to reduce aggressive impulses. It has the additional advantage of hurting those people around them.

Psychoanalytic theories make some intuitive sense since many alcoholics have immature social skills. They often turn to alcohol to help cope with life stresses. Despite this intuitive appeal, there are little prospective data to support these theories. An alcohol dependent person may exhibit dependent traits, however, these traits are just as likely to result from chronic alcohol use as they are to lead to it. Even if correlations exist between alcohol abuse and dependent personalities, it is not clear which is the cause and which is the effect. In summary, there is little evidence to support the oral fixation theory.

Tension Reduction. Another important theory for alcohol abuse is that alcohol drinking is reinforced because alcohol reduces tension. Conger (1951) proposed the Tension Reduction Hypothesis as a model for alcohol drinking. The model assumes that alcohol can reduce tension and people learn to drink alcohol to avoid or reduce unpleasant stress. Clinical observations and studies appear to support this theory.

First, alcohol dependence and anxiety symptoms often coexist. Many anxious patients say that drinking alcohol helps them reduce anxiety. This is especially true of phobic patients who often use alcohol to help face their fears. One patient could only travel over bridges after drinking five or more beers. Another patient needed to drink before attending any social function. She would have one or two drinks while getting dressed and another two or three at the social function to help her feel more relaxed. One can easily see how using alcohol in this way can quickly lead to the sorts of problems we have outlined.

Alcohol relapse often occurs following a negative life event such as loss of a job or death of a spouse (Marlatt and Gordon, 1980). For example, one patient had a very severe relapse following the breakup with his girlfriend. Stress from the breakup may have increased the patient's desire to use alcohol to relieve this stress. Epidemiological studies also support the Tension Reduction Hypothesis, since alcohol drinking is associated with cultural stress. States with high rates of divorce, births, unemployment and other stressful life events also have high rates of alcohol abuse (Linksky, Straus, and Colby, 1985).

While clinical and epidemiological studies support the Tension Reduction Hypothesis, experimental studies fail to show that increased tension leads to increased drinking. If people drink alcohol to reduce tension, we would expect that alcohol drinking would increase during tension-arousing situations. This prediction led to many conflicting results. For example, in laboratory studies, subjects who are threatened with an electric shock or who receive feedback that they have done poorly on a test do not increase drinking.

How can we account for these conflicting results? The tension reducing properties of alcohol may be specific to certain situations. Alcohol may reduce tension only for social stress but not for other sorts of stresses. Also, alcohol may reduce tension only in particular doses (low doses but not high doses) and under certain conditions (in naturalistic but not experimental situations). In addition, alcohol may reduce tension only for some individuals who carry a gene for alcoholism. Finally, alcohol may not reduce tension but may dampen the impact of a stressful situation. The results of several studies support this hypothesis. Experienced male drinkers who are threatened with electric shock or social evaluation show less subjective and physiological signs of anxiety when intoxicated than when sober (Levenson, et al., 1980).

Recent reviews suggest yet another view of the relationship between stress and alcohol drinking. According to this analysis people do not drink alcohol to reduce tension. Rather, they drink once tension has stopped and a sense of relief has set in. This is known as the "happy hour" effect. It accounts for the frequent observation that anxiety and alcohol drinking often go together. However, it is the sudden removal of stress that sets the occasion for drinking, rather than the situation causing stress . For example, Volpicelli et al. (1990) found that rats increased their alcohol drinking following, but not during, uncontrollable stress. In another study, rats living in a fearful environment tended to drink less alcohol than rats removed from the fearful environment and placed in a safe, home cage (Volpicelli, et al., 1982). One study of college students showed similar results. After completing a difficult (stressful) test, half the students were told they did poorly, scoring in the lower 15th percentile of their peers. The other half were told they did well, scoring in the upper l5th percentile. The relieved subjects--who thought they did well on the test -- drank more alcohol than subjects who believed they did poorly (Lisman, 1986).


Genetics. Researchers have discovered that alcohol dependence runs in families. A classic study by Goodwin (1974), compared the adopted children of alcohol-dependent parents to the adopted children of non-alcohol-dependent parents. In the children of alcohol-dependent biological parents, the risk of becoming alcohol dependent increased. In contrast, if the adoptive parents were alcohol-dependent, there was no increased risk of alcoholism. In general, if one biological parent is alcoholic, the likelihood of a child becoming dependent increases nearly three times. If both parents are alcoholic, the likelihood of alcohol dependence increases about five times. However, the likelihood of alcohol dependence does not increase in children whose nonbiological parent is dependent on alcohol. This work shows that genetic factors affect the risk of alcohol dependence more than the family environment.

In an attempt to determine what specific inherited factor(s) increase their risk of alcohol abuse, researchers have conducted a series of studies comparing the biological children of alcohol dependent parents to the biological children of non-alcoholic parents. Several differences emerge between these two groups.

One source of biological vulnerability suggests that high risk subjects have some instability in their nervous system that can be counteracted by drinking alcohol. For example, sons of alcohol dependent fathers are less able to hold their body still when asked to stand at attention, compared to sons of nonalcoholic fathers (Hegedus et al., 1984). Typically, people without alcoholic fathers sway more when intoxicated. However, when sons of alcoholic fathers drink alcohol, there is less body sway (Schuckit, 1985). Also, patients who have an inherited disorder in which their hand shakes, familial essential tremor, are more likely to abuse alcohol. When they drink alcohol, the tremor vanishes.

Another biological mechanism that may put people at risk for alcohol dependence is increased sensitivity to the pleasure producing effects of alcohol. Alcohol dependent patients will often report that they noticed a wonderful calm high the very first time they drank alcohol. Alcohol dependent patients also show pain relief, analgesia, following a small dose of alcohol. These studies suggest that alcoholics receive more pleasure or obtain more pain relief compared to non-alcohol abusing people.

Similarly people who are not abusing alcohol, but have alcohol dependent parents, are more sensitive to the pleasure producing effects from alcohol. They report more pleasure associated with their first drink (Negoshi and Wilson,1987). Also, high risk people show increased alpha waves (a measure of relaxation) after a small dose of alcohol. Finally, studies show that in subjects with alcoholic parents, small doses of alcohol increase peripheral levels of beta-endorphin by 170 percent. In contrast, subjects without alcoholic parents do not have this large increase in beta-endorphin (Gianoulakis, 1990).


    Goodwin, D. W. (1989). Alcoholism. In H. I. Kaplan and B. J. Sadock (Eds.), Comprehensive Textbook of Psychiatry. 5th ed. (pp. 686-698). Baltimore: Williams & Wilkins.

    U. S. Department of Health. (1990). Alcohol and Health. U.S. Gov't. Publication Office: DHHS Publication No. (ADM) 90-1656.

    Schuckit, M. A. (1992). Genetic contributions to alcoholism. Clinical Neuropharmacology, 15, 72A-73A.

    Volpicelli, J. R. (1987). Uncontrollable events and alcohol drinking. British Journal of Addiction, 82, 381-392.

Alexander DeLuca, M.D., FASAM.
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Revised: November 24th, 2001.
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