Psychiatric Annals

CME Article 

The Physician's Role in Recognition and Treatment of Alcohol Dependence and Comorbid Conditions

Joseph Pagano, MD; Noni A. Graham, MPH; Kimberly Frost-Pineda, MPH; Mark S. Gold, MD

Abstract

Alcoholism — or alcohol dependence, as the diagnosis is listed in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV)1 — is a chronic, often progressive disease that can be fatal without intervention and treatment. It starts with a drink, then drinking, then develops into an all-consuming preoccupation with alcohol and impaired control over alcohol intake. There may be attempts (or failed attempts) to curtail or cut down the amount of alcohol consumed. Rationing or other attempts to control use fail as pathological attachment to the drug develops. Use continues despite serious adverse health, personal, work-related, and financial consequences.

Alcoholism usually involves physical dependence on alcohol; however, tolerance and withdrawal are just two of the criteria used to diagnose alcohol dependence. Comorbidity, genetic, and psychosocial factors contribute to the risk of developing this disease.

Alcoholism is common, serious, and expensive to both those afflicted and society at large.2 The list of medical complications of alcoholism is exhaustive and includes almost every organ system: alcoholic hepatitis, cirrhosis, gastritis, pancreatitis, high blood pressure, cardiomyopathy, congestive heart failure, stroke, hypoglycemia and diabetes, erectile dysfunction in men, fetal alcohol syndrome, esophageal cancer, liver cancer, and colorectal cancer.

Physicians often make the diagnosis of alcohol abuse only after evaluation of a physical illness, such as cirrhosis, cardiomyopathy, pancreatitis or gastrointestinal bleeding; a charge of driving while intoxicated; or another major problem that can only be attributed to loss of control over alcohol. Wernicke encephalopathy and Korsakoff psychosis are much less common and usually develop late in the course of the disease. Fetal alcohol syndrome and fetal alcohol affect are 100% preventable and are directly attributable to alcohol use during pregnancy. In addition to medical problems, physicians often diagnose alcohol abuse or dependence after a suicide attempt, fight, domestic violence incident, argument, or homicide.

Alcohol affects virtually every organ system in the body and, in high enough doses, will cause coma and death. Alcohol dependence occurs gradually as alcohol alters the balance of several neurotransmitter systems, including opiate receptors (eg, mu, delta, kappa), gamma-amino butyric acid (GABA) receptors, and the glutamate, serotonin, and dopaminergic systems.

The pleasurable effects of alcohol are thought to be related to dopamine and opiate receptors. Numerous studies suggest these neurotransmitters are associated with risk of alcohol dependence. Excessive, long-term drinking can deplete or increase the levels of some of these neurotransmitters, leading to continued drinking to either to restore good feelings or to avoid negative feelings.3 Alcohol's effect on the GABA receptor causes the anxiolytic and sedative effects. Alcohol is an inhibitor of the receptor for glutamate; chronic alcohol ingestion results in the upregulation of glutamate receptors.4 Alcohol and the anticipation of alcohol availability raise dopamine levels in the mesocorticolimbic brain, which is associated with its pleasurable aspects.5

When alcohol is withdrawn, the central nervous system experiences increased excitability. Long-term alcoholics are more prone to alcohol withdrawal syndrome and suffer a more severe withdrawal. Chronic alcohol ingestion can lead to cell death and cerebellar degeneration, Wernicke-Korsakoff syndrome, and most commonly, withdrawal seizures when alcohol use is decreased or ceased.3

In the adult population of the United States, estimates of past year alcohol abuse and dependence are 7.5% to 9.5% with a lifetime prevalence of 13.5% to 23.5%.2 Social and cultural factors send many people messages that it is all right to drink excessively. Having friends or a close partner who drinks regularly but who may not abuse alcohol could increase the risk of excessive drinking on the patient's part.5

Age. People who begin drinking at an early age (by age 14) are at a higher risk of alcoholism. The…

Alcoholism — or alcohol dependence, as the diagnosis is listed in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV)1 — is a chronic, often progressive disease that can be fatal without intervention and treatment. It starts with a drink, then drinking, then develops into an all-consuming preoccupation with alcohol and impaired control over alcohol intake. There may be attempts (or failed attempts) to curtail or cut down the amount of alcohol consumed. Rationing or other attempts to control use fail as pathological attachment to the drug develops. Use continues despite serious adverse health, personal, work-related, and financial consequences.

Alcoholism usually involves physical dependence on alcohol; however, tolerance and withdrawal are just two of the criteria used to diagnose alcohol dependence. Comorbidity, genetic, and psychosocial factors contribute to the risk of developing this disease.

Alcoholism is common, serious, and expensive to both those afflicted and society at large.2 The list of medical complications of alcoholism is exhaustive and includes almost every organ system: alcoholic hepatitis, cirrhosis, gastritis, pancreatitis, high blood pressure, cardiomyopathy, congestive heart failure, stroke, hypoglycemia and diabetes, erectile dysfunction in men, fetal alcohol syndrome, esophageal cancer, liver cancer, and colorectal cancer.

