eMedicine Specialties > Psychiatry > Addiction
Alcoholism: Treatment & Medication
Updated: Dec 15, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
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.
Medical Care
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.
- 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.
- Present the diagnosis.
- 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:
- Brief physician advice makes a difference.
- While a trial period of controlled drinking with careful follow-up might be appropriate for a diagnosis of alcohol abuse, this approach increases a physician's professional liability. Complete abstinence is the only treatment for alcohol dependence. Emphasize that the most common error is underestimating the amount of help that will be needed to stop drinking. The differential diagnosis between alcohol abuse and dependence can be a difficult judgment call.
- Hospitalize patients if they have a history of delirium tremens or if they have significant comorbidity. Consider inpatient treatment if the patient has poor social support, significant psychiatric problems, or a history of relapse after treatment.
- Strongly recommend AA.
- Encourage hospitalized patients to call AA from the hospital. AA will send someone to talk to them if the patient makes the contact. Patients need to attend meetings regularly (daily at first) and for a sufficient length of time (usually 2 y or more) because recovery is a difficult and lengthy process.
- In the beginning of treatment, and perhaps ongoing, patients should remove alcohol from their homes and avoid bars and other establishments where strong pressures to drink may influence successful abstinence.
- If the patient has an antisocial personality (ie, severe problems with family, peers, school, and police before age 15 y and before the onset of alcohol problems), recovery is less likely. If the patient has primary depression, anxiety disorder, or another potentially contributory disorder (the other disorder must antedate the problems with alcohol or it must be a significant problem during long periods of sobriety), treat this primary problem aggressively.
- 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.
Medication
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).34 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.
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 was recently 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.
Glutamate receptor blockers
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.
Acamprosate (Campral)
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.
Adult
666 mg PO tid; initiate as soon as possible after alcohol withdrawal when abstinence has been achieved; if <60 kg, may need to decrease dose by 333-666 mg/d
CrCl 30-50 mL/min: 333 mg PO tid
Pediatric
Not established
Coadministration with naltrexone increases acamprosate C max and AUC, but no dosage adjustment necessary
Documented hypersensitivity; severe renal impairment (ie, CrCl <30 mL/min)
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Diarrhea is most common adverse effect (20%), but dropouts are few; additional common adverse effects are dizziness, itching, nausea, flatulence, headache, and increased sexual desire; depression and anxiety incidence slightly higher than that of placebo in 1 study
Aldehyde dehydrogenase inhibitors
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.
Disulfiram (Antabuse)
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.
Adult
250 mg PO qd
Pediatric
Not established
Do not administer with metronidazole; use with caution in patients on phenytoin (levels of phenytoin might increase)
Documented hypersensitivity, severe myocardial disease, coronary occlusion
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Adverse effects are uncommon, but hepatitis, optic neuritis, neuropathy, and skin rash reported
Opiate antagonists
Alcohol has been shown to bind to opiate receptors in the brain. Studies show that blocking opiate receptors decreases cravings for alcohol.
Naltrexone (ReVia, Vivitrol)
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.
Adult
Oral: 50 mg PO qd
Some physicians give 25 mg for the first 2 d of therapy; some believe 100 mg works better than 50 mg, but no trials demonstrate this
Extended-release injection: 380 mg IM every month; administer into gluteal muscle, alternating injection site between buttocks each month
Pediatric
Not established
Inhibits effects of opiates; patients currently taking opiates or who have been on long-term opiate therapy in previous 7 d can experience severe opiate withdrawal
Documented hypersensitivity, acute hepatitis or liver failure; physiologic opioid dependence or acute opiate withdrawal; extended-release injection for IM administration only, must not be administered IV
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Nausea/vomiting, abdominal pain, daytime sleepiness, and nasal congestion were more common vs placebo in largest randomized trial to date; discontinuation due to adverse effects was uncommon in most clinical trials; IM injection may cause serious injection site reactions including cellulitis, induration, hematoma, abscess, sterile abscess, and necrosis (some requiring surgical intervention); instruct patients to monitor the injection site and contact their physician if they develop pain, swelling, tenderness, induration, bruising, pruritus, or redness at the injection site that does not improve or worsens within 2 wk
More on Alcoholism |
| Overview: Alcoholism |
| Differential Diagnoses & Workup: Alcoholism |
Treatment & Medication: Alcoholism |
| Follow-up: Alcoholism |
| Multimedia: Alcoholism |
| References |
| « Previous Page | Next Page » |
References
Vaillant GE. A long-term follow-up of male alcohol abuse. Arch Gen Psychiatry. Mar 1996;53(3):243-9. [Medline].
