1.

Alcohol Abuse

v Alcohol : What You Don't Know Can Harm You

Alcohol is the oldest and most widely used drug in the world. Nearly half of all Americans over the age of 12 are consumers of alcohol. Although most drink only occasionally or moderately, there are an estimated 10 to 15 million alcoholics or problem drinkers in the United States, with more than 100,000 deaths each year attributed to alcohol. Among the nation's alcoholics and problem drinkers are as many as 4.5 million adolescents, and adolescents are disproportionately involved in alcohol-related automobile accidents, the leading cause of death among Americans 15 to 24 years old.

If you are like many Americans, you may drink alcohol occasionally. Or, like others, you may drink moderate amounts of alcohol on a more regular basis. If you are a woman or someone over the age of 65, this means that you have no more than one drink per day; if you are a man, this means that you have no more than two drinks per day. Drinking at these levels usually is not associated with health risks and can help to prevent certain forms of heart disease.

But did you know that even moderate drinking, under certain circumstances, is not risk free? And that if you drink at more than moderate levels, you may be putting yourself at risk for serious problems with your health and problems with family, friends, and coworkers? This chapter explains some of the consequences of drinking that you may not have considered.

Dealing with drunkenness and with alcohol-related accidents, crime, violence, and disturbances consumes more resources than any other aspect of police operations, while the health consequences of alcohol abuse add enormously to national health care costs. Illegal drugs can be more rapidly addicting than alcohol and may well have a more powerful effect on human behavior, but the high level of alcohol consumption, which is many times greater than the level of illegal drug use, makes it one of America's most serious drug problems.

Signs and symptoms of alcohol use and intoxication:

Smell of alcohol on breath

Irritability

Euphoria

Loss of physical coordination

Inappropriate or violent behavior

Loss of balance

Unsteady gait

Slurred and/or incoherent speech

Loss of consciousness

Slowed thinking

Depression

Impaired short-term memory

Blackouts

Signs and symptoms of alcohol withdrawal, experienced by alcoholics and problem drinkers:

Tremors

Agitation

Anxiety and panic attacks

Paranoia and delusions

Hallucinations (usually visual)

Nausea and vomiting

Increased body temperature

Elevated blood pressure and heart rate

Convulsions

Seizures

What Is a Drink

A standard drink is:

One 12-ounce bottle of beer* or wine cooler

One 5-ounce glass of wine

1.5 ounces of 80-proof distilled spirits.

* Beer ranges considerably in its alcohol content, with malt liquor being higher in its alcohol content than most other brewed beverages.

Drinking and Driving

It may surprise you to learn that you don't need to drink much alcohol before your ability to drive becomes impaired. For example, certain driving skills—such as steering a car while, at the same time, responding to changes in traffic—can be impaired by blood alcohol concentrations (BACs) as low as 0.02 percent. (The BAC refers to the amount of alcohol in the blood.) A 160-pound man will have a BAC of about 0.04 percent 1 hour after consuming two 12-ounce beers or two other standard drinks on an empty stomach (see above, "What Is a Drink?"). And the more alcohol you consume, the more impaired your driving skills will be.

Although most States set the BAC limit for adults who drive after drinking at 0.08 to 0.10 percent, impairment of driving skills begins at much lower levels.

Interactions With Medications

Alcohol interacts negatively with more than 150 medications. For example, if you are taking antihistamines for a cold or allergy and drink alcohol, the alcohol will increase the drowsiness that the medication alone can cause, making driving or operating machinery even more hazardous. And if you are taking large doses of the painkiller acetaminophen and drinking alcohol, you are risking serious liver damage. Check with your doctor or pharmacist before drinking any amount of alcohol if you are taking any over-the-counter or prescription medications.

Interpersonal Problems

The more heavily you drink, the greater the potential for problems at home, at work, with friends, and even with strangers. These problems may include:

• Arguments with or estrangement from your spouse and other family members;
• Strained relationships with coworkers;
• Absence from or lateness to work with increasing frequency;
• Loss of employment due to decreased productivity; and
• Committing or being the victim of violence.

