Alcoholism

Back

Practice Essentials

Alcohol use is the fourth leading cause of preventable death in the United States (after smoking, high blood pressure, and obesity). According to a 2018 report from the WHO, in 2016 the harmful use of alcohol resulted in about 3 million deaths, or 5.3% of all deaths around the world, with most of these occurring among men.[1, 2] The economic costs of excessive alcohol consumption in 2010 were estimated at $249 billion, or $2.05 a drink.[3]

Signs and symptoms

The diagnosis of an alcohol problem is best made by the history. Screening instruments for alcohol problems include the CAGE ([need to] cut down [on drinking], annoyance, guilt [about drinking], [need for] eye-opener) questionnaire and the AUDIT (alcohol use disorders identification test). The CAGE questions should be given face-to-face, whereas AUDIT can be given as a paper-and-pencil test.

The following are signs and symptoms of alcohol withdrawal:

The following are signs of delirium tremens (ie, alcohol withdrawal delirium):

The following are signs of chronic alcoholism:

Complications of alcoholism manifest as follows:

See Clinical Presentation for more detail.

Diagnosis

Alcohol biomarkers are physiologic indicators of alcohol exposure or ingestion and may reflect the presence of an alcohol use disorder. These biomarkers are not meant to be a substitute for a comprehensive history and physical examination. Indirect alcohol biomarkers, which suggest heavy alcohol use by detecting the toxic effects of alcohol, include the following[4] :

Direct alcohol biomarkers include alcohol itself and ethyl glucuronide (EtG).[4] A blood alcohol level detects alcohol intake in the previous few hours and thus is not necessarily a good indicator of chronic excessive drinking.[5] Blood alcohol levels that indicate alcoholism with a high degree of reliability are as follows:

Features of EtG are as follows:

See Workup for more detail.

Management

The first step in treatment is brief intervention.

Further treatment of alcoholism involves the following:

See Treatment and Medication for more detail.

Background

Alcoholism is common, serious, and expensive. Physicians encounter alcohol-related cirrhosis, cardiomyopathy, pancreatitis, and gastrointestinal bleeding, as well as intoxication and alcohol addiction, on a daily basis. Alcoholism is also associated with many cancers. Wernicke encephalopathy and Korsakoff psychosis are also important causes of chronic disability as well as dementia. Fetal alcohol syndrome is a leading cause of mental retardation. In addition, accidents (especially automobile), depression, dementia, suicide, and homicide are important consequences of alcoholism.

Alcohol-related diseases are discussed in separate articles. The focus of this article is screening, diagnosis, treatment, and new research findings on the natural history and heritability of alcoholism.

Pathophysiology

Alcohol affects virtually every organ system in the body and, in high doses, can cause coma and death. It affects several neurotransmitter systems in the brain, including opiates, GABA, glutamate, serotonin, and dopamine. Increased opiate levels help explain the euphoric effect of alcohol, while its effects on GABA cause anxiolytic and sedative effects.

Alcohol inhibits the receptor for glutamate. Long-term ingestion results in the synthesis of more glutamate receptors. When alcohol is withdrawn, the central nervous system experiences increased excitability. Persons who abuse alcohol over the long term are more prone to alcohol withdrawal syndrome than persons who have been drinking for only short periods. Brain excitability caused by long-term alcohol ingestion can lead to cell death and cerebellar degeneration, Wernicke-Korsakoff syndrome, tremors, alcoholic hallucinosis, delirium tremens, and withdrawal seizures. Opiate receptors are increased in the brains of recently abstinent alcoholic patients, and the number of receptors correlates with cravings for alcohol.

Frequency

United States

According to the 2015 National Survey on Drug Use and Health (NSDUH), 86.4% of people ages 18 or older reported that they drank alcohol at some point in their lifetime; 70.1% reported that they drank in the past year; 56.0% reported that they drank in the past month.[8]

These statistics are based on the US National Longitudinal Alcohol Epidemiologic Study. Alcoholism is prevalent in 20% of adult hospital inpatients. One in 6 patients in community-based primary care practices had problem drinking. The following apply to the US adult population:

Alcoholism is slightly more common in lower income and less educated groups. Vaillant studied the natural history of alcoholism and the differences between college-educated and inner-city alcoholic persons. He followed 2 cohorts (over 400 patients) of alcoholic patients over many years.[9]

According to Vaillant's research, inner-city men began problem drinking approximately 10 years earlier than college graduates (age 25–30 y vs age 40–45 y). Inner-city men were more likely to be abstinent from alcohol consumption than college graduates (30% vs 10%) but more likely to die from drinking (30% vs 15%). A large percentage of college graduates alternated between controlled drinking and alcohol abuse for many years. Returning to controlled drinking from alcohol abuse is uncommon, no more than 10%; however, this figure is likely to be high because it was obtained from self-reported data. Mortality in both groups was related strongly to smoking. Abstinence for less than 5–6 years did not predict continued abstinence (41% of men abstinent for 2 y relapsed).

According to the 2015 NSDUH, 12.5% of college students ages 18–22 reported heavy alcohol use in the past month compared with 8.5% of other persons of the same age.[8] Regarding binge drinking, 37.9% of college students ages 18–22 reported binge drinking in the past month compared with 32.6% of other persons of the same age.[8]

The National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) study suggests the transition from use to dependence was highest for nicotine users, followed by cocaine, alcohol, and cannabis users.[10] An increased risk of transition to dependence among minorities and those with psychiatric or dependence comorbidity highlights the importance of promoting outreach and treatment of these populations.

Binge drinking statistics from the CDC estimate more than 38 million US adults binge drink an average of 4 times a month and the most drinks they consume on average is 8. The report found that binge drinking is more common among households with incomes ≥$75,000, but the largest number of drinks consumed per occasion is highest among households with incomes of < $25,000.[11]  According to the 2015 National Survey on Drug Use and Health (NSDUH), 26.9% of people ages 18 or older reported that they engaged in binge drinking in the past month; 7% reported that they engaged in heavy alcohol use in the past month.[8]

International

The World Health Organization examined mental disorders in primary care offices and found that alcohol dependence or harmful use was present in 6% of patients. In Britain, 1 in 3 patients in community-based primary care practices had at-risk drinking behavior. Alcoholism is more common in France than it is in Italy, despite virtually identical per capita alcohol consumption.

Mortality/Morbidity

According to a 2018 report from the WHO, in 2016 the harmful use of alcohol resulted in about 3 million deaths, or 5.3% of all deaths around the world, with most of these occurring among men. Globally, an estimated 237 million men and 46 million women have alcohol-use disorders, with the highest prevalence in Europe and the Americas.[1, 2]

Worldwide, alcohol is responsible for a percentage of a number of conditions, as follows:

An analysis in the United Kingdom in 2010 found that overall, alcohol was found to be the most harmful drug to the person consuming and to others. However, this study does not mean that substances other than alcohol have no harmful consequences; heroin, cocaine, and methamphetamine were found to be the most harmful drugs to individuals themselves. In addition, this study did not address the issue of polydrug abuse, which is a common phenomenon in individuals abusing substances. The combination of alcohol and other substances can lead to serious adverse effects, and such combinations were not explored in this study.[12]

Below are the statistically significant relative risks from a study by the American Cancer Society for men and women who consume 4 or more drinks daily. A drink is defined as one 12-oz beer, one 4- to 5-oz glass of wine, or one mixed drink containing 1.5 oz of spirits (80 proof). The relative risk for the noted maladies with consumption of 4 or more drinks daily is as follows:

Moderate alcohol consumption (1–2 drinks/d) reduces the risk of cardiovascular disease in men and women by approximately 30%.[13, 14, 15] The effect of heavy alcohol consumption on the risk of cardiovascular disease varies in different studies. The person's drinking pattern appears to have an effect on cardiovascular disease. Drinking with meals may reduce the risk, while binge drinking increases risk (even in otherwise moderate drinkers).

Moderate alcohol consumption appears to increase the risk of breast cancer in women. Total mortality is reduced with moderate alcohol consumption but not with heavy alcohol consumption; the cardiovascular benefit is offset by cirrhosis, cancer, and injuries. The amount of alcohol associated with the lowest mortality appears to be 2 drinks per day in men and 1 drink or fewer per day in women. Moderate alcohol consumption reduces the risk of developing diabetes, but heavy alcohol consumption may increase the risk. The cardiovascular benefit becomes important in men older than 40 years and in women older than 50 years. The risk of hypertension is increased with 3 or more drinks daily.

No benefits are noted in people at low risk for coronary disease (men < 40 y and women < 50 y). Recent data suggest an increase in coronary calcification with moderate alcohol consumption in young adults.[16] This effect was exacerbated by binge drinking.

Of men aged 18–25 years, 60% binge drink. (Binge drinking is defined as 5 alcoholic drinks for men [4 for women] in a row.) Binge drinking significantly increases the risk of injury and contracting sexually transmitted diseases. Women who binge drink at this age are at higher risk of becoming pregnant and potentially harming an unborn child. (Any amount of alcohol consumption during pregnancy is risky.) Cohort data from the Prospective Epidemiological Study of Myocardial Infarction (PRIME) investigated alcohol use patterns on ischemic heart disease in Northern Ireland and France. Regular and moderate alcohol use throughout the week, a typical pattern in middle-aged men in France, was associated with a lower risk of ischemic heart disease, whereas the binge drinking pattern more prevalent in Northern Ireland was associated with a higher risk of ischemic heart disease.[17]

More than three quarters of all foster children in the United States are children of alcohol- or drug-dependent parents. From 60–70% of reported domestic violence incidents involve alcohol. Half of all violent crime is alcohol or drug related.