Physicians often make the diagnosis of alcohol abuse only after evaluation of a physical illness, such as cirrhosis, cardiomyopathy, pancreatitis or gastrointestinal bleeding; a charge of driving while intoxicated; or another major problem that can only be attributed to loss of control over alcohol. Wernicke encephalopathy and Korsakoff psychosis are much less common and usually develop late in the course of the disease. Fetal alcohol syndrome and fetal alcohol affect are 100% preventable and are directly attributable to alcohol use during pregnancy. In addition to medical problems, physicians often diagnose alcohol abuse or dependence after a suicide attempt, fight, domestic violence incident, argument, or homicide.

Neurological Effects

Alcohol affects virtually every organ system in the body and, in high enough doses, will cause coma and death. Alcohol dependence occurs gradually as alcohol alters the balance of several neurotransmitter systems, including opiate receptors (eg, mu, delta, kappa), gamma-amino butyric acid (GABA) receptors, and the glutamate, serotonin, and dopaminergic systems.

The pleasurable effects of alcohol are thought to be related to dopamine and opiate receptors. Numerous studies suggest these neurotransmitters are associated with risk of alcohol dependence. Excessive, long-term drinking can deplete or increase the levels of some of these neurotransmitters, leading to continued drinking to either to restore good feelings or to avoid negative feelings.3 Alcohol's effect on the GABA receptor causes the anxiolytic and sedative effects. Alcohol is an inhibitor of the receptor for glutamate; chronic alcohol ingestion results in the upregulation of glutamate receptors.4 Alcohol and the anticipation of alcohol availability raise dopamine levels in the mesocorticolimbic brain, which is associated with its pleasurable aspects.5

Alcohol Withdrawal

When alcohol is withdrawn, the central nervous system experiences increased excitability. Long-term alcoholics are more prone to alcohol withdrawal syndrome and suffer a more severe withdrawal. Chronic alcohol ingestion can lead to cell death and cerebellar degeneration, Wernicke-Korsakoff syndrome, and most commonly, withdrawal seizures when alcohol use is decreased or ceased.3

Epidemiology

In the adult population of the United States, estimates of past year alcohol abuse and dependence are 7.5% to 9.5% with a lifetime prevalence of 13.5% to 23.5%.2 Social and cultural factors send many people messages that it is all right to drink excessively. Having friends or a close partner who drinks regularly but who may not abuse alcohol could increase the risk of excessive drinking on the patient's part.5

Risk Factors

Age. People who begin drinking at an early age (by age 14) are at a higher risk of alcoholism. The prevalence of alcohol dependence declines with increasing age. The prevalence in elderly populations is unclear but is probably around 3%. However, this population is growing, and alcohol problems are higher in elderly patients for a given amount of alcohol consumed than in younger adult drinkers.2,6

Gender. Men are more likely to become alcoholics or abuse alcohol than are women, with an average lifetime prevalence of 20% in men and 8% in women.

Family history. The risk of alcoholism is higher for people who have a parent or parents who abused alcohol. In addition, identical twins have greater concordance of alcohol dependence than fraternal twins.7

Occupation. According to a press release from Ensuring Solutions to Alcohol Problems, those who work in construction and mining, wholesale, and retail have the highest odds of problem drinking (alcohol abuse or dependence), at 25% to 45% more likely than the average US worker.8 However, those involved in government or professional services (eg, careers in law, medicine, or architecture) have much smaller numbers (government = 69 per 1,000 employees, professional = 54 per 1,000 employees), compared with the US average of 91 per 1,000 employees.

Ethnicity. Studies have reported a lower prevalence of alcoholism in blacks than whites in the US. Compared with whites, the prevalence was equal or higher in Hispanics, higher in Native Americans, and lower in Asian Americans.

Consequences of Alcohol Use

Alcohol use is the third leading cause of preventable death in the US, after smoking and obesity. Cigarette smoking remains the number one cause of death both in the general population and among alcoholics. Annually, 100,000 deaths are attributable to alcohol at a cost of $166 billion. Almost half of these deaths are attributable to alcohol-related injury.2

Beneficial Effects of Alcohol

Moderate alcohol consumption is associated with decreased all-cause mortality. The relationship between alcohol consumption and heart disease can best be understood as a J-shaped curve. Those who are abstinent from alcohol have higher rates of heart disease; that rate decreases for low and moderate consumers and then increases dramatically at a high level of alcohol use.9 This point is exemplified in an interview with Dr. Eric Rimm, where review of several epidemiologic studies in the literature has suggested that moderate alcohol consumption reduces heart disease10 (Table).

Risk Reduction in Coronary Artery Disease Associated with Moderate Alcohol Consumption*

Table.