Alcohol-Related Birth Defects

If you are a pregnant woman or one who is trying to conceive, you can prevent alcohol-related birth defects by not drinking alcohol during your pregnancy. Alcohol can cause a range of birth defects, the most serious being fetal alcohol syndrome (FAS). Children born with alcohol-related birth defects can have lifelong learning and behavior problems. Those born with FAS have physical abnormalities, mental impairment, and behavior problems. Because scientists do not know exactly how much alcohol it takes to cause alcohol-related birth defects, it is best not to drink any alcohol during this time.

Long-Term Health Problems

Some problems, like those mentioned above, can occur after drinking over a relatively short period of time. But other problems—such as liver disease, heart disease, certain forms of cancer, and pancreatitis—often develop more gradually and may become evident only after long-term heavy drinking. Women may develop alcohol-related health problems after consuming less alcohol than men do over a shorter period of time. Because alcohol affects many organs in the body, long-term heavy drinking puts you at risk for developing serious health problems, some of which are described below.

Alcohol-related liver disease. More than 2 million Americans suffer from alcohol-related liver disease. Some drinkers develop alcoholic hepatitis, or inflammation of the liver, as a result of long-term heavy drinking. Its symptoms include fever, jaundice (abnormal yellowing of the skin, eyeballs, and urine), and abdominal pain. Alcoholic hepatitis can cause death if drinking continues. If drinking stops, this condition often is reversible. About 10 to 20 percent of heavy drinkers develop alcoholic cirrhosis, or scarring of the liver. Alcoholic cirrhosis can cause death if drinking continues. Although cirrhosis is not reversible, if drinking stops, one's chances of survival improve considerably. Those with cirrhosis often feel better, and the functioning of their liver may improve, if they stop drinking. Although liver transplantation may be needed as a last resort, many people with cirrhosis who abstain from alcohol may never need liver transplantation. In addition, treatment for the complications of cirrhosis is available.

Heart disease. Moderate drinking can have beneficial effects on the heart, especially among those at greatest risk for heart attacks, such as men over the age of 45 and women after menopause. But long-term heavy drinking increases the risk for high blood pressure, heart disease, and some kinds of stroke.

Cancer. Long-term heavy drinking increases the risk of developing certain forms of cancer, especially cancer of the esophagus, mouth, throat, and voice box. Women are at slightly increased risk of developing breast cancer if they drink two or more drinks per day. Drinking may also increase the risk for developing cancer of the colon and rectum.

Pancreatitis. The pancreas helps to regulate the body's blood sugar levels by producing insulin. The pancreas also has a role in digesting the food we eat. Long-term heavy drinking can lead to pancreatitis, or inflammation of the pancreas. This condition is associated with severe abdominal pain and weight loss and can be fatal.

If you or someone you know has been drinking heavily, there is a risk of developing serious health problems. Because some of these health problems are both reversible and treatable, it is important to see your doctor for help. Your doctor will be able to advise you about both your health and your drinking.

Research Directions

The National Institute on Alcohol Abuse and Alcoholism (NIAAA), National Institutes of Health, supports about 90 percent of the Nation's research on alcohol use and related consequences. Today, alcohol researchers are working on the cutting edge of medical science to answer questions such as:

Who is at risk for alcohol-related problems?

How does alcohol affect the body, including the brain?

How is the risk for alcoholism inherited?

What are the health benefits and risks of moderate drinking?

What therapies, including medications, show promise for treating alcohol dependence more effectively?

Each new discovery made by alcohol researchers provides a piece of the answer to the ages old question of how to prevent and treat the alcohol-related troubles that plague individuals, families, and society. We see the future of alcohol research both as a challenge and as a reward: A challenge, because with more answers come more questions, and we still have far to go. A reward, because the answers we find ultimately will help diminish a public health threat that has existed for far too long.