Overall, morbidity and mortality are related strongly to smoking, and people who drink heavily are less likely to quit smoking. Additionally, persons who begin smoking early are more likely to develop problems with alcohol.

With regard to pregnancy, fetal alcohol syndrome is the leading known cause of mental retardation (1 in 1000 births). More than 2000 infants annually are born with this condition in the United States. Alcohol-related birth defects and neurodevelopmental problems are estimated to be 3 times higher. Even small amounts of alcohol consumption may be risky in pregnancy. A 2001 study by Sood et al reported that children aged 6–7 years whose mothers consumed alcohol even in small amounts had more behavioral problems.[18] In a study from 2003, Baer et al showed that moderate alcohol consumption while pregnant resulted in a higher incidence of offspring problem drinking at age 21 years, even after controlling for family history and other environmental factors.[19] All women who are pregnant or planning to become pregnant should avoid alcohol.

Race

The two largest studies, the US National Comorbidity Survey and the Epidemiologic Catchment Area Survey, both showed a lower prevalence of alcoholism in African Americans than in white Americans. The prevalence was equal or higher in Hispanic Americans compared with white Americans.

Studies of Native Americans and Asian Americans are smaller. These studies indicate the prevalence of alcoholism is higher in Native Americans and lower in Asian Americans when compared with white Americans.

Sex

Alcoholism is at least twice as prevalent in men as it is in women. In the National Comorbidity Survey, it was 2.5 times more prevalent in men than in women. The lifetime prevalence was 20% in men and 8% in women. For alcohol abuse or dependence in the past year, the rates were 10% for men and 4% for women.

Women do not metabolize alcohol as efficiently as men. Hazardous drinking (not alcoholism) is greater than 1 drink daily for women and greater than 2 drinks daily for men.

Problem drinking in women is much less common than it is in men, and the typical onset of problem drinking in females occurs later than in males. However, progression is more rapid, and females usually enter treatment earlier than males. Women more commonly combine alcohol with prescription drugs of abuse than do males. Women living with substance-abusing men are at high risk.

Alcohol problems are less likely to be recognized in women, and women with alcohol problems are less likely to be treated. This may be because women are less likely than men to have job, financial, or legal troubles as a result of drinking.

Age

The prevalence of alcoholism declines with increasing age. The prevalence in elderly populations is unclear but is probably approximately 3%. A study of the US Medicare population found that alcohol-related hospitalizations were as common as hospitalizations for myocardial infarction.

Because of the growing population of older Americans, the number of heavy drinkers will increase from 1 million currently to 2 million by 2060.[20] The 2012—2013 National Epidemiologic Survey on Alcohol and Related Conditions III (NESARC III) found that 55.2% of adults age 65 and over drink alcohol. Most of them don’t have a drinking problem, but some of them drink above the recommended daily limits.[21]

Among older patients with alcoholism, from one third to one half develop alcoholism after age 60 years. This group is harder to recognize. A population-based study found that problem drinking (>3 drinks/d) was observed in 9% of older men and in 2% of older women. Alcohol levels are higher in elderly patients for a given amount of alcohol consumed than in younger patients.

Among younger individuals (such as college students), weekly or daily consumption of energy drinks (highly caffeinated beverages) has been strongly associated with alcohol dependence. This population is an important target population for alcohol use disorder prevention.[22]  

More than a quarter (27%) of all 15- to 19-year-olds worldwide consume alcohol. Rates are highest in Europe (44%), followed by the Americas (38%) and the Western Pacific (38%). Total alcohol consumption per capita among those older than 15 years around the world rose from 5.5 liters of pure alcohol in 2005 to 6.4 liters in 2010 and remained at that level in 2016.[1, 2]

History

Diagnosis

The diagnosis of an alcohol problem is best made by the history. Laboratory tests have a sensitivity of no better than 50%, and physical examination is helpful only after the consequences of alcoholism are apparent. Early diagnosis based on a careful history can prevent such consequences. Physicians should use terms such as "person with an alcohol problem" rather than "alcoholic" or "addict," which are commonly used but demeaning shorthand terms.

Although the dangers of alcoholism are well known, data suggest that physicians frequently fail to make the diagnosis. Less than 50% of people who went to their doctor because of alcohol-related issues were asked about the problem. Multiple studies on medical inpatients and surgical patients in university and community hospitals, as well as outpatients in internal medicine and family medicine practices, show a low recognition rate and an even poorer treatment rate. The following are possible reasons that alcohol-related problems are missed during diagnosis.

Screening

The US Preventive Services Task Force (USPSTF) recommends that clinicians screen all adult patients 18 years of age or older for alcohol misuse, as well as provide patients engaged in risky or hazardous drinking with brief behavioral counseling interventions to reduce alcohol misuse.[23, 24]

The USPSTF recommends the following screening tools:

The AUDIT (alcohol use disorders identification test) is the best test for screening because it detects hazardous drinking and alcohol abuse. Furthermore, it has a greater sensitivity in populations with a lower prevalence of alcoholism. One study suggested that questions 1, 2, 4, 5, and 10 were nearly as effective as the entire questionnaire. If confirmed, AUDIT would be easier to administer.

Table 1. AUDIT Questions and Scoring System



View Table

See Table

The AUDIT can be administered as a paper-and-pencil test, but the CAGE questionnaire should be administered face to face.

The CAGE ([need to] cut down [on drinking], annoyance, guilt [about drinking], [need for] eye-opener) questionnaire is the best-known and most-studied short screening test for alcohol problems. The CAGE questions should be given face-to-face (not as a paper and pencil test) and should be asked before questions on quantity and frequency (the sensitivity of the questions drops if quantity questions precede them).

The following 4 questions make up the CAGE questionnaire:

Patients who answer affirmatively to 2 questions are 7 times more likely to be alcohol dependent than the general population. Those who answer negatively to all 4 questions are one-seventh as likely to have alcoholism as the general population.

The sensitivity of the CAGE questionnaire was thought to be 75%. More recent studies, however, show that the sensitivity is lower, particularly in populations with a lower prevalence, such as among female and elderly populations. The CAGE questionnaire also may fail to identify binge drinkers and cannot identify those who have not experienced the consequences of alcoholism. Nevertheless, the CAGE questionnaire is brief and easy to administer

The CAGE questions are not useful for diagnosing hazardous drinking. Women should consume no more than 3 standard alcohol drinks on any one occasion and no more than 7 drinks per week[25] and men younger than 65 years should consume no more than 4 drinks on any one occasion and no more than 13 standards drinks per week. Men older than 65 years should follow recommendations for women. Other drinking considered hazardous is any use of alcohol by children, teens, by those with a personal or family history of alcohol dependence, women who are pregnant or breastfeeding, and use before or during situations requiring attention or skill (e.g., driving)

By itself, the CAGE questionnaire is not an adequate screening for alcohol problems.The CAGE questionnaire is less reliable when given after asking questions on frequency. If the patient answers questions on the CAGE questionnaire or AUDIT affirmatively, following up with additional questions about circumstances and reasons is important. Additional useful questions are found below (see Additional questions).

The diagnosis of alcohol dependence relies more on the consequences of alcohol use and less on the amount of alcohol consumed. Thus, if one suspects alcohol problems from answers to screening questions, attempt to determine what consequences of alcohol abuse the patient has experienced.

The Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5) changed from differentiating Alcohol Abuse and Alcohol Dependence to a single category of Alcohol Use Disorder. DSM-5 criteria are as follows:

A maladaptive pattern of substance use leading to clinically significant impairment or distress, as manifested by 2 or more of the following, occurring at any time in the same 12-month period:

Specify if the Alcohol Use Disorder is:

Specify if the Alcohol Use Disorder is:

Specify if the patient is in a controlled environment where access to alcohol is limited.[26]

Additional questions, as follows, may be helpful when screening for alcoholism:

Physical

The following are signs and symptoms of alcohol withdrawal:

The following are signs of delirium tremens (ie, alcohol withdrawal delirium):

The following are signs of chronic alcoholism:

Ataxia, ophthalmoplegia (usually lateral gaze palsy), and confusion indicate Wernicke encephalopathy.

Anterograde and retrograde amnesia, often with confabulation and preceded by Wernicke encephalopathy, indicates Korsakoff syndrome.

Asterixis and confusion suggest hepatic encephalopathy.

Causes

Patients commonly use a psychiatric disorder to deny alcohol abuse. Unless strong evidence indicates that the psychiatric disorder clearly precedes the alcoholism or is present during a long period of sobriety, the best plan is to proceed as if alcoholism is the primary diagnosis. Arrange a consultation with a psychiatrist for difficult cases because some patients who are treated for psychiatric conditions stop drinking and do very well.

The physician should, nonetheless, perform a brief mental status exam to help guide the referral process. Basic elements that should be covered in the mental status exam include an assessment of mood, perceptual problems such as hallucinations, and a safety screen. The use of a standardized instrument helps ensure important questions are asked and the results transmitted with some degree of objectivity. Several validated instruments exist, including The Patient Health Questionnaire from the Primary Care Evaluation of Mental Disorders (PRIME-MD)[27] and the Cornell Psychiatric Screen.[28]

Genetic psychiatric disorders, such as schizophrenia and bipolar disorder, are associated with alcoholism.[29] The presence of both a serious, persistent mental illness and alcoholism is called dual diagnosis. The physician must address both. Family history commonly reveals members with bipolar disorder, alcoholism, or both. Despite this and despite an intensive search for a gene for alcoholism, study results remain inconclusive. Nevertheless, some evidence indicates that genetics plays a major role in alcohol abuse.