Risk Reduction in Coronary Artery Disease Associated with Moderate Alcohol Consumption

Furthermore, alcohol consumption is associated with benefits regardless of whether the alcohol is consumed in wine, beer, or spirits. Alcohol increases serum concentration of high-density lipoprotein cholesterol and positively affects fibrinolysis and other blood clotting functions. Wine, however, is the best-studied alcoholic beverage, “found to contain antioxidants, vasorelaxants, and stimulants to antiaggregatory mechanisms.”18 The amount of alcohol associated with the lowest mortality appears to be 2 drinks per day in men and 1 drink or less per day in women. A drink is defined as “12 oz of beer, 5 oz of wine, or 1.5 oz of 80-proof distilled spirits.”19

Moderate consumption of alcohol specifically reduces risk of coronary heart disease. However, despite the benefit of alcohol in cardiovascular disease, the risk of hypertension is increased with more than 2 more drinks daily. The cardiovascular benefit is offset somewhat by cirrhosis, cancer, high blood pressure, stroke, suicide, accidents, and injuries.19 For non-problem drinkers without a family history of alcoholism, the benefits of moderate consumption appear to outweigh the risk of accidents, abuse and dependence, disability, and death. However, any consumption makes it especially important for physicians to screen their patients and, when appropriate, make an early diagnosis and offer brief intervention or referral for specialized treatment.

Making the Diagnosis

The diagnosis of an alcohol problem is difficult but essential in preventing alcohol-related morbidity and mortality. The first step is taking a comprehensive history that includes questions about current drinking and family history. Early diagnosis means identifying pathological attachment rather than cirrhosis. Routine laboratory tests have a sensitivity of no better than 50%, and physical examination is helpful only with the later consequences of alcoholism.

Although the dangers of alcoholism are well known, physicians frequently fail to make the diagnosis. Fewer than 50% of people who went to their doctor because of alcohol problems were asked about their alcohol use. Patients frequently deny they have a problem and might not link alcohol with its consequences. Patients might be unaware that a positive family history increases their own risk for the disease. Furthermore, they might fear being reported to their employers or be too ashamed to report their problem.20

Alcohol and the Law

Often, alcohol problems are detected in relation to legal problems. In the field, police officers often deal with intoxicated persons who may be putting themselves or others at risk. DSM-IV alcohol intoxication includes inappropriate aggressive or sexual behavior, lability of mood, slurred speech, poor coordination, unsteady gait, nystagmus, flushed face, stupor or coma, and impairment in judgment, attention, or memory.1

Police often find an intoxicated person driving or attempting to drive. In observing motor vehicle operation, officers may find drivers with problems staying in their lane: drifting, swerving, straddling lanes. There may also be issues with speed (too fast or too slow), braking distance, disobeying traffic signals and signs, no headlights, improper signaling or turns, and road rage.21

In any of these instances, or in a case of public intoxication, the odor of an alcoholic beverage may be most apparent, cueing police to ask a person to perform a mental, eye, or dexterity test, or request sobriety tests such as breath or blood tests. However, in the case of an alcohol-dependent person with higher tolerance, signs of intoxication are not as obvious. Brick and Carpenter2,25 conducted a study in which police (raters) had to identify drinkers (targets) on video and rate their sobriety. Unfortunately, even with blood alcohol concentration (BAC) levels above the legal limit (up to 0.13%), raters were unable to identify if targets had been drinking or not.

Screening for Alcoholism

Every patient should be asked about alcohol use and screened for problem use. Despite the importance of screening, physicians may not be prepared to screen for and diagnose alcoholism. “How much do you drink?” probably is the question most commonly asked by doctors. This question has less than 50% sensitivity for alcohol problems. Blood tests, such as liver function tests and mean corpuscular volume (MCV), are not particularly effective; even gamma glutamyl transferase (GGT) has a sensitivity of only about 50%. Recently, sialic acid and carbohydrate-deficient transferrin have been touted as possible tests, but the sensitivities of both appear to be too low to be useful.

Recent use often is detected by measuring BAC, which is best accomplished by a blood test. Breath tests can only estimate BAC, which is why breath tests are not used or admissible in court in every state. Breath tests use infrared absorption spectroscopy, which provides a quantitative measure of how alcohol vapor absorbs light of a particular color, or more specifically, methyl group structures. Unfortunately, breath-testing instruments are not very specific; more than 100 compounds can be found in human breath at any one time. Approximately 70% to 80% of these compounds contain methyl group structure and may be incorrectly detected as ethyl alcohol.23

Screening Tools

The best-known and most-studied short screening test is the CAGE questionnaire. CAGE is an acronym used to help remember Cut down, Annoyed, Guilty, and Eye-opener questions. The questions are:

  • Have you ever felt the need to cut down on your drinking?
  • Have people annoyed you by criticizing your drinking?
  • Have you ever felt bad or guilty about your drinking?
  • Have you ever had a drink first thing in the morning to steady your nerves or get rid of a hangover?