Resources

If you or someone you know needs help or more information, contact:

¨ Al-Anon Family Group Headquarters
    1600 Corporate Landing Parkway
    Virginia Beach, VA 23454-5617
    Internet address: http://www.al-anon.alateen.org

Makes referrals to local Al-Anon groups, which are support groups for spouses and other significant adults in an alcoholic person's life. Also makes referrals to Alateen groups, which offer support to children of alcoholics.

Locations of Al-Anon or Alateen meetings worldwide can be obtained by calling   1-888-4AL-ANON Monday through Friday, 8 a.m.-6 p.m. (e.s.t.).

Free informational materials can be obtained by calling the toll-free numbers (operating 7 days per week, 24 hours per day):

U.S.: (800) 356-9996

Canada: (800) 714-7498

¨ Alcoholics Anonymous (AA) World Services
    475 Riverside Drive, 11th Floor
    New York, NY 10115
    (212) 870-3400
    Internet address: http://www.alcoholics-anonymous.org

Makes referrals to local AA groups and provides informational materials on the AA program. Many cities and towns also have a local AA office listed in the telephone book.

¨ National Council on Alcoholism and Drug Dependence (NCADD)
    12 West 21st Street
    New York, NY 10010
    (800) NCA-CALL
    Internet address: http://www.ncadd.org

Provides telephone numbers of local NCADD affiliates (who can provide information on local treatment resources) and educational materials on alcoholism via the above toll-free number.

¨ National Institute on Alcohol Abuse and Alcoholism
    Scientific Communications Branch
    6000 Executive Boulevard, Suite 409
    Bethesda, MD 20892-7003
    (301) 443-3860
    Internet address: http://www.niaaa.nih.gov

Makes available free publications on all aspects of alcohol abuse and alcoholism. Many are available in Spanish. Call, write, or search the World Wide Web site for a list of publications and ordering information.

Source: National Institute on Alcohol Abuse and Alcoholism (1999)
National Institutes of Health

v     Epidemiology of Alcoholism

Alcohol Use and Abuse: Where Do the Numbers Come From?

Newspapers and magazines regularly publish stories that report estimates of the number of people who are problem drinkers, the number of traffic deaths that involve alcohol, or the amount of alcohol that Americans consume. Where do these numbers come from, and how realistic are they?

Estimates such as these often come from research in epidemiology, the study of the distribution and determinants of disease, injuries, and other health-related conditions such as alcohol use, abuse, and associated consequences (MacMahan & Pugh 1960; Mausner & Bahn 1974). These studies can tell us how many people suffer from alcohol-related problems and what groups (e.g., according to sex, age, race, occupation, place of residence) are at greater risk, thereby providing information for developing treatment and prevention programs. Studies in alcohol epidemiology address the following areas: drinking levels and patterns, prevalence of alcohol dependence, and problems arising from alcohol abuse. Our information in these areas is generally good, but there are some limitations based on the types of data available.

First, the question of how much and what types of alcoholic beverages (beer, wine, spirits) Americans are drinking and whether overall drinking levels are increasing or decreasing can be studied by monitoring the sales of alcoholic beverages (Brooks et al. 1989). Because sales data are the basis for tax collection, such reports are carefully monitored and are generally accurate. Average or per capita consumption based on overall alcohol sales is particularly useful for international comparisons (Smart 1989) but does not tell us anything about what groups may be at risk for excessive drinking.

The most common way to assess group-specific drinking patterns (e.g., typical quantity and frequency, beverage preferences, drinking contexts) is to conduct population surveys in which respondents report drinking behavior. Research has demonstrated that properly constructed questionnaires can improve reliability and validity for self-reports of drinking behavior (Williams et al.1985; Hilton 1989), and there have been many surveys of drinking behavior (e.g., Malin et al. 1986; Williams et al 1986; Hilton 1987; Brooks et al. 1989).