Twin studies

Identical twins have a higher concordance for drinking behavior and possibly alcoholism than fraternal twins.

In a well-conducted twin study of 542 families, a single underlying trait for conduct disorder, antisocial personality, alcohol dependence, and drug dependence was found, which was highly heritable and was observed in both sexes.[30] Additionally, the study found that maximal alcohol consumption of fathers was predictive of their children having behavior and substance abuse problems (>24 drinks in 24 h yielded especially high risk). Not all at-risk children developed substance use or behavior problems. The environment seemed to determine which, if any, manifested. Deviant peers and poor parent-child relationships predicted early use (age < 15 y) of alcohol, which predicted later alcohol abuse and antisocial personality. This study applies to early-onset alcoholism and type 2 alcoholism. More work is needed on later-onset alcoholism and type 1 alcoholism.

Adoption studies

Whether reared by biologic or adoptive parents, sons of males with alcoholic problems are 4 times more likely to have problems with alcohol than sons of persons who are not.

Two Swedish studies have suggested the following 2 types of male alcoholism:

Data from adoption studies on daughters of persons with alcohol problems are less clear. Daughters might be at increased risk if the biological mother has alcoholism. A recent twin study in women found higher concordance in monozygotic twins than in dizygotic twins.

Experimental studies

Schuckit and Smith found that sons of persons with alcoholism respond differently to an alcohol challenge.[31] They report decreased subjective ratings for feeling intoxicated, and they objectively have less body sway when given the same amount of alcohol as sons of persons without alcoholism. The study population consisted of white, male college students who drank alcohol but were not alcohol dependent themselves. The fathers in this study could not have psychopathology other than alcoholism (i.e., no sociopathy, no bipolar illness).

Ten-year follow-up data have been published recently for the first half of this cohort. Of the sons of persons with alcoholism, 26% were alcohol dependent by age 30 years, as opposed to 9% of the control group. Furthermore, 56% of the sons of persons with alcoholism with lesser objective and subjective responses to alcohol became alcohol dependent, as opposed to 14% of the sons of persons with alcoholism who did not demonstrate these decreased responses. This also held true for the sons of fathers who did not have alcoholism, although the numbers were small.

Positive family history and lesser response to alcohol increased the likelihood of later development of alcohol dependence.

Psychological studies

Behavioral models explain alcohol abuse in terms of learning theory. Through operant conditioning, the reinforcing elements of alcohol use become habitual.

Cognitive models explain alcohol abuse in terms of “automatic thoughts,” which precede the person’s more identifiable feelings about alcohol. For example, an automatic thought might be “I deserve a drink because I’ve had a rough day."

Psychoanalytic models explain alcohol abuse in terms of ego defenses and intrapsychic conflicts. The alcohol serves as a way to escape the uncomfortable internal conflict.

Laboratory Studies

Biomarkers

Alcohol biomarkers are physiological indicators of alcohol exposure or ingestion and may reflect the presence of an alcohol use disorder. These biomarkers are not meant to be a substitute for a comprehensive history and physical examination by an appropriate health professional. Instead, alcohol biomarkers should be a complement to self-reported measures of drinking.[4]

In a population of psychiatric patients, research evidence has shown the usefulness of biological measures in the detection of alcohol use disorders when compared with patient self-report. A 2007 study of 486 consecutively admitted psychiatric patients showed a low correlation between self-reported consumption of alcohol and illicit drugs and biological measures; 52% of the patients underreported their consumption of illicit drugs when compared with urine toxicology screening results; 56% of patients underreported alcohol use as evaluated by carbohydrate-deficient transferrin (CDT), and 37% of patients underreported alcohol use as evaluated by CDT + gamma glutamyltransferase (GGT).[39] Replication of such research in a primary care population is needed to show that biological measures aid the primary care clinician in detecting alcohol use disorders.

Alcohol biomarkers are generally divided into indirect and direct biomarkers.[4]

Indirect alcohol biomarkers suggest heavy alcohol use by detecting the toxic effects that alcohol may have had on organ systems or body chemistry.[4]

Direct alcohol biomarkers are analytes of alcohol metabolism.[4]

Table 2. Sensitivity and Specificity of Alcohol Biomarkers*



View Table

See Table

Other Tests

The possibility of polysubstance abuse/dependence justifies performing a blood/urine toxicology screen for other substances of abuse.

Medical Care

A number of serious problems are closely linked to alcohol intoxication. In fact, according to the NIAAA, intoxication is present in 30% of homicides, 22% of suicides, and 33% of car crashes. Any patient who presents an imminent safety risk to themselves or another person should be considered a candidate for hospitalization. This may require the assistance of family members or medical consultation with a psychiatrist.

Many physicians believe no effective treatment is available for alcoholism; therefore, these physicians do not refer their patients for treatment. However, more than 13 studies representing more than 4000 patients demonstrate that brief interventions make a difference. Most of the patients in these studies drank heavily but did not yet have a problem with alcohol.

One study performed in Norway demonstrated that brief advice given early can affect gamma glutamyl transferase levels and reported alcohol consumption. Early warning makes a difference to persons who drink heavily. In a study of 200 workers with alcoholism, recalling a physician's warning about drinking at the beginning of the study was associated with a better prognosis 2 years later. Unfortunately, less than 25% had received warnings from their physicians, again illustrating the problem of missed diagnosis.

Alcoholism can also be categorized into 2 types: early-onset (biological predisposition to the disease) or late-onset (brought on by environmental or psychosocial triggers). Understanding and studying the difference between early- and late-onset alcoholism facilitate the selection of the appropriate therapy. Drugs that affect the rewarding behavior of neural activities, such as ondansetron, naltrexone, topiramate, and baclofen, have been shown to alter drinking behavior.[46]

The first step in treatment is brief intervention. The physician states unequivocally that the patient has a problem with alcohol and emphasizes that this determination stems from the consequences of alcohol in that patient's life, not from the quantity of alcohol consumed. Emphasizing the effects on family, friends, and occupation, as well as any physical manifestations, is important. Pointing out that loss of control and compulsive use indicate alcohol dependence also is important.

Present the diagnosis. Use explicit evidence; emphasize the consequences endured by the patient as a result of alcohol abuse. Be empathic and nonjudgmental. Avoid arguments about the diagnosis. Avoid use of the word alcoholic.

Indicate the responsibility for change is with the patient. Listen to the patient's goals and point out discrepancies between his or her goals and actions.

Determine the patient's readiness for change. Motivating a reluctant patient is one of the great challenges in treatment. To enhance the prospects of successful treatment, the clinician needs to have a basic concept of the stages of change. The 5 stages of change (Prochaska,) provide fundamental guidance for enhancing motivation. The Substance Abuse and Mental Health Services Administration, the Center for Substance Abuse Treatment presents this concept in detail through a Treatment Improvement Protocol titled "Enhancing Motivation for Change in Substance Abuse Treatment." The 5 stages of change are precontemplation, contemplation, preparation, action, and maintenance. Specific strategies aligned with each of the 5 stages help a clinician motivate and prepare the patient for change. The 5 stages of change represent a cycle, permitting and explaining behavior that moves in both progressive and regressive directions.

In the precontemplation phase, the individual does not express any interest in the need for change. Many individuals with substance use problems are firmly entrenched in this stage. The options in dealing with patients in this stage are limited and include pointing out the discrepancy between patient action and patient goals, suggesting that the patient bring a family member to the next appointment, and suggesting a 2-week abstinence trial.

Contemplation represents the first evidence of dynamic behavior. The individual expresses a tentative belief in the possibility that alcohol use might be harmful. The hallmark of this stage is ambivalence and skepticism. Skepticism is not the same as denial but instead allows some degree of personal reflection. The patient is receptive to new information, or just as likely reassured that current behavior is acceptable, in the absence of information. Thus, the clinician should influence the ambivalence characteristic of contemplation in a direction favoring change. This can include pointing out that the patient's actions are not congruent with their goals, giving pamphlets concerning alcohol abuse, and suggesting an abstinence trial.

When the clinician successfully alters the balance in favor of a healthy choice, the patient enters the preparation stage. The preparation stage is a thoughtful phase focused on making plans.

The action stage of change represents full recognition of a problem along with observable evidence of steps taken to reduce alcohol use. The clinician should reinforce and praise the decision to change. Emphasizing that the biggest error at this stage is to underestimate the amount of help needed to quit drinking is critical. The patient should be given a list of options for treatment including AA and pharmacotherapy.

Maintenance is the final and most mature stage of change. During the maintenance stage, motivational efforts are directed toward promoting hard won gains and preventing slips. Relapse prevention efforts are sustained by the patient's appreciation of specific environmental and biobehavioral triggers, which contribute to recurrence. See Follow-up.

As mentioned previously, the stages of change represent a cycle permitting both forward and backward movement.

The physician must state firmly, but empathically, that alcohol is a problem for the patient and that the patient determines the solution. Patients come for treatment through several means, often from a mixture of both coercion and concern. The clinician needs to understand the extent of resistance to effectively work with the patient. A good strategy is to learn about patients' goals and indicate discrepancies between their goals and their choices. Pointing out discrepancies is more effective initially than statements such as, "You have to quit," or, "You have to go to AA."