Patients who answer affirmatively to two of these questions are 7 times more likely to be alcohol dependent. The sensitivity of the CAGE questionnaire was once thought to be about 75%, but more recent studies show sensitivity is lower in populations with lower prevalence, such as women and the elderly. The CAGE questionnaire might also fail to identify binge drinkers and will not identify those who have not suffered the consequences of alcoholism. Nevertheless, the CAGE questionnaire is brief and easily administered.24 Other screening tests include the Alcohol Use Disorders Identification Test (AUDIT), which detects hazardous drinking as well as alcohol abuse.24

A 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, the next step is to attempt to determine what consequences of alcohol abuse the patient has experienced. The diagnosis of alcohol dependence requires three of the seven DSM-IV criteria: tolerance; withdrawal; loss of control exhibited by regularly using more than intended; preoccupation evidenced by an inordinate time spent drinking and recovering and/or neglect of family, friends, occupation and pleasurable activities; failed attempts to control, moderate, or quit completely; or continued drinking despite physical or psychological consequences caused or exacerbated by alcohol.1

Physical Examination

Signs and symptoms of alcohol withdrawal include nausea and vomiting, diaphoresis, agitation and anxiety, headache, tachycardia, tremor, seizures, and visual and auditory hallucinations, all of which can occur in the absence of delirium tremens. Signs of delirium tremens (alcohol withdrawal delirium) include tachycardia and hypertension, temperature elevation, and delirium.

Stigmata of chronic alcoholism include gynecomastia, spider angiomas, dupuytren contractures (these also might be congenital), testicular atrophy, enlarged or shrunken liver, enlarged spleen, ataxia, ophthalmoplegia, and confusion. Anterograde and retrograde amnesia, often with confabulation and preceded by Wernicke type encephalopathy, indicates Korsakoff syndrome. Asterixis and confusion suggest hepatic encephalopathy.25

Comorbidity

Alcohol and Psychiatric Diseases

There is a strong genetic influence in the development of alcohol dependence and in the development of numerous psychiatric disorders. Alcohol abuse can cause, mimic, minimize, or exacerbate symptoms of psychiatric disorders. Emotional state (ie, high levels of stress, anxiety or emotional pain) can lead some people to drink alcohol to block out turmoil. Loss, trauma, and terrorism have all been associated with relapse to drinking, overdrinking, and abuse by novice drinkers. Other factors, such as low self-esteem, untreated depression, and poor impulse control, may make the patient more likely to use and abuse alcohol.

Major depression, bipolar disorders, cigarette smoking, antisocial personality disorders, and schizophrenia are commonly comorbid with alcohol problems.26 In a study by Lapham et al.,27 among convicted drunk drivers, “50% of women and 33% of men had at least 1 additional psychiatric disorder other than drug abuse or dependence, mainly posttraumatic stress disorder or major depression.” In addition to these issues, physicians are often faced with the challenging task of distinguishing some of these comorbid conditions from alcohol-induced psychiatric symptoms, which may mimic comorbid disorders.

Poly-Substance Abuse

Substances of abuse are rarely used alone. Other substances may be used to improve the positive effects or minimize the adverse effects. With alcohol, the most common other substances used include tobacco, marijuana, cocaine, and prescription opiates. Although these other substances cause a range of biological and intoxicating effects, addiction is independent of substance of choice.

Alcohol and tobacco use. According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA), at least 80% of alcoholics smoke cigarettes.28 Alcohol and tobacco are used concurrently to either increase the desired effects of each other or to decrease the unpleasant effects of the other. Concomitant use increases risk of diseases of the heart and lungs and various cancers. Relative risk for developing mouth and throat cancer is 38 times greater for those who use both tobacco and alcohol.28

A study of nonsmall-cell lung cancer by Ahrendt et al.29 found p53 gene mutations were present in 76% of the drinkers who also smoked. The p53 gene is one of the most frequently mutated genes in human cancer. In addition, Obot et al.30 found that children with alcohol dependent parents are more likely than other children to have past year tobacco use (odds ratio = 3.2; confidence interval = 2.05 to 4.98).

Alcohol and marijuana use. Prevalence of marijuana use and admissions for treatment have increased in recent decades due to both increasing potency of the marijuana used and the rising rate of judicial referrals. Young people may abuse alcohol and marijuana together or use whichever is more easily accessible.

Like tobacco smoke, marijuana smoke contains a number of carcinogens, and when combined with alcohol, the risk of adverse effects increases. Ramaekers et al.31 stated that the tetrahydrocannabinol (THC) in marijuana enhances alcohol-induced impairment (even in small doses), displaying an increased crash risk [odds ratio 2.9; 95% confidence interval = 1.1 to 7.7). In a twin study by Lynskey et al.,32 those who used cannabis before the age of 17 had a 1.6- to 6.0-fold increase in odds of alcohol and other drug abuse/dependence, relative to their twin who had not used cannabis by age 17, regardless of whether or not the pair were monozygotic.

Alcohol and cocaine use. When alcohol is combined with cocaine, the effects are more severe than either drug used alone. Cocaethylene is a psychoactive metabolite formed from simultaneous use of alcohol and cocaine. It blocks dopamine pathways, provokes enhanced postsynaptic receptor stimulation, and may “be more euphorigenic and rewarding than cocaine.”33 In a small double-blind, double-dummy randomized controlled crossover study (n= 8), Farre et al.34 reported increase in heart rate, rate-pressure product, plasma cortisol, and euphoria in healthy volunteers receiving cocaine and alcohol in combination.