Although useful, surveys do have limitations. First, their costs often limit sample size, which can increase the margin of error a special problem when studying subpopulations, such as racial or ethnic minorities and certain age groups, unless the survey plan provides for over sampling of these special groups. Even then, sample sizes are seldom large enough to identify small changes in drinking over time. Second, comparisons from one survey to another can be handicapped by differences in definitions and questions asked. Finally, self-reports of consumption in surveys tend to underestimate consumption compared with beverage sales data (Harford et al. 1988). Household and telephone surveys by their very nature tend to under sample heavier drinkers who may not live in households or who are frequently unavailable for interview. Also, some people underreport their consumption for fear that the interviewer will judge them negatively; yet individual respondents do report consuming amazingly large quantities of alcohol.

A second major area of research involves the question asked most frequently of alcohol epidemiologists: How many people are alcoholic? Early attempts at estimating the prevalence of alcoholism used variations of the Jellinek formula, based on the number of cirrhosis deaths (Brenner 1960; Schmidt & deLint 1970), or formulas based on per capita consumption (Ledermann 1956; deLint & Schmidt 1968). Other researchers used survey methods to measure the prevalence of alcohol-related problems as an indication of the prevalence of alcoholism (Cahalan et al. 1969; Cahalan 1970; Cahalan & Room 1974), but these same studies also demonstrated that not all alcohol problems are limited to persons who are alcohol dependent.

Newer and improved estimates of the prevalence of alcoholism are based on the concept of an "alcohol dependence syndrome" (Edwards & Gross 1976), defined in the International Classification of Diseases (ICD) and in the Diagnostic and Statistical Manual of Mental Disorders of the American Psychiatric Association. Diagnostic criteria for this syndrome have been used to develop operational definitions of dependence based on self-reported symptoms; surveys with questions based on these definitions can provide estimates of the numbers of persons whose alcohol dependence makes them appropriate candidates for treatment (Williams et al. 1987; Regier et al. 1988; Moore et al. 1989; Williams et al. in press). Because this is a relatively new area of research, methods are still evolving and refinements in diagnostic criteria and related survey questions (Grant 1989) will lead to new estimates.

A third major area of interest in alcohol epidemiology is assessing the scope of various health and social problems resulting from alcohol abuse. Many problems (e.g., with marriage or family, job, or the law) can be recognized by respondents as related to drinking and can be measured by self-reports from population surveys, with the same survey-related limitations mentioned earlier. For data on alcohol-related mortality and morbidity, however, researchers often rely on more objective sources. The three primary sources are death certificate data, the Fatal Accident Reporting System (FARS), and the National Hospital Discharge Survey (NHDS).

Alcohol-related mortality is estimated using death certificate data collected by the National Center for Health Statistics (NCHS) for all U.S. deaths (1988). The major methodological issue for studies of mortality lies in the determination of which deaths are alcohol related. Certain causes of death are by definition alcohol related (e.g., alcoholic psychoses, alcohol dependence syndrome, nondependent abuse of alcohol, certain categories of cirrhosis, excessive blood level of alcohol, and accidental poisoning by alcohol). There may be some underreporting of alcohol-related codes in mortality data to the extent that "sympathetic" certifiers of the cause of death may believe they are protecting an individual's reputation by recording a cause of death that does not directly implicate alcohol.

Individual studies have reported that a certain proportion of other diseases (e.g., certain cancers) and many accidents also are alcohol related (Ravenholt 1984; Roizen 1988). Researchers apply such estimates to overall cause-specific mortality to estimate additional alcohol-related mortality. The Public Health Service has proposed use of two new codes in the 10th Revision of the ICD for identifying alcohol involvement in mortality based on measures of blood alcohol content or other evidence of intoxication (Grant et al. 1987). These new codes should improve our ability to identify alcohol-related mortality.