The patient's response determines the physician's next step. If the patient denies the problem, recommending joining AA will not work. Involving the family and/or suggesting a trial of abstinence is useful, and, importantly, the physician should follow up with the patient in a few weeks. The patient might be angry initially and storm out of the office, but then the patient might recall the physician's warning months or years later and stop drinking. For patients who recognize a problem and will consider referral, the cheapest (free) and most accessible option is AA.

The AA 12-step approach involves psychosocial techniques used in changing behavior (eg, rewards, social support networks, role models). Each new person is assigned an AA sponsor (a person recovering from alcoholism who supervises and supports the recovery of the new member). The sponsor should be older and should be of the same sex as the patient (opposite sex if the patient is homosexual).

Patients do not need a strong religious background to be successful in AA; they only need the belief in a power higher than themselves. Urge patients to use aspects of the program that can help them stay sober and ignore aspects that are not helpful.

Patients who have tried AA may have had a bad past experience. Patients should try at least 5-10 different meetings before giving up on the AA approach because each meeting is different. For example, women often do better at meetings for women only because the issues for female patients with alcoholism are different from the issues for male patients with alcoholism. A meeting in the suburbs might not be appropriate for someone from the inner city and vice versa.

The physician should have AA literature in the office (dates and places of meetings), have the AA phone number available, and know about other treatment services in the community, including referrals for medical consultants or specialists in chemical dependency. No randomized trials of AA have been performed, but a US Veterans Administration study suggested that patients who attended meetings did much better than those who refused to go.

AA can be reached via their Web site (Alcoholics Anonymous) or by mail (AA General Service; PO Box 459; Grand Central Station; New York, NY 10163). Physicians can order pamphlets and other patient education material from these sources.

Additional sources of help include the Substance Abuse Treatment FACILITY LOCATOR, Self-Help Group Sourcebook Online, and SMART Recovery. The acronym SMART is for Self-Management and Recovery Training.

Treatment of alcoholism involves the following:

Strongly encourage family members of patients with alcoholism to contact Al-Anon and Alateen via its Web site (Al-Anon/Alateen) or mailing address (Al-Anon Family Group Headquarters; PO Box 182; Madison Square Garden Station; New York, NY 10159-0182).

Consultations

Consultation with a psychiatrist might be indicated in cases in which questions of suicide, violence, or comorbid psychiatric disorders might be present.

Diet

Persons with alcoholism often have a poor diet. Folate deficiency is common. Advise patients to eat plenty of fruits and vegetables and consider a multivitamin supplement. Supplemental enteral nutrition improves survival in persons with advanced liver disease.

Guidelines Summary

Substance Abuse and Mental Health Services Administration

In March 2020, the Substance Abuse and Mental Health Services Administration (SAMHSA) released considerations for the care and treatment of mental and substance use disorders in the COVID-19 pandemic.[47]

SAMHSA advises that outpatient treatment options be used to the greatest extent possible. Inpatient facilities should be reserved for those for whom outpatient measures are not considered an adequate clinical option. SAMHSA strongly recommends the use of telehealth and/or telephonic services to provide evaluation and treatment of patients.

SAMHSA urges providers to consider utilizing benzodiazepines in situations in which they believe that the individual would not benefit from administration of anticonvulsant medications that have been effective in treatment of alcohol withdrawal.

US Preventive Services Task Force

The US Preventive Services Task Force (USPSTF) recommends screening adults 18 and older, including pregnant women, for unhealthy alcohol use in primary care settings. Those patients who engage in risky or hazardous drinking should be offered brief behavioral counseling interventions to reduce unhealthy alcohol use. The USPSTF also concludes the evidence is insufficient regarding screening for alcohol use in adolescents 12 to 17 in primary care settings.[48]

American Psychiatric Association

The American Psychiatric Association (APA) released the following guidelines in 2018:

The guideline also includes statements related to assessment and treatment planning. Evidence-based psychotherapeutic treatments for alcohol use disorder, including cognitive-behavioral therapy (CBT), 12-step facilitation, and motivational enhancement therapy, also play a major role in treatment. In addition, community-based peer support groups such as Alcoholics Anonymous (AA) and other programs are helpful for many patients.[49]  

Medication Summary

Treatment of alcohol withdrawal is best accomplished with benzodiazepines. Avoid fixed-dose therapy, and treat patients for symptoms. This results in use of lower doses of benzodiazepines, less patient sedation, and earlier patient discharge. Lorazepam and oxazepam are preferred for patients with significant liver disease because the half-lives of other benzodiazepines can be significantly prolonged. These shorter-acting benzodiazepines require more frequent patient monitoring. Use longer-acting drugs (eg, chlordiazepoxide) when monitoring is not reliable.

Other agents that have been used with some success in the treatment of withdrawal include beta-blockers, clonidine, phenothiazines, and anticonvulsants. All can be used with benzodiazepines, but none has been proven to be adequate as monotherapy. A number of medications have been tried in the treatment of alcoholism. Disulfiram (Antabuse) has been used as an adjunct to counseling and AA with motivated patients to reduce the risk of relapse. Patients are reminded of the risks of adverse effects when tempted to drink. Disulfiram causes nausea, vomiting, and dysphoria with coincident alcohol use. In a large trial, disulfiram did not increase abstinence. If a patient asks for disulfiram and thinks it will help, it might be worth considering.

Naltrexone blocks opiate receptors and works by decreasing the craving for alcohol, resulting in fewer relapses. A recent positron emission tomography study demonstrated that persons with alcoholism have increased opiate receptors in the nucleus accumbens of the brain and that the number of receptors correlates with craving.

Most, but not all, studies found that naltrexone decreases relapses but the effect is modest (12–20%). Combining naltrexone therapy with cognitive behavioral therapy enhanced benefit. One study showed benefit with an intensive primary care intervention. Studies suggest that virtually all placebo patients who sampled alcohol relapsed, while only half the naltrexone patients who sampled alcohol relapsed.

Most studies are of short duration, and more long-term trials are needed. In short-term studies when naltrexone was stopped, patients relapsed. Naltrexone has a greater effect on reducing relapse to heavy drinking than it does on maintaining abstinence. Extended-release intramuscular naltrexone resulted in reduced relapse to heavy drinking in a large, randomized trial. Its effects on complete abstinence were more modest. The main adverse effects are nausea and/or vomiting, abdominal pain, sleepiness, and nasal congestion.

In 2001, Sinclair reviewed 8 studies and suggested that naltrexone is safe to administer in patients who are still drinking and that it will gradually result in the patient consuming less alcohol (this is the case in laboratory animals).[50] Patients should take the naltrexone daily initially and then only when they have a strong urge to drink. Patients should carry naltrexone with them indefinitely. Patients should agree to always take the naltrexone prior to drinking alcohol. Daily naltrexone may be counterproductive in patients who remain abstinent. It is most helpful in those who sample alcohol after stopping (lower chance of a relapse). More data are needed before this approach can be adapted because it challenges the conventional wisdom that complete abstinence is always the goal of treatment.

Nalmefene is another opioid antagonist, and it blocks delta, kappa, and mu receptors; naltrexone acts primarily on mu receptors. One randomized trial with 100 patients using 10 mg PO bid has been completed, and nalmefene appears to have efficacy similar to naltrexone (reduces relapse to heavy drinking in patients who sample alcohol). At present, the drug is approved only for intravenous use for opiate addiction.

The 2010 Cochrane review on opioid antagonists for alcohol dependence included 50 studies with 7793 participants.[51] In most studies, treatment was provided over 3 months. The review showed that more patients who took naltrexone were able to reduce the amount and frequency of drinking compared with patients who took placebo. On average, 1 in 9 patients were helped by naltrexone. For injectable formulations of naltrexone, which can be advantageous for patients who have problems with taking their medication on schedule, and for the second opioid antagonist (nalmefene), the evidence was too limited to allow final conclusions. Nevertheless, available studies indicated that these drugs might have effects on drinking comparable to oral naltrexone.

A number of studies have focused on antidepressants. Early studies with the selective serotonin reuptake inhibitors (SSRIs) have been disappointing. Two fairly good studies used tricyclic antidepressants (ie, desipramine, imipramine), which showed some short-term benefit. More data are needed. SSRIs probably do not benefit patients who are not depressed but might benefit those who are depressed. Topiramate facilitates GABA function and antagonizes glutamate, which should decrease mesocorticolimbic dopamine after alcohol and reduce cravings. One double-blinded trial with 150 subjects for 12 weeks suggests this is the case (decreased drinking, decreased craving, and greater abstinence). Topiramate is not approved for this use by the US Food and Drug Administration.

The largest and longest studies on the treatment of alcohol abuse have been performed in Europe with acamprosate (Campral). At 1 year, the continuous abstinence rates were 18% in the acamprosate group and 7% in the placebo group. At 2 years, the continuous abstinence rates were 12% in the acamprosate group and 5% in the placebo group. Most patients returned to drinking while still using the drug. The drug is approved in the United States. It stimulates GABA transmission, inhibits glutamate, and decreases alcohol consumption in alcohol-dependent rats. The main adverse effect is diarrhea.

Two short-term trials have compared acamprosate and naltrexone. Both found naltrexone to be superior. One of these studies compared the combination with either drug alone and with placebo. The combination was statistically superior to placebo and acamprosate alone and superior (but not statistically) to naltrexone alone. Larger and longer trials of the combination therapy are needed.

Results from a 12-week, randomized, placebo-controlled trial of 150 adults with current alcohol dependence showed that patients treated with the anticonvulsant gabapentin were more likely to stop drinking or at least abstain from heavy drinking than those taking a placebo. In addition, gabapentin significantly reduced cravings, sleeplessness, and depression.[52, 53, 54]

A 2015 study funded by the National Institutes of Health (NIH) found that an antibiotic typically used to treat tuberculosis reduces alcohol cravings and may enhance cue-related extinction therapies in individuals with alcohol use disorders. Results showed that low doses of D-cycloserine (50 mg) significantly reduced alcohol cravings for up to 3 weeks, leading to significant reductions in alcohol consumption.[55, 56]

Acamprosate (Campral)

Clinical Context:  Synthetic compound with a chemical structure similar to that of the endogenous amino acid homotaurine (structural analogue of GABA). Mechanism of action to maintain alcohol abstinence not completely understood. Hypothesized to interact with glutamate and GABA neurotransmitters centrally to restore neuronal excitation and inhibition balance. Not associated with tolerance or dependence development. Use does not eliminate or diminish alcohol withdrawal symptoms. Indicated to maintain alcohol abstinence as part of a comprehensive management program that includes psychosocial support. Available as a 333-mg tab.

Class Summary

Mechanism of action is unknown, but it enhances GABA transmission and inhibits glutamate transmission. Compared with placebo, reduces drinking frequency and effectively increases abstinence in patients with alcoholism.

Disulfiram (Antabuse)

Clinical Context:  Decreases number of drinking days but does not increase abstinence. Directly observed therapy might be more beneficial but has not been studied in a good randomized trial.

Class Summary

Disulfiram inhibits aldehyde dehydrogenase, and, as a result, acetaldehyde accumulates. This leads to nausea, hypotension, and flushing if a person drinks alcohol while taking disulfiram.

Naltrexone (ReVia, Vivitrol)

Clinical Context:  Patients must be abstinent for 5-7 d before beginning therapy. Monitor liver function during treatment. Expensive, approximately $4.50/pill. Pure antagonist and is not addicting.

IM administration of Vivitrol reduces first-pass hepatic metabolism as compared with oral naltrexone. No significant increase from baseline in mean AST or ALT levels.

Vivitrol does not appear to be a hepatotoxin at recommended doses but patients should be warned of risk of hepatic injury. Preparation is considered nonaddicting.

Class Summary

Alcohol has been shown to bind to opiate receptors in the brain. Studies show that blocking opiate receptors decreases cravings for alcohol.

Further Outpatient Care

Frequent follow-up is essential to support the patient in recovery. The most common mistake physicians make is assuming too soon that the patient is stable. Ask patients about attendance at AA meetings and about their relationships with their sponsors. Less than 20% of patients remain abstinent for a full year. Among patients who have been sober for 2 years, the relapse rate is 40%. Patients who have been sober for 5 years are likely to remain sober, but they are still at risk for relapse.

Warning signs for physicians that a patient has relapsed include missing appointments or attending AA meetings less frequently. Warn patients to avoid testing themselves, particularly early in sobriety. Encouraging involvement in exercise and other leisure activities also is helpful.

The key step for the patient is to realize that treatment does not end with sobriety. Recovery means that patients can handle the stresses of everyday life without alcohol. Therefore, the patient must develop and rehearse strategies to cope with high-risk situations.

Successful recovery requires the patient to be able to do the following:

Patients should have a list of phone numbers of people they can call when they are having a difficult time coping. Importantly, patients should write out the list and put it in a convenient location because sometimes during high-stress periods they may become emotionally and mentally disorientated, necessitating written instructions.

Patients should spend time thinking about circumstances during which they feel at highest risk for relapse. They should anticipate these situations and make a written list. Most persons with alcoholism can quickly list the circumstances and/or emotions that led them to drink.

Patients need to identify specific responses (thoughts as well as behaviors) to each of these high-risk situations. Encourage patients to be very specific when considering their responses. For example, ask patients exactly what they are going to say and do when asked at parties what they want to drink. Once patients have made the list, they should practice responses to their high-risk situations.

When patients have the urge to drink, there are several techniques that can be used to deal with the situation, including (1) self-distraction (i.e. getting involved with an alternate activity that they enjoy), (2) thought stopping (i.e. patients should not dwell on thoughts of drinking but should stop these thoughts), (3) reprogramming (ie, patients should avoid activities that remind them of drinking), and (4) use of social support structure. The most common cause of relapse is failure to use coping strategies.

If the patient has a relapse, find out what happened (make a diagnosis) in order to formulate a new treatment plan. Below is an outline for dealing with relapses. Insist that the patient be actively involved in devising solutions; do not attempt to solve the problem for the patient.

Make a diagnosis.

Institute a treatment plan.

A 2010 study investigated a 10-year comparison of public endorsement of treatment and prejudice of the diagnoses of schizophrenia, depression, and alcohol dependence. Regarding alcohol dependence, high proportions of respondents in this study endorsed treatment, with general increases in the proportion endorsing treatment from doctors and specific increases in the proportions endorsing treatment from psychiatrists (from 61% in 1996 to 79% in 2006). This study found that more of the public embraces a neurobiological understanding of mental illness, which translates into support for services but not necessarily into a decrease in stigma.[57]

Prognosis

The prognosis for alcoholism should not be considered hopeless. As many as 30% of persons with alcoholism stop drinking. Even a patient with cirrhosis might have a favorable prognosis if alcohol cessation is achieved.

Patient Education

For patient education resources, see the Mental Health Center, Infections Center, and Digestive Disorders Center. Also, see the patient education articles Alcoholism, Drug Dependence and Abuse, Alcohol Intoxication, Hepatitis B, Hepatitis C, and Cirrhosis.

Involving family in the patient’s treatment of alcoholism can be a vital step on the path toward recovery. At a minimum, the destructive behaviors that occurred before treatment should be addressed by the patient with his or her family members. This is an important acknowledgment by the patient as they begin to grapple with the significance of their previous alcohol-centered lifestyle. Family members may find support through Al Anon, a fellowship devoted to sharing experiences and learning from others how to achieve serenity when a loved one struggles with alcohol.

What is mortality rate associated with alcoholism?How is alcoholism diagnosed?What are the signs and symptoms of alcohol withdrawal?What are the signs and symptoms of delirium tremens associated with alcoholism?What are the signs and symptoms of chronic alcoholism?What are possible complications of alcoholism?Which indirect biomarkers are used to detect the toxic effects of alcohol?Which blood alcohol levels are reliable indicators of alcoholism?Which ethyl glucuronide (EtG) findings suggest alcoholism?What is the first step in treatment of alcoholism?What are treatment options for alcoholism?What are the manifestations of chronic alcoholism?Which organ systems are affected by alcoholism?What is the pathogenesis of alcoholism?How does education affect the likelihood of alcoholism in the US?What percentage of US adults drink alcohol?What is the prevalence of alcoholism in the US?How does socioeconomic status affect the likelihood of alcoholism in the US?What factors increase the risk of alcohol dependence?What is the incidence of binge drinking in the US?What is the prevalence of comorbid mental disorders and alcoholism?What is the mortality rate associated with alcoholism?What is the global incidence of alcohol-related mortality?How harmful is alcohol compared to other misused substances?What are the maladies associated the consumption of 4 or more daily drinks of alcohol?What are the benefits and risks to moderate alcohol consumption?How is binge drinking defined, and what are the risks?What are alcohol-related risks to children and families?What is the relationship between alcoholism and smoking?What is fetal alcohol syndrome?How does the prevalence of alcoholism vary by race?How does the prevalence of alcoholism vary by sex?How does the prevalence of alcoholism vary by age?How is the CAGE questionnaire administered to screen from alcohol misuse?How is alcoholism diagnosed?Which factors lead to misdiagnosis of alcohol-related problems?What are the USPSTF recommendations for alcohol misuse screening?Which alcohol misuse screening tools are recommended by the USPSTF?What is the alcohol use disorders identification test (AUDIT)?How are alcohol screening tests administered?What are the 4 questions asked to screen from alcohol misuse in the CAGE questionnaire?Which CAGE questionnaire answers indicate an increased likelihood of alcohol dependence?What is the sensitivity of the CAGE questionnaire for alcohol misuse screening?What are the limitations of the CAGE questionnaire for alcohol misuse screening?What does the diagnosis of alcohol dependence rely on?What are the DSM-5 criteria for Alcohol Use Disorder?What are the different severity levels of Alcohol Use Disorder?What is the difference between early and sustained remission is Alcohol Use Disorder?What is a controlled environment according to DSM-5 Alcohol Use Disorder criteria?Which questions may be helpful to ask when screening for alcoholism?What are the signs and symptoms of alcohol withdrawal?What are the signs and symptoms of delirium tremens (DTs)?What are some signs and symptoms of chronic alcoholism?What are the signs and symptoms of alcoholism-related Wernicke encephalopathy?What are the signs and symptoms of alcoholism-related Korsakoff syndrome?What are the signs and symptoms of alcoholism-related hepatic encephalopathy?How are psychiatric disorders and alcoholism differentiated?What is the role of a mental status exam in the evaluation of alcoholism?What is the genetic etiology of alcoholism?What do twin studies reveal about the inheritability of alcoholism?What have adoptive studies revealed about the inheritability of alcoholism among males?What 2 types of male alcoholism have been proposed?What have adoptive studies revealed about the inheritability of alcoholism among females?What factors have been shown to increase the likelihood of later development of alcohol dependence?What are the psychological theories of alcoholism?Which mental health disorders may be included in a dual diagnosis with alcohol use disorder?Which other types of drug abuse should be included in the differential diagnosis of alcoholism?What is prevalence of comorbid psychiatric disorders and alcoholism?What is the prevalence of comorbid posttraumatic stress disorder (PTSD) and alcoholism?What are the differential diagnoses for Alcoholism?What is the role of biomarkers in the diagnosis of alcoholism?What is the reliability of biological measures for the detection of alcohol use disorders?What are the types of alcohol biomarkers?How are indirect alcohol biomarkers used to detect the toxic effects of alcohol?How are direct alcohol biomarkers used to detect the toxic effects of alcohol?When is a toxicology screen indicated in the evaluation of alcoholism?What are the indications for inpatient treatment of alcoholism?How does brief advice from a physician early in alcoholism affect prognosis?How is alcoholism categorized?What is the initial treatment of alcoholism?How should the diagnosis of alcoholism be presented?What is the significance of readiness to change in the treatment of alcoholism?What are the 5 stages of change for patients with alcoholism?What is the precontemplation stage of change for alcoholism?What is the contemplation stage of change for alcoholism?When does the preparation phase of change for alcoholism begin?What is the action stage of change for alcoholism?What is the maintenance stage of change for alcoholism?What is the significance of stages of change for alcoholism?What is the role of the physician in the stages of change for alcoholism?What is the AA 12-step approach for the treatment of alcoholism?What can increase the likelihood of success of AA for the treatment of alcoholism?What information about AA should a physician provide to patients with alcoholism?What are sources of help for patients with alcoholism?What are treatment options for alcoholism?When are specialist consultations indicated in the management of alcoholism?What are dietary modifications for patients with alcoholism?What are the USPSTF guidelines for alcoholism screening in primary care settings?What are the APA treatment guidelines for alcoholism?How is alcohol withdrawal treated?Which medications are used for the treatment of alcoholism?What is the role of naltrexone in the treatment of alcoholism?How should naltrexone be administered in the treatment of alcoholism?What is the role of nalmefene in the treatment of alcoholism?What is the efficacy of opioid antagonists in the treatment of alcohol dependence?What is the role of antidepressants in the treatment of alcoholism?What is the efficacy of acamprosate in the treatment of alcoholism?What is the efficacy of naltrexone in the treatment of alcoholism?What is the role of gabapentin in the treatment of alcoholism?What is the role of antibiotics in the treatment of alcoholism?Which medications in the drug class Opiate antagonists are used in the treatment of Alcoholism?Which medications in the drug class Aldehyde dehydrogenase inhibitors are used in the treatment of Alcoholism?Which medications in the drug class Glutamate receptor blockers are used in the treatment of Alcoholism?Why is frequent follow-up needed during recovery from alcoholism?What are warning signs of alcoholism relapse?What strategies are needed during the recovery phase of alcoholism treatment?What factors are required for a patient with alcoholism to make a successful recovery?What can aid in recovery from alcoholism?What techniques can be used to cope with the urge to drink in patients with alcoholism?How are alcoholic relapses managed?What effect does public endorsement of treatment of alcoholism have on patient services?What is the prognosis of alcoholism?What information about alcoholism should patients and their families receive?

Author

Warren Thompson, MD, FACP, Associate Professor, Department of Internal Medicine, Mayo Medical School

Disclosure: Nothing to disclose.

Coauthor(s)

Raj K Kalapatapu, MD, Fellow, Addiction Psychiatry, Columbia University College of Physicians and Surgeons

Disclosure: Nothing to disclose.

R Gregory Lande, DO, FACN, Clinical Consultant, Army Substance Abuse Program, Department of Psychiatry, Walter Reed Army Medical Center

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Glen L Xiong, MD, Associate Clinical Professor, Department of Psychiatry and Behavioral Sciences, Department of Internal Medicine, University of California, Davis, School of Medicine; Medical Director, Sacramento County Mental Health Treatment Center

Disclosure: Nothing to disclose.

References

  1. Anderson P. WHO Reports 3 Million Alcohol-Related Deaths in 2016. Medscape Medical News. Available at https://www.medscape.com/viewarticle/902614. September 27, 2018; Accessed: October 2, 2018.
  2. Poznyak V, Rekve D. Global status report on alcohol and health 2018. World Health Organization. September 21, 2018. Available at http://www.who.int/substance_abuse/publications/global_alcohol_report/gsr_2018/en/
  3. Sacks JJ, Gonzales KR, Bouchery EE, Tomedi LE, Brewer RD. 2010 National and State Costs of Excessive Alcohol Consumption. Am J Prev Med. 2015 Nov. 49 (5):e73-9. [View Abstract]
  4. Substance Abuse and Mental Health Services Administration. Center for Substance Abuse Treatment. The Role of Biomarkers in the Treatment of Alcohol Use Disorders. US Department of Health and Human Services. September 2006. Available at http://kap.samhsa.gov/products/manuals/advisory/pdfs/0609_biomarkers.pdf
  5. Das SK, Dhanya L, Vasudevan DM. Biomarkers of alcoholism: an updated review. Scand J Clin Lab Invest. 2008. 68(2):81-92. [View Abstract]
  6. Niemelä O. Biomarkers in alcoholism. Clin Chim Acta. 2007 Feb. 377(1-2):39-49. [View Abstract]
  7. Peterson K. Biomarkers for alcohol use and abuse. Alcohol Research & Health. 2004/2005. 28:
  8. Substance Abuse and Mental Health Services Administration (SAMHSA). 2015 National Survey on Drug Use and Health (NSDUH). SAMHSA. Available at https://www.samhsa.gov/data/sites/default/files/NSDUH-DetTabs-2015/NSDUH-DetTabs-2015/NSDUH-DetTabs-2015.htm#tab2-46b. 2015; Accessed: September 12, 2017.
  9. Vaillant GE. A long-term follow-up of male alcohol abuse. Arch Gen Psychiatry. 1996 Mar. 53(3):243-9. [View Abstract]
  10. Lopez-Quintero C, Cobos JP, Hasin DS, et al. Probability and predictors of transition from first use to dependence on nicotine, alcohol, cannabis, and cocaine: Results of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC). Drug Alcohol Depend. 2011 May 1. 115(1-2):120-30. [View Abstract]
  11. CDC Press Release. Binge drinking is bigger problem than previously thought. Centers for Disease Control and Prevention. Available at http://www.cdc.gov/media/releases/2012/p0110_binge_drinking.html. Accessed: January 10, 2012.
  12. Nutt DJ, King LA, Phillips LD. Drug harms in the UK: a multicriteria decision analysis. Lancet. 2010 Nov 6. 376(9752):1558-65. [View Abstract]
  13. Doll R, Peto R, Boreham J, Sutherland I. Mortality in relation to alcohol consumption: a prospective study among male British doctors. Int J Epidemiol. 2005 Feb. 34(1):199-204. [View Abstract]
  14. Knoops KT, de Groot LC, Kromhout D, Perrin AE, Moreiras-Varela O, Menotti A. Mediterranean diet, lifestyle factors, and 10-year mortality in elderly European men and women: the HALE project. JAMA. 2004 Sep 22. 292(12):1433-9. [View Abstract]
  15. Thun MJ, Peto R, Lopez AD, et al. Alcohol consumption and mortality among middle-aged and elderly U.S. adults. N Engl J Med. 1997 Dec 11. 337(24):1705-14. [View Abstract]
  16. Pletcher MJ, Varosy P, Kiefe CI, Lewis CE, Sidney S, Hulley SB. Alcohol consumption, binge drinking, and early coronary calcification: findings from the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Am J Epidemiol. 2005 Mar 1. 161(5):423-33. [View Abstract]
  17. Ruidavets JB, Ducimetiere P, Evans A, Montaye M, Haas B, Bingham A. Patterns of alcohol consumption and ischaemic heart disease in culturally divergent countries: the Prospective Epidemiological Study of Myocardial Infarction (PRIME). BMJ. 2010. 341:c6077. [View Abstract]
  18. Sood B, Delaney-Black V, Covington C, et al. Prenatal alcohol exposure and childhood behavior at age 6 to 7 years: I. dose-response effect. Pediatrics. 2001 Aug. 108(2):E34. [View Abstract]
  19. Baer JS, Sampson PD, Barr HM, et al. A 21-year longitudinal analysis of the effects of prenatal alcohol exposure on young adult drinking. Arch Gen Psychiatry. 2003 Apr. 60(4):377-85. [View Abstract]
  20. Ault, A. Proven Screening Tool for Alcohol Abuse Underutilized. Medscape Medical News. Available at http://www.medscape.com/viewarticle/861116. March 29, 2016; Accessed: April 7, 2016.
  21. Grant BF, Goldstein RB, Saha TD, Chou SP, Jung J, Zhang H, et al. Epidemiology of DSM-5 Alcohol Use Disorder: Results From the National Epidemiologic Survey on Alcohol and Related Conditions III. JAMA Psychiatry. 2015 Aug. 72 (8):757-66. [View Abstract]
  22. Arria AM, Caldeira KM, Kasperski SJ, Vincent KB, Griffiths RR, O'Grady KE. Energy Drink Consumption and Increased Risk for Alcohol Dependence. Alcohol Clin Exp Res. 2010 Nov 12. [View Abstract]
  23. Brauser D. New Guidelines for Alcohol Misuse in Adults Released. Medscape Medical News. Available at http://at http://www.medscape.com/viewarticle/804212
  24. Moyer VA; U.S. Preventive Services Task Force. Screening and Behavioral Counseling Interventions in Primary Care to Reduce Alcohol Misuse: U.S. Preventive Services Task Force Recommendation Statement. Ann Intern Med. 2013 May 14. doi:10.7326/0003-4819-159-3-201308060-00652. [Epub ahead of print].
  25. Enoch MA, Goldman D. Problem drinking and alcoholism: diagnosis and treatment. Am Fam Physician. 2002 Feb 1. 65(3):441-8. [View Abstract]
  26. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Washington, DC: American Psychiatric Association; 2013.
  27. Spitzer RL, Kroenke K, Williams JB. Validation and utility of a self-report version of PRIME-MD: the PHQ primary care study. Primary Care Evaluation of Mental Disorders. Patient Health Questionnaire. JAMA. 1999 Nov 10. 282(18):1737-44. [View Abstract]
  28. Boutin-Foster C, Ferrando SJ, Charlson ME. The Cornell Psychiatric Screen: a brief psychiatric scale for hospitalized medical patients. Psychosomatics. 2003 Sep-Oct. 44(5):382-7. [View Abstract]
  29. Nery FG, Stanley JA, Chen HH, Hatch JP, Nicoletti MA, Serap Monkul E, et al. Bipolar disorder comorbid with alcoholism: A (1)H magnetic resonance spectroscopy study. J Psychiatr Res. 2009 Oct 7. [View Abstract]
  30. Hicks BM, Krueger RF, Iacono WG, McGue M, Patrick CJ. Family transmission and heritability of externalizing disorders: a twin-family study. Arch Gen Psychiatry. 2004 Sep. 61(9):922-8. [View Abstract]
  31. Schuckit MA, Smith TL. An 8-year follow-up of 450 sons of alcoholic and control subjects. Arch Gen Psychiatry. 1996 Mar. 53(3):202-10. [View Abstract]
  32. Chengappa KN, Levine J, Gershon S, Kupfer DJ. Lifetime prevalence of substance or alcohol abuse and dependence among subjects with bipolar I and II disorders in a voluntary registry. Bipolar Disord. 2000 Sep. 2(3 Pt 1):191-5. [View Abstract]
  33. Jacobsen LK, Southwick SM, Kosten TR. Substance use disorders in patients with posttraumatic stress disorder: a review of the literature. Am J Psychiatry. 2001 Aug. 158(8):1184-90. [View Abstract]
  34. Vlahov D, Galea S, Ahern J, Resnick H, Boscarino JA, Gold J. Consumption of cigarettes, alcohol, and marijuana among New York City residents six months after the September 11 terrorist attacks. Am J Drug Alcohol Abuse. 2004 May. 30(2):385-407. [View Abstract]
  35. Marshall RD, Galea S. Science for the community: assessing mental health after 9/11. J Clin Psychiatry. 2004. 65 Suppl 1:37-43. [View Abstract]
  36. Shipherd JC, Stafford J, Tanner LR. Predicting alcohol and drug abuse in Persian Gulf War veterans: what role do PTSD symptoms play?. Addict Behav. 2005 Mar. 30(3):595-9. [View Abstract]
  37. Green B. Post-traumatic stress disorder: symptom profiles in men and women. Curr Med Res Opin. 2003. 19(3):200-4. [View Abstract]
  38. Dobie DJ, Kivlahan DR, Maynard C, Bush KR, Davis TM, Bradley KA. Posttraumatic stress disorder in female veterans: association with self-reported health problems and functional impairment. Arch Intern Med. 2004 Feb 23. 164(4):394-400. [View Abstract]
  39. de Beaurepaire R, Lukasiewicz M, Beauverie P, Castéra S, Dagorne O, Espaze R, et al. Comparison of self-reports and biological measures for alcohol, tobacco, and illicit drugs consumption in psychiatric inpatients. Journal of European Psychiatry. November 2007. 22 (8):540-548. [View Abstract]
  40. Hannuksela ML, Liisanantti MK, Nissinen AE, Savolainen MJ. Biochemical markers of alcoholism. Clin Chem Lab Med. 2007. 45(8):953-61. [View Abstract]
  41. Sommers MS, Savage C, Wray J, Dyehouse JM. Laboratory measures of alcohol (ethanol) consumption: strategies to assess drinking patterns with biochemical measures. Biol Res Nurs. 2003 Jan. 4(3):203-17. [View Abstract]
  42. Bergström JP, Helander A. Clinical Characteristics of Carbohydrate-Deficient Transferrin (%Disialotransferrin) Measured by HPLC: Sensitivity, Specificity, Gender Effects, and Relationship with other Alcohol Biomarkers. Alcohol Alcohol. 2008 Apr 24. [View Abstract]
  43. Neumann T, Spies C. Use of biomarkers for alcohol use disorders in clinical practice. Addiction. 2003 Dec. 98 Suppl 2:81-91. [View Abstract]
  44. Bean P. State of the art contemporary biomarkers of alcohol consumption. MLO Med Lab Obs. 2005 Nov. 37(11):10-2, 14, 16-7; quiz 18-9. [View Abstract]
  45. Hietala J, Koivisto H, Anttila P, Niemelä O. Comparison of the combined marker GGT-CDT and the conventional laboratory markers of alcohol abuse in heavy drinkers, moderate drinkers and abstainers. Alcohol Alcohol. 2006 Sep-Oct. 41(5):528-33. [View Abstract]
  46. Johnson BA. Medication treatment of different types of alcoholism. Am J Psychiatry. 2010 Jun. 167(6):630-9. [View Abstract]
  47. Substance Abuse and Mental Health Services Administration. Considerations for the Care and Treatment of Mental and Substance Use Disorders in the COVID-19 Epidemic. Substance Abuse and Mental Health Services Administration. Available at https://www.samhsa.gov/sites/default/files/considerations-care-treatment-mental-substance-use-disorders-covid19.pdf. March 20, 2020; Accessed: March 23, 2020.
  48. US Preventive Services Task Force., Curry SJ, Krist AH, Owens DK, Barry MJ, Caughey AB, et al. Screening and Behavioral Counseling Interventions to Reduce Unhealthy Alcohol Use in Adolescents and Adults: US Preventive Services Task Force Recommendation Statement. JAMA. 2018 Nov 13. 320 (18):1899-1909. [View Abstract]
  49. Reus VI, Fochtmann LJ, Bukstein O, Eyler AE, Hilty DM, Horvitz-Lennon M, et al. The American Psychiatric Association Practice Guideline for the Pharmacological Treatment of Patients With Alcohol Use Disorder. Am J Psychiatry. 2018 Jan 1. 175 (1):86-90. [View Abstract]
  50. Sinclair JD. Evidence about the use of naltrexone and for different ways of using it in the treatment of alcoholism. Alcohol Alcohol. 2001 Jan-Feb. 36(1):2-10. [View Abstract]
  51. Rosner S, Hackl-Herrwerth A, Leucht S, Vecchi S, Srisurapanont M, Soyka M. Opioid antagonists for alcohol dependence. Cochrane Database Syst Rev. 2010 Dec 8. 12:CD001867. [View Abstract]
  52. Cassels C. Anticonvulsant Promising for Alcohol Dependence. Medscape Medical News. Available at http://www.medscape.com/viewarticle/813817. Accessed: November 13, 2013.
  53. Mason BJ, Quello S, Goodell V, Shadan F, Kyle M, Begovic A. Gabapentin Treatment for Alcohol Dependence: A Randomized Clinical Trial. JAMA Intern Med. 2013 Nov 4. [View Abstract]
  54. Nunes EV. Gabapentin: A New Addition to the Armamentarium for Alcohol Dependence?. JAMA Intern Med. 2013 Nov 4. [View Abstract]
  55. Davenport, L. Antibiotic Cuts Alcohol Cravings, May Enhance Psychotherapy. Medscape Medical News. Available at http://www.medscape.com/viewarticle/845066. Accessed: May 22, 2015.
  56. MacKillop J, Few LR, Stojek MK, Murphy CM, Malutinok SF, Johnson FT, et al. D-cycloserine to enhance extinction of cue-elicited craving for alcohol: a translational approach. Transl Psychiatry. 2015 Apr 7. 5:e544. [View Abstract]
  57. Pescosolido BA, Martin JK, Long JS, Medina TR, Phelan JC, Link BG. "A disease like any other"? A decade of change in public reactions to schizophrenia, depression, and alcohol dependence. Am J Psychiatry. 2010 Nov. 167(11):1321-30. [View Abstract]
  58. CDC. Alcohol-Related Disease Impact (ARDI). Centers for Disease Control and Prevention. Available at http://nccd.cdc.gov/DPH_ARDI/default/default.aspx. Accessed: March 4, 2016.
  59. Stahre M, Roeber J, Kanny D, Brewer RD, Zhang X. Contribution of excessive alcohol consumption to deaths and years of potential life lost in the United States. Prev Chronic Dis. 2014 Jun 26. 11:E109. [View Abstract]
  60. World Health Organization. Global status report on alcohol and health. 2014. Available at http://www.who.int/substance_abuse/publications/global_alcohol_report/msb_gsr_2014_1.pdf?ua=1
  61. Saitz R. Clinical practice. Unhealthy alcohol use. N Engl J Med. 2005 Feb 10. 352(6):596-607. [View Abstract]
  62. American Medical Association. Alcoholism in the elderly. Council on Scientific Affairs, American Medical Association. JAMA. 1996 Mar 13. 275(10):797-801. [View Abstract]
  63. Anton RF, Moak DH, Waid LR, et al. Naltrexone and cognitive behavioral therapy for the treatment of outpatient alcoholics: results of a placebo-controlled trial. Am J Psychiatry. 1999 Nov. 156(11):1758-64. [View Abstract]
  64. Bigby JA. Substance Abuse Education and General Internal Medicine: A Manual for Faculty. Washington, DC: Society of General Internal Medicine; 1993.
  65. Brauser D. CDC Urges Physicians to Ask About Alcohol. Medscape Medical News. Available at http://www.medscape.com/viewarticle/818793. Accessed: January 16, 214.
  66. Brauser D. Inflammatory Markers May Predict Alcohol Dependence. Medscape Medical News. Available at http://www.medscape.com/viewarticle/836307. Accessed: December 12, 2014.
  67. Brooks M. Alcohol remains a leading cause of premature death. Medscape Medical News. June 27, 2014.
  68. Brooks M. Binge Drinking Boosts Mortality Risk in Older Adults. Medscape Medical News. Mar 3 2014.
  69. CDC. Alcohol Screening and Counseling: An effective but underused health service. Available. Medscape Medical News. Available at http://www.cdc.gov/vitalsigns/alcohol-screening-counseling/index.html.. Accessed: January 16, 214.
  70. Fleming MF, Barry KL, Manwell LB, et al. Brief physician advice for problem alcohol drinkers: A randomized controlled trial in community-based primary care practices. JAMA. 1997. 277:1039-1045. [View Abstract]
  71. Garbutt JC, Kranzler HR, O'Malley SS. Efficacy and tolerability of long-acting injectable naltrexone for alcohol dependence: a randomized controlled trial. JAMA. 2005 Apr 6. 293(13):1617-25. [View Abstract]
  72. Heinz A, Reimold M, Wrase J, et al. Correlation of stable elevations in striatal {micro}-opioid receptor availability in detoxified alcoholic patients with alcohol craving: a positron emission tomography study using carbon 11-labeled carfentanil. Arch Gen Psychiatry. 2005 Jan. 62(1):57-64. [View Abstract]
  73. Holahan CJ, Schutte KK, Brennan PL, et al. Episodic Heavy Drinking and 20-Year Total Mortality Among Late-Life Moderate Drinkers. Alcohol Clin Exp Res. 2014 Mar 3. [View Abstract]
  74. Kiefer F, Jahn H, Tarnaske T, et al. Comparing and combining naltrexone and acamprosate in relapse prevention of alcoholism: a double-blind, placebo-controlled study. Arch Gen Psychiatry. 2003 Jan. 60(1):92-9. [View Abstract]
  75. Malone SM, Iacono WG, McGue M. Drinks of the father: father's maximum number of drinks consumed predicts externalizing disorders, substance use, and substance use disorders in preadolescent and adolescent offspring. Alcohol Clin Exp Res. 2002 Dec. 26(12):1823-32. [View Abstract]
  76. Mayo-Smith MF, American Society of Addiction Medicine Working Group on Pharmacology. Pharmacological management of alcohol withdrawal: A meta-analysis and evidence-based practice guideline. JAMA. 1997. 278:144-151. [View Abstract]
  77. Melville N. Confirmed: Gabapentin Improves Alcohol Dependence Outcomes. Medscape [serial online]. Available at http://www.medscape.com/viewarticle/817472. Accessed: December 16, 2013.
  78. Mendelson JH, Mello NK. Medical Diagnosis and Treatment of Alcoholism. New York, NY: McGraw-Hill; 1992.
  79. National Institute on Alcohol Abuse and Alcoholism. Etiology and Natural History of Alcoholism.
  80. NIAAA. Alcohol Involvement in Accidental Death, Homicide, and Suicide.
  81. O'Connor PG, Schottenfeld RS. Patients with alcohol problems. N Engl J Med. 1998 Feb 26. 338(9):592-602. [View Abstract]
  82. O'Malley SS, Jaffe AJ, Chang G, et al. Six-month follow-up of naltrexone and psychotherapy for alcohol dependence. Arch Gen Psychiatry. 1996 Mar. 53(3):217-24. [View Abstract]
  83. O'Malley SS, Rounsaville BJ, Farren C, et al. Initial and maintenance naltrexone treatment for alcohol dependence using primary care vs specialty care: a nested sequence of 3 randomized trials. Arch Intern Med. Apr 6 2005. 163(14):1695-704. [View Abstract]
  84. Piccinelli M, Tessari E, Bortolomasi M, et al. Efficacy of the alcohol use disorders identification test as a screening tool for hazardous alcohol intake and related disorders in primary care: a validity study. BMJ. 1997 Feb 8. 314(7078):420-4. [View Abstract]
  85. Pletcher MJ, Varosy P, Kiefe CI, et al. Alcohol consumption, binge drinking, and early coronary calcification: findings from the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Am J Epidemiol. 2005 Mar 1. 161(5):423-33. [View Abstract]
  86. Room R, Babor T, Rehm J. Alcohol and public health. Lancet. 2005 Feb 5. 365(9458):519-30. [View Abstract]
  87. Saitz R. Clinical practice. Unhealthy alcohol use. N Engl J Med. 2005 Feb 10. 352(6):596-607. [View Abstract]
  88. Saitz R, O'Malley SS. Pharmacotherapies for alcohol abuse. Withdrawal and treatment. Med Clin North Am. 1997 Jul. 81(4):881-907. [View Abstract]
  89. Samet JH, Rollnick S, Barnes H. Beyond CAGE. A brief clinical approach after detection of substance abuse. Arch Intern Med. 1996 Nov 11. 156(20):2287-93. [View Abstract]
  90. Sigvardsson S, Bohman M, Cloninger CR. Replication of the Stockholm Adoption Study of alcoholism. Confirmatory cross-fostering analysis. Arch Gen Psychiatry. 1996 Aug. 53(8):681-7. [View Abstract]
  91. Stahre M, Roeber J, Kanny D, Brewer RD, Zhang X. Contribution of excessive alcohol consumption to deaths and years of potential life lost in the United States. Prev Chronic Dis. 2014 Jun 26. 11:E109. [View Abstract]
  92. Steinbauer JR, Cantor SB, Holzer CE 3rd, Volk RJ. Ethnic and sex bias in primary care screening tests for alcohol use disorders. Ann Intern Med. 1998 Sep 1. 129(5):353-62. [View Abstract]
  93. Thun MJ, Peto R, Lopez AD, Monaco JH, Henley SJ, Heath CW Jr. Alcohol consumption and mortality among middle-aged and elderly U.S. adults. N Engl J Med. 1997 Dec 11. 337(24):1705-14. [View Abstract]
  94. Volpicelli JR, Alterman AI, Hayashida M, O'Brien CP. Naltrexone in the treatment of alcohol dependence. Arch Gen Psychiatry. 1992 Nov. 49(11):876-80. [View Abstract]
  95. Walden B, McGue M, Lacono WG, et al. Identifying shared environmental contributions to early substance use: the respective roles of peers and parents. J Abnorm Psychol. 2004 Aug. 113(3):440-50. [View Abstract]
  96. Walsh DC, Hingson RW, Merrigan DM, Levenson SM, Coffman GA, Heeren T, et al. The impact of a physician's warning on recovery after alcoholism treatment. JAMA. 1992 Feb 5. 267(5):663-7. [View Abstract]
  97. Wilk AI, Jensen NM, Havighurst TC. Meta-analysis of randomized control trials addressing brief interventions in heavy alcohol drinkers. J Gen Intern Med. 1997 May. 12(5):274-83. [View Abstract]