Mokdad AH, Marks JS, Stroup DF, Gerberding JL. Actual causes of death in the United States, 2000. JAMA. Mar 10 2004;291(10):1238-45. [Medline].
Saitz R. Clinical practice. Unhealthy alcohol use. N Engl J Med. Feb 10 2005;352(6):596-607. [Medline].
Doll R, Peto R, Boreham J, Sutherland I. Mortality in relation to alcohol consumption: a prospective study among male British doctors. Int J Epidemiol. Feb 2005;34(1):199-204. [Medline].
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. Sep 22 2004;292(12):1433-9. [Medline].
Thun MJ, Peto R, Lopez AD, et al. Alcohol consumption and mortality among middle-aged and elderly U.S. adults. N Engl J Med. Dec 11 1997;337(24):1705-14. [Medline].
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. Mar 1 2005;161(5):423-33. [Medline].
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. Aug 2001;108(2):E34. [Medline].
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. Apr 2003;60(4):377-85. [Medline].
Enoch MA, Goldman D. Problem drinking and alcoholism: diagnosis and treatment. Am Fam Physician. Feb 1 2002;65(3):441-8. [Medline].
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. Nov 10 1999;282(18):1737-44. [Medline].
Boutin-Foster C, Ferrando SJ, Charlson ME. The Cornell Psychiatric Screen: a brief psychiatric scale for hospitalized medical patients. Psychosomatics. Sep-Oct 2003;44(5):382-7. [Medline].
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. Oct 7 2009;[Medline].
Hicks BM, Krueger RF, Iacono WG, McGue M, Patrick CJ. Family transmission and heritability of externalizing disorders: a twin-family study. Arch Gen Psychiatry. Sep 2004;61(9):922-8. [Medline].
Schuckit MA, Smith TL. An 8-year follow-up of 450 sons of alcoholic and control subjects. Arch Gen Psychiatry. Mar 1996;53(3):202-10. [Medline].
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. Sep 2000;2(3 Pt 1):191-5. [Medline].
Jacobsen LK, Southwick SM, Kosten TR. Substance use disorders in patients with posttraumatic stress disorder: a review of the literature. Am J Psychiatry. Aug 2001;158(8):1184-90. [Medline].
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. May 2004;30(2):385-407. [Medline].
Marshall RD, Galea S. Science for the community: assessing mental health after 9/11. J Clin Psychiatry. 2004;65 Suppl 1:37-43. [Medline].
Shipherd JC, Stafford J, Tanner LR. Predicting alcohol and drug abuse in Persian Gulf War veterans: what role do PTSD symptoms play?. Addict Behav. Mar 2005;30(3):595-9. [Medline].
Green B. Post-traumatic stress disorder: symptom profiles in men and women. Curr Med Res Opin. 2003;19(3):200-4. [Medline].
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. Feb 23 2004;164(4):394-400. [Medline].
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. Pages 1-8. [Full Text].
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. [Medline].
Das SK, Dhanya L, Vasudevan DM. Biomarkers of alcoholism: an updated review. Scand J Clin Lab Invest. 2008;68(2):81-92. [Medline]. [Full Text].
Hannuksela ML, Liisanantti MK, Nissinen AE, Savolainen MJ. Biochemical markers of alcoholism. Clin Chem Lab Med. 2007;45(8):953-61. [Medline]. [Full Text].
Niemelä O. Biomarkers in alcoholism. Clin Chim Acta. Feb 2007;377(1-2):39-49. [Medline].
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. Jan 2003;4(3):203-17. [Medline].
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. Apr 24 2008;[Medline].
Peterson K. Biomarkers for alcohol use and abuse. Alcohol Research & Health. 2004/2005;28.
Neumann T, Spies C. Use of biomarkers for alcohol use disorders in clinical practice. Addiction. Dec 2003;98 Suppl 2:81-91. [Medline].
Bean P. State of the art contemporary biomarkers of alcohol consumption. MLO Med Lab Obs. Nov 2005;37(11):10-2, 14, 16-7; quiz 18-9. [Medline].
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. Sep-Oct 2006;41(5):528-33. [Medline].
Sinclair JD. Evidence about the use of naltrexone and for different ways of using it in the treatment of alcoholism. Alcohol Alcohol. Jan-Feb 2001;36(1):2-10. [Medline].
American Medical Association. Alcoholism in the elderly. Council on Scientific Affairs, American Medical Association. JAMA. Mar 13 1996;275(10):797-801. [Medline].
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR). Washington, DC: American Psychiatric Association; 2000.
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. Nov 1999;156(11):1758-64. [Medline].
Bigby JA. Substance Abuse Education and General Internal Medicine: A Manual for Faculty. Washington, DC: Society of General Internal Medicine; 1993.
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. [Medline].
Garbutt JC, Kranzler HR, O'Malley SS. Efficacy and tolerability of long-acting injectable naltrexone for alcohol dependence: a randomized controlled trial. JAMA. Apr 6 2005;293(13):1617-25. [Medline].
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. Jan 2005;62(1):57-64. [Medline].
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. Jan 2003;60(1):92-9. [Medline].
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. Dec 2002;26(12):1823-32. [Medline].
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. [Medline].
Mendelson JH, Mello NK. Medical Diagnosis and Treatment of Alcoholism. New York, NY: McGraw-Hill; 1992.
National Institute on Alcohol Abuse and Alcoholism. Etiology and Natural History of Alcoholism. Available at http://pubs.niaaa.nih.gov/publications/Social/Module2Etiology&NaturalHistory/Module2.html.
NIAAA. Alcohol Involvement in Accidental Death, Homicide, and Suicide. Available at http://pubs.niaaa.nih.gov/publications/Social/Module1Epidemiology/AlcoholInvolvement.html.
O'Connor PG, Schottenfeld RS. Patients with alcohol problems. N Engl J Med. Feb 26 1998;338(9):592-602. [Medline].
O'Malley SS, Jaffe AJ, Chang G, et al. Six-month follow-up of naltrexone and psychotherapy for alcohol dependence. Arch Gen Psychiatry. Mar 1996;53(3):217-24. [Medline].
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. [Medline].
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. Feb 8 1997;314(7078):420-4. [Medline].
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. Mar 1 2005;161(5):423-33. [Medline].
Room R, Babor T, Rehm J. Alcohol and public health. Lancet. Feb 5 2005;365(9458):519-30. [Medline].
Saitz R. Clinical practice. Unhealthy alcohol use. N Engl J Med. Feb 10 2005;352(6):596-607. [Medline].
Saitz R, O'Malley SS. Pharmacotherapies for alcohol abuse. Withdrawal and treatment. Med Clin North Am. Jul 1997;81(4):881-907. [Medline].
Samet JH, Rollnick S, Barnes H. Beyond CAGE. A brief clinical approach after detection of substance abuse. Arch Intern Med. Nov 11 1996;156(20):2287-93. [Medline].
Sigvardsson S, Bohman M, Cloninger CR. Replication of the Stockholm Adoption Study of alcoholism. Confirmatory cross-fostering analysis. Arch Gen Psychiatry. Aug 1996;53(8):681-7. [Medline].
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. Sep 1 1998;129(5):353-62. [Medline].
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. Dec 11 1997;337(24):1705-14. [Medline].
Volpicelli JR, Alterman AI, Hayashida M, O'Brien CP. Naltrexone in the treatment of alcohol dependence. Arch Gen Psychiatry. Nov 1992;49(11):876-80. [Medline].
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. Aug 2004;113(3):440-50. [Medline].
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. Feb 5 1992;267(5):663-7. [Medline].
Wilk AI, Jensen NM, Havighurst TC. Meta-analysis of randomized control trials addressing brief interventions in heavy alcohol drinkers. J Gen Intern Med. May 1997;12(5):274-83. [Medline].
Further Reading
Keywords
alcoholism, alcohol, alcohol dependence, alcohol abuse, alcohol use, Alcoholics Anonymous, AA, chronic alcohol use, chronic alcohol abuse, substance abuse, ethanol abuse, binge drinking, bender, alcoholic
Treatment & Medication: Alcoholism