The National Highway Traffic Safety Administration operates FARS, which counts every death from a traffic crash occurring on public roads within 30 days of the accident and records alcohol-related deaths based upon blood alcohol measurement, issuance of a citation for driving under the influence, or the determination of the responding police officer (USDOT 1985). The lack of uniformity among jurisdictions in the use of blood alcohol testing results in some underreporting of alcohol involvement in FARS data, and there is no information on the race of decedents.

As in the case of mortality, studies of alcohol-related morbidity or illness depend upon the specification of diseases that are associated with alcohol abuse. Data for such studies come from NHDS, an ongoing NCHS survey of discharges from short-stay community hospitals that provides codes for conditions diagnosed during the hospital stay (NCHS 1985; Stinson 1989). The availability of multiple diagnostic codes on each record allows for the examination of comorbidity of alcohol-related and other diseases. Sample sizes are large (typically in excess of 200,000 records per year) but not always large enough for reliable estimates when examining specific disease codes or when studying smaller age or race groups.

Even with the limitations described above, studies in alcohol epidemiology give us the data we need to assess the problems resulting from alcohol abuse. Such information is useful in estimating the societal costs of various health problems (Harwood et al. 1985), often providing the basis for justifying program development and implementation. Surveillance, an ongoing form of descriptive epidemiology characterized primarily by uniformity of methods for repeated observations over time, is conducted to monitor change and provides one means of evaluating the effectiveness of treatment and prevention programs (Stinson et al. 1987; Brooks et al. 1989; Grant &. Zobeck 1989; Zobeck et al. 1989). In addition, through the identification of nonrandom variations in the distribution of alcohol-related problems. epidemiologic research can generate hypotheses for testing in analytical studies

Conclusion

There are many different and sometimes conflicting statistics on the nature and extent of alcohol-related problems. Consequently, many alcohol professionals and the lay public are skeptical about the legitimacy of alcohol-related data, and often ask "How do you know what you know about alcohol-related problems?". We hope that the general description of alcohol epidemiological research in this chapter sheds some light on this question and helps alcohol program personnel. policymakers, and others to interpret better the many alcohol-related facts they see and hear.

The good news is that alcohol-related data are getting better and better. Refined data collection methodology and analysis and better reporting continue to increase information validity and reliability. Alcohol epidemiological research also has raised important questions for future alcohol research–questions that will help us to better prevent and treat alcohol abuse, alcoholism, and related consequences. For example, epidemiological research findings show that only a minority of alcoholics develop cirrhosis. Thus, a need has been identified for research on risk factors other than alcohol (e.g., genetic, nutritional, viral) that may be involved in cirrhosis development.

References

1. Brenner, B. Estimating the prevalence of alcoholism from vital rates. Quarterly Journal of Studies on Alcohol 21:140-141, 1960.

2. Brooks, S.; Williams, G.: Stinson, F.; and Noble, J. Surveillance Report #13: Apparent Per Capita Alcohol Consumption: National, State and Regional Trends. 1977-1987. Rockville, MD: National Institute on Alcohol Abuse and Alcoholism, Division of Biometry and Epidemiology, Alcohol Epidemiologic Data System, Sept. 1989.

3. Cahalan, D. & Room. R. Problem Drinking Among American Men. Monograph No. 7. New Brunswick, NJ: Rutgers Center for Alcohol Studies, 1974.

4. Cahalan, D. Problem Drinkers. San Francisco: Jossey-Bass, 1970.

5. Cahalan, D.; Cisin, l.; and Crossley, H. American Drinking Practices. Monograph No. 6. New Brunswick, NJ: Rutgers Center for Alcohol Studies, 1969.

6. Delint, J. & Schmidt, W. The distribution of alcohol consumption in Ontario. Quarterly Journal of Studies on Alcohol 29:968-973, 1968.

7. Edwards, G. & Gross, M.M. Alcohol dependence: Provisional description of a clinical syndrome. British Medical Journal 1:1058-1061, 1976.

8. Grant, B. DSM III-R and ICD- 10 classifications of alcohol use disorders and associated disabilities: A structural analysis. International Review of Psychiatry 1:21-39, 1989.