Deaths while intoxicated. Data from the National Institute on Alcohol Abuse and Alcoholism (NIAAA).

Questions 0 Points 1 Point 2 Points 3 Points 4 Points
1. How often do you have a drink containing alcohol?NeverMonthly or less2-4 times a month2-3 times a week4 or more times a week
2. How many drinks containing alcohol do you have on a typical day when you are drinking?1 or 23 or 45 or 67-910 or more
3. How often do you have 6 or more drinks on 1 occasion?NeverLess than monthlyMonthlyWeeklyDaily or almost daily
4. How often during the past year have you found that you were not able to stop drinking once you had started?NeverLess than monthlyMonthlyWeeklyDaily or almost daily
5. How often during the past year have you failed to do what was normally expected of you because of drinking?NeverLess than monthlyMonthlyWeeklyDaily or almost daily
6. How often during the past year have you needed a first drink in the morning to get yourself going after a heavy drinking session?NeverLess than monthlyMonthlyWeeklyDaily or almost daily
7. How often during the past year have you had a feeling of guilt or remorse after drinking?NeverLess than monthlyMonthlyWeeklyDaily or almost daily
8. How often during the past year have you been unable to remember what happened the night before because you had been drinking?NeverLess than monthlyMonthlyWeeklyDaily or almost daily
9. Have you or has someone else been injured as a result of your drinking?No Yes, but not in the past year Yes, during the past year
10. Has a relative, friend, or a doctor or other health care worker been concerned about your drinking or suggested you cut down?No Yes, but not in the past year Yes, during the past



year



Biomarker Sensitivity (%) Specificity (%)
AST15-6947-68
ALT18-5850-57
GGT34-8511-95
MCV34-8926-95
CDT39-9482-100
CDT + GGT90 †98
Alcohol0-1000-100
EtG76-9177-92
*Values vary considerably according to gender, age, drinking pattern, prevalence of alcohol abuse/dependence, and prevalence of comorbidity, among other factors.[40, 6, 41, 43, 44]



† The sensitivity comes from one study in Finland, which uses a special formula. This study needs to be replicated.[45]