Cocaethylene exerts cardiovascular toxicity and potentiates cocaine hepatotoxicity in humans and mice.33 Xu et al.35 found that cocaethylene blocks cardiac sodium channels in guinea pigs, and suggested it may be the reason for increased incidence of sudden death in concomitant alcohol and cocaine users. Furthermore, cocaine and cocaethylene have been shown to stimulate HIV replication in culture, leading to overall accelerated progression to AIDS.36

Cocaine and other psychostimulants, including methamphetamine and even prescription methylphenidate, also are used with alcohol to reverse alcohol's sedating effects and allow the drinking person to drink more or drive home. This sometimes has tragic consequences, when the stimulant wears off before the alcohol.

Alcohol and HIV/AIDS

People who abuse alcohol also are more likely to indulge in high-risk sexual behaviors and injection drug use, the two primary modes of HIV-transmission. Some people deliberately use alcohol to reduce inhibitions, providing an excuse for indulging in risky behaviors.

Alcohol use increases susceptibility to HIV and conditions that are complications of AIDS, including TB, pneumonia, hepatitis C, and AIDS-related brain damage. Alcohol use also may aid in decrease of medication compliance and poor response to HIV/AIDS therapies.37

Intervention

Brief Intervention

The first step in addressing problem drinking is brief intervention. The physician must state unequivocally that the patient has a problem with alcohol and that this determination stems not only from the quantity of alcohol consumed but also from the consequences of alcohol in that patient's life. 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 is also important. In some cases presenting the DSM-IV criteria with specific examples can be extremely helpful.

The next step is to present the diagnosis using explicit evidence and emphasizing the consequences suffered by the patient as a result of alcohol abuse. In this intervention, it is important to be empathic and nonjudgmental and to avoid arguments about the diagnosis. Indicate responsibility for change is with the patient. Listen to the patient's goals and point out discrepancies between his or her goals and actions.

Next, determine the patient's readiness for change. If the patient does not believe a problem exists, suggest bringing a family member to the next appointment or suggest a 2-week trial of abstinence. The differential diagnosis between alcohol abuse and dependence can be a difficult judgment call.

Motivational Interview

Another approach to treatment is the motivational interview, a type of counseling that helps the patient focus on examining and resolving ambivalent behavior/attitudes to elicit change. Rollnick and Miller38 instruct providers to use the steps listed in the Sidebar (see page 478). This type of intervention makes the relationship between physician and patient more of a partnership than the “expert/recipient roles.”

Sidebar.

Steps for Motivational Interviewing

Seek to understand the person's frame of reference via reflective listening.

Express acceptance and affirmation.

Elicit and reinforce the person's own self-motivational statements; express:

  • Problem recognition.
  • Concern.
  • Desire and intention to change.
  • Ability to change.

Monitor the person's degree of readiness to change (do not generate resistance by jumping ahead of the client).

Affirm the person's freedom of choice and self-direction.

12-step Groups

If the patient is thinking about changing his or her lifestyle, pamphlets concerning alcohol abuse should be provided and an abstinence trial suggested. If the patient is ready to change, reinforcement and praise for the decision should be given. Emphasize that the biggest error at this stage is for the patient to underestimate the amount of help needed to quit drinking. Consider the need for detoxification and pharmacotherapy and give the patient a list of options. For patients who recognize a problem and will consider referral, the cheapest (free) and most accessible option is Alcoholics Anonymous (AA).

The AA 12-step approach involves psychosocial techniques used in changing behavior (eg, use of rewards, social support networks, role models). It is strongly suggested that each new person obtain an AA sponsor who is a recovering alcoholic that supports the recovery of the new member and introduces 12-step recovery. The sponsor should be of the same sex as the patient. Patients do not need a strong religious background to be successful in AA, only the belief in a higher power.

Patients should be urged to follow the entire program and to discuss reservations with their sponsor.39,40 Patients should try at least five to 10 different meetings before giving up on the AA approach, because each meeting is different. The physician should have AA literature in the office, maintain a list of dates and places of meetings, and have the AA intergroup phone number available. No randomized trials of AA have been performed, but no other single treatment for alcoholism has helped as many recover as AA.

Treatment

The first and final point in the treatment of alcoholism is that the treatment does not have an endpoint. There is no “cure” for alcoholism but like many other chronic illnesses it requires lifelong maintenance treatment. The mainstay of treatment is group and individual counseling and therapy to support recovery from the psychological aspects of alcoholism. Sometimes, emotional or withdrawal symptoms of the disease may mimic psychiatric disorders. Effective treatment is nearly impossible unless patients accept that they're addicted and unable to control their drinking. Psychopharmacologic treatments increase the success of long-term treatment and include disulfiram, naltrexone, and acamprosate (Volpicelli, see page 484). Drug testing is both an outcome measure and a treatment in its own right.41

Many alcoholics and alcohol abusers enter treatment reluctantly because they deny that they have a problem. Patients commonly use a psychiatric disorder to deny alcohol abuse. Unless there is strong evidence that the psychiatric disorder clearly precedes the alcoholism or is present during a long period of sobriety, it is best to proceed as if alcoholism is the primary diagnosis. Health or legal problems also may prompt treatment. Intervention is sometimes required for some alcoholics to recognize and accept the need for treatment.42

A wide range of treatments are available for alcoholism. Treatment is tailored to the individual and may involve an evaluation, a brief intervention, an outpatient program or counseling, or a residential inpatient stay. Many residential alcoholism treatment programs in the US include abstinence, individual and group therapy, participation in AA, educational lectures, family involvement, work assignments, activity therapy, and the use of counselors and professional staff, many of whom also are in recovery.39

Our program uses naltrexone and acamprosate, plus urine testing and a 12-step model for recovery. In addition, we take a long-term view and believe that years of abuse cannot be reversed by days of treatment. We have reported 5-year outcomes for impaired physician alcoholics with full return to work and stable abstinent recovery of more than 80%.43 Detoxification from alcohol is not treatment; however, treatment may begin with detoxification, usually taking about 4 to 7 days. A long-acting benzodiazepine generally is used to prevent delirium tremens or other withdrawal seizures. It is best to 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 in patients with significant liver disease because the half-lives of other benzodiazepines are longer. These shorter-acting benzodiazepines require more frequent patient monitoring. 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 have been proven to be adequate by themselves.44 Treatment is important to prevent kindling and recurrent seizures. After detoxification, most patients will have an increase in appetite and will gain weight without a dietary consultation or exercise plan.

Summary

Alcohol abuse and dependence are the cause of significant morbidity and mortality in the US. Comorbid psychiatric disorders and polysubstance abuse are the rule rather than the exception. Physicians are ideally positioned to educate, prevent, diagnose, intervene, and treat or refer patients with substance abuse problems. Twelve-step recovery is the mainstay in lifelong maintenance of recovery and should be encouraged in all chemically dependent treatments, regardless of primary treatment plan.

References

  1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders [text revision]. 4th ed. Washington, DC: American Psychiatric Publishing; 2000.
  2. Alcoholism and Drug Dependence Are America's Number One Health Problem. National Council on Alcoholism and Drug Dependence. 2002. Available at: http://www.ncadd.org/facts/numberoneprob.html. Accessed May 2, 2005.
  3. Doweiko HE. Concepts of Chemical Dependency. Pacific Grove, CA: Brooks/Cole; 2002.
  4. Malcolm R, Gorman J, Myrick H. The role of GABA in the pathogenesis and treatment of anxiety and other neuropsychiatric disorders. Part 2: The treatment of alcohol withdrawal. Virginia Commonwealth University. 2001. Available at: http://www.vcu-cme.org/gaba2/overview.html. Accessed May 2, 2005.
  5. Bowirrat A, Oscar-Berman M. Relationship between dopaminergic neurotransmission, alcoholism, and Reward Deficiency syndrome. Am J Med Genet B Neuropsychiatr Genet. 2005;132(1):29–37. doi:10.1002/ajmg.b.30080 [CrossRef]
  6. Alcoholism in the elderly. Council on Scientific Affairs, American Medical Association. JAMA. 1996;275(10):797–801. doi:10.1001/jama.275.10.797 [CrossRef]8598598
  7. National Institute on Alcohol Abuse and Alcoholism. The genetics of alcoholism. Alcohol Alert. 1992;18:357.
  8. Giller J. Construction and Mining, Wholesale, Retail Top List of Industries With Problem Drinkers in the Workforce. Washington, DC: The George Washington University Medical Center; 2005.
  9. Rehm J, Greenfield TK, Rogers JD. Average volume of alcohol consumption, patterns of drinking, and all-cause mortality: results from the US National Alcohol Survey. Am J Epidemiol. 2001;153(1):64–71. doi:10.1093/aje/153.1.64 [CrossRef]11159148
  10. Rimm EB, Gold MS, ed. Alcohol consumption and good health. Psychiatry Today (University of Florida Department of Psychiatry). Available at: http://www.psychiatry.ufl.edu/newsletters/Content/rimm.pdf. Accessed May 2, 2005.
  11. Rimm EB, Giovannucci EL, Willett WC, et al. Prospective study of alcohol consumption and risk of coronary disease in men. Lancet. 1991;338(8765):464–468. doi:10.1016/0140-6736(91)90542-W [CrossRef]1678444
  12. Fuchs CS, Stampfer MD, Colditz GA, et al. Alcohol consumption and mortality among women. N Engl J Med. 1995;332(19):1245–1250. Erratum in: N Engl J Med 1997;336(7):523. doi:10.1056/NEJM199505113321901 [CrossRef]7708067
  13. Klatsky AL, Armstrong MA, Friedman GD. Red wine, white wine, liquor, beer, and risk for coronary artery disease hospitalization. Am J Cardiol. 1997;80(4):416–420. doi:10.1016/S0002-9149(97)00388-3 [CrossRef]9285651
  14. Renaud SC, Gueguen R, Siest G, Salamon R. Wine, beer, and mortality in middle-aged men from eastern France. Arch Intern Med. 1999;159(16):1865–1870. doi:10.1001/archinte.159.16.1865 [CrossRef]10493316
  15. Yuan JM, Ross RK, Gao YT, Henderson BE, Yu MC. Follow up study of moderate alcohol intake and mortality among middle aged men in Shanghai, China. BMJ. 1997;314(7073):18–23. doi:10.1136/bmj.314.7073.18 [CrossRef]9001474
  16. Kitamura A, Iso H, Sankai T, et al. Alcohol intake and premature coronary heart disease in urban Japanese men. Am J Epidemiol. 1998;147(1):59–65. doi:10.1093/oxfordjournals.aje.a009367 [CrossRef]9440399
  17. Rehm JT, Bondy SJ, Sempos CT, Vuong CV. Alcohol consumption and coronary heart disease morbidity and mortality. Am J Epidemiol. 1997;146(6):495–501. doi:10.1093/oxfordjournals.aje.a009303 [CrossRef]9290510
  18. Rimm EB, Klatsky A, Grobbee D, Stampfer MJ. Review of moderate alcohol consumption and reduced risk of coronary heart disease: is the effect due to beer, wine, or spirits?BMJ. 1996;312(7033):731–736. doi:10.1136/bmj.312.7033.731 [CrossRef]8605457
  19. Alcoholic beverages. In: US Department of Health and Human Services and US Department of Agriculture. Dietary Guidelines for Americans 2005. Available at: http://www.health.gov/dietaryguidelines/dga2005/document/pdf/Chapter9.pdf. Accessed May 2, 2005.
  20. Fleming MF, Barry KL, Manwell LB, Johnson K, London R. Brief physician advice for problem alcohol drinkers. A randomized controlled trial in community-based primary care practices. JAMA. 1997;277(13):1039–1045. doi:10.1001/jama.1997.03540370029032 [CrossRef]9091691
  21. Standard Field Sobriety Tests (SFST). Impaired Driving on Trial. Indiana Governor's Council on Impaired and Dangerous Driving. 2002. Available at: http://www.iupui.edu/∼iutox/Impaired_Driving/dui_detection.htm#Standard%20Field%20Sobriety%20Tests%20(SFST). Accessed May 2, 2005.
  22. Brick J, Carpenter JA. The identification of alcohol intoxication by police. Alcohol Clin Exp Res. 2001;25(6):850–855. doi:10.1111/j.1530-0277.2001.tb02290.x [CrossRef]11410721
  23. Hanson DJ. Alcohol Research and Statistics: Deceptive Reports, Alcohol Problems and Solutions. 2004. Available at: http://www2.potsdam.edu/alcohol-info/Controversies/1098894305.html. Accessed May 25, 2005.
  24. Caetano R. The identification of alcohol dependence criteria in the general population. Addiction. 1999;94(2):255–267. doi:10.1046/j.1360-0443.1999.9422559.x [CrossRef]10396793
  25. Webner D. Delirium tremens. US National Library of Medicine and National Institutes of Health, Medline Plus. 2003. Available at: http://www.nlm.nih.gov/medlineplus/ency/article/000766.htm. Accessed May 2, 2005.
  26. Le Fauve CE, Litten RZ, Randall CL, et al. Pharmacological treatment of alcohol abuse/dependence with psychiatric comorbidity. Alcohol Clin Exp Res. 2004;28(2):302–312. doi:10.1097/01.ALC.0000113413.37910.D7 [CrossRef]15112938
  27. Lapham SC, Smith E, C'de Baca J, et al. Prevalence of psychiatric disorders among persons convicted of driving while impaired. Arch Gen Psychiatry. 2001;58(10):943–949. doi:10.1001/archpsyc.58.10.943 [CrossRef]11576032
  28. National Institute on Alcohol Abuse and Alcoholism. Alcohol and tobacco. Alcohol Alert. 1998;39. Available at: http://www.niaaa.nih.gov/publications/aa39.htm. Accessed May 25, 2005.
  29. Ahrendt SA, Chow JT, Yang SC, et al. Alcohol consumption and cigarette smoking increase the frequency of p53 mutations in non-small cell lung cancer. Cancer Res. 2000;60(12):3155–3159.10866304
  30. Obot IS, Wagner FA, Anthony JC. Early onset and recent drug use among children of parents with alcohol problems: data from a national epidemiologic survey. Drug Alcohol Depend. 2001;65(1):1–8. doi:10.1016/S0376-8716(00)00239-8 [CrossRef]11714584
  31. Ramaekers JG, Berghaus G, van Laar M, Drummer OH. Dose related risk of motor vehicle crashes after cannabis use. Drug Alcohol Depend. 2004;73(2):109–119. doi:10.1016/j.drugalcdep.2003.10.008 [CrossRef]14725950
  32. Lynskey MT, Heath AC, Bucholz KK, et al. Escalation of drug use in early-onset cannabis users vs co-twin controls. JAMA. 2003;289(4):427–433. doi:10.1001/jama.289.4.427 [CrossRef]12533121
  33. Landry MJ. An overview of cocaethylene, an alcohol-derived, psychoactive, cocaine metabolite. J Psychoactive Drugs. 1992;24(3):273–276. doi:10.1080/02791072.1992.10471648 [CrossRef]1432406
  34. Farre M, De La Torre R, Gonzalez ML, et al. Cocaine and alcohol interactions in humans: neuroendocrine effects and cocaethylene metabolism. J Pharmacol Exp Ther. 1997;283(1):164–176.9336321
  35. Xu YQ, Crumb WJ Jr, Clarkson CW. Cocaethylene, a metabolite of cocaine and ethanol, is a potent blocker of cardiac sodium channels. J Pharmacol Exp Ther. 1994;271(1):319–325.7965731
  36. Shapshak P, Shah S, Weatherby N, et al. Cocaine and cocaethylene accelerate HIV progression in African American women. Presented at: Fourth Conference on Retroviruses and Opportunistic Infections, AIDSLINE, National Library of Medicine. ; May 4–7, 1997. ; Washington, DC. .
  37. National Institute on Alcohol Abuse and Alcoholism. Alcohol and HIV/AIDS. Alcohol Alert. 2002;57. Available at: http://www.niaaa.nih.gov/publications/aa57.htm. Accessed May 25, 2005.
  38. Rollnick S, Miller WR. What is motivational interviewing?Behavioural and Cognitive Psychotherapy. 1995;23:325–334. doi:10.1017/S135246580001643X [CrossRef]
  39. Gorski TT. Understanding the Twelve Steps. New York, NY: Fireside Press; 1991.
  40. Flores PJ. Group Psychotherapy with Addicted Populations: An Integration of Twelve-Step and Psychodynamic Theory. New York, NY: Hawthorne Press; 1997.
  41. Frost-Pineda K, Gold MS, Pomm R, Jacobs WS. Randomized urine testing: a safe and effective intervention for drug addiction. J Clin Pharm. 2003;43:64.
  42. Connors GJ, Donovan DM, DiClemente CC. Substance Abuse Treatment and the Stages of Change: Selecting and Planning Interventions. New York, NY: The Guilford Press; 2001
  43. Gold MS, Pomm R, Kennedy Y, Jacobs WS, Frost-Pineda K. 5-year state-wide study of physicians addiction treatment outcomes confirmed by urine testing. Presented at: Society for Neuroscience's 31st Annual Meeting. ; November 10–15, 2001. ; San Diego, CA. .
  44. Wesson DR. SAMHSA/CSAT Treatment Improvement Protocols. TIP 19: Detoxification From Alcohol and Other Drugs. US Department of Health and Human Services, Public Health Service, Substance Abuse and Mental Health Services Administration, Center for Substance Abuse Treatment. 1995. Available at: http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=hstat5.chapter.39784. Accessed May 2, 2005.

Risk Reduction in Coronary Artery Disease Associated with Moderate Alcohol Consumption*

StudyPopulationCountryRisk Reduction
Health Professionals Follow-Up Study1150,000 male healthcare professionalsUS35%
Nurses' Health Study12120,000 female nursesUS35%
Kaiser Permanente13124,000 men and womenUS30%
Eastern France1436,000 menFrance35%
Shanghai Follow-up Study1518,000 menChina35%
Japanese Employee Study168,500 menJapan45%
National Health and Nutrition Examination Study173,000 men and 4,000 womenUS35%

Educational Objectives

  1. Identify people at risk for alcoholism in the outpatient setting.

  2. Discuss the basic concepts and treatment strategies of alcohol withdrawal.

  3. Describe the basic concepts of alcohol treatment and rehabilitation.

Sidebar.

Steps for Motivational Interviewing

Seek to understand the person's frame of reference via reflective listening.

Express acceptance and affirmation.

Elicit and reinforce the person's own self-motivational statements; express:

  • Problem recognition.
  • Concern.
  • Desire and intention to change.
  • Ability to change.

Monitor the person's degree of readiness to change (do not generate resistance by jumping ahead of the client).

Affirm the person's freedom of choice and self-direction.

Authors

Dr. Pagano is clinical assistant professor, Department of Psychiatry, University of Florida College of Medicine, Gainesville, FL. Ms. Graham is research coordinator, Division of Addiction Medicine, Department of Psychiatry, University of Florida College of Medicine. Ms. Frost-Pineda is director of Public Health Research, Division of Addiction Medicine, and assistant in psychiatry, University of Florida College of Medicine. Dr. Gold is distinguished professor, Departments of Psychiatry, Neuroscience, Anesthesiology, Community Health & Family Medicine, and chief, Division of Addiction Medicine, University of Florida McKnight Brain Institute.

Address reprint requests to: Mark S. Gold, MD, University of Florida McKnight Brain Institute, Box 100256, Gainesville, FL 32610-0256.

The authors have no industry relationships to disclose.

10.3928/00485713-20050601-04

Sign up to receive

Journal E-contents