9. Grant. B.F.; Dufour, M.; Stinson, F.; Towle, L.; and Bertolucci, D. Epidemiologic Bulletin No. 17: Proposed coding of alcohol's role in casualties. Alcohol Health & Research World 12(1):48-50, 1987.

10. Grant, B. & Zobeck, T. Surveillance Report #11: Liver Cirrhosis Mortality in the United States, 1972- 86. Rockville. MD: National Institute on Alcohol Abuse and Alcoholism, Division of Biometry and Epidemiology, Alcohol Epidemiologic Data System, June 1989.

11. Harford, T.C; Zobeck, T.S.; Grant, B.F.; Stinson, F.S.; Aitken. S.S.; Dufour, M.; and Stoil, M.J. Epidemiologic Bulletin No. 19: The alcohol surveillance program of the Division of Biometry and Epidemiology: History, growth, and future directions. Alcohol Health & Research World 12(4):309- 313, 1988.

12. Harwood, H.; Kristiansen, P.; and Rachal, J. Social and economic costs of alcohol abuse and alcoholism. Issue Report No. 2. Research Triangle Park, NC: Research Triangle Institute, 1985.

13. Hilton, M. Drinking patterns and drinking problems in 1984: Results from a general population survey. Alcoholism: Clinical and Experimental Research 11:167-175, 1987.

14. Hilton, M. A comparison of a prospective diary and two summary recall techniques for recording alcohol consumption. British Journal of Addiction 84:1085- 1092. 1989.

15. Lederman S. Alcohol, Alcoholism, Alcoholization; Donnes Scientifiques de Caractere Physiologique, Economique et Social. (Institut National d'Etudes Demographiques, Travaux et Documents, Cahier No. 29.) Paris: Presses Universitaires, 1956. 

16. Macmahon, B. & Pugh. T. Epidemiologic Methods. Boston: Little, Brown, 1960.

17. Malin, H.; Wilson, R.; Williams, G.; and Aitken, S. Epidemiologic Bulletin 10: 1983 Alcohol Health Practices Supplement. Alcohol Health & Research World 10(2):48-50 1986.

18. Mausner, J. & Bahn, A. Epidemiology: An Introductory Text Philadelphia: W.B. Saunders, 1974.

19. Moore, R.; Bone. L.; Geller, G.; Mamon, J.; Stokes, E.; and Levine, D. Prevalence, detection, and treatment of alcoholism in hospitalized patients. Journal of the American Medical Association 261 :403-407, 1989. National Center for Health Statistics. Utilization of short-stay hospitals, United States. 1983, annual summary. Vital and Health Statistics. Series 13. No. 83. DHHS Pub. No. (PHS)85-1744. Public Health Service. Washington, DC U.S. Govt. Print. Off., 1985. * National Center for Health Statistics. Advance Report of Final Mortality Statistics. 1986. (Monthly Vital Statistics Report, Vol. 37, No. 6) DHHS Pub. No. (PHS)88-1120. Washington, DC: Supt. of Docs., U.S. Govt. Print. Off., 1988.

20. Ravenholt, R. Addiction mortality in the United States. 1980: Tobacco, alcohol, and other substances. Population and Development Review 10:697-724. 1984.

21. Regier, D.; Boyd. J.; Burke, J.; Rae, D.: Myers, J.; Kramer, M.; Robins, L.; George. L.; Karno, M.: and Locke, B. One-month prevalence of mental disorders in the United States. Archives of General Psychiatry 45:977-986. 1988.

22. Roizen, J. Alcohol and trauma. In: Giesbrecht, N.; Gonzales, R.; Grant, M.; Osterberg, E.; Room, R.; Rootman. I.; and Towle, L., eds. Drinking and Casualties: Accidents, Poisonings, and Violence in an International Perspective. London: Routledge, 1988.

23. Schmidt, W. & deLint, J. Estimating the prevalence of alcoholism from alcohol consumption and mortality data. Quarterly Journal of Studies on Alcohol 31 :957-964, 1970.

24. Smart, R. ls the postwar drink ing binge ending? Cross-national trends in per capita alcohol consumption. British Journal of Addiction 84:743-748, 1989.

25. Stinson, F. U.S. Epidemiologic Data Reference Manual, Vol. 4: Hospital Discharges with Alcohol- Related Conditions. National Institute on Alcohol Abuse and Alcoholism. Washington, DC: U.S. Govt. Print. Off., 1989.

26. Stinson, F. & Williams, G. Surveillance Report #4: Trends in Alcohol-Related Morbidity Among Short-Stay Community Hospital Discharges, 1979-84. Rockville, MD: National Institute on Alcohol Abuse and Alcoholism, Division of Biometry and Epidemiology, Alcohol Epidemiologic Data System, Jan. 1987. U.S. Department of Transportation. Fatal Accident Reporting System 1983. Washington, DC: the Department, 1985.

27. Williams, G.; Aitken. S.; and Malin, H. Reliability of self-reported alcohol consumption in a general population survey. Journal of Studies on Alcohol 46:223-227, 1985.

28. Williams, G.; Dufour, M., and Bertolucci, D. Drinking levels, knowledge, and associated characteristics, 1985 NHIS findings. Public Health Reports 101:593-598. 1986.

29. Williams, G.D.; Stinson, F.S.; Parker, D.A.; Harford, T.C.; and Noble, J. Epidemioiogic Bulletin No. 15: Demographic trends. alcohol abuse and alcoholism, 1985-1995. Alcohol Health & Research World 11 (3):80-83, 1987.

30. Williams, G.; Grant, B.; Harford, T.; and Noble, J. Population projections using DSM-III criteria: Alcohol abuse and dependence, 1990-2000. Alcohol Health & Research World, in press.

31. Zobeck, T.; Grant, B.; Williams, G.; and Bertolucci, D. Surveillance report #12: Trends in Alcohol- Related Fatal Traffic Crashes, United States: 1977-1987. Rockville, MD: National Institute on Alcohol Abuse and Alcoholism, Division of Biometry and Epidemiology, Alcohol Epidemiologic Data System, Aug. 1989.

Source: National Institute on Alcohol Abuse and Alcoholism (1999) National Institutes of Health

v Screening for Alcoholism

It is estimated that at least 20 percent of adults who visit a physician have had an alcohol problem at one time ⁽¹⁾. In a survey of patients admitted to an inpatient service, 12 to 30 percent screened positively for alcoholism ⁽²⁾. Yet, several recent studies indicate that physicians in various health care settings often do not recognize and treat alcoholism ^(3,2,4). These findings underscore the need for effective and accurate procedures that will enable clinicians to screen for alcoholism.

Alcohol screening identifies individuals in a patient population who have begun to develop or who are at risk for developing alcoholism. Although physicians customarily take a patient's medical history, routine use of a standard alcoholism-detection instrument is valuable because these instruments provide a structured, disciplined, and consistent means to detect individuals at risk.

Alcoholism-Screening Instruments

Two types of alcoholism-screening instruments are available. The first type includes self-report questionnaires and structured interviews; the second type includes clinical laboratory tests which can detect pathophysiology associated with excessive alcohol consumption . Both types of screening instruments should be valid (i.e., measure what the clinician or researcher is attempting to measure) and should yield reliable results (i.e., consistent across raters and time).

Sensitivity and specificity, key properties of every screening test, are related to validity. Sensitivity refers to the test's accuracy in identifying individuals with an alcohol problem (i.e., persons with the disease test as positive). Specificity refers to the test's effectiveness in identifying people who do not have an alcohol problem (i.e., persons without the disease test as negative).

Two issues should be addressed in the discussion of sensitivity and specificity. First, it is not possible to optimize both properties in a screening instrument. The likelihood of over-identifying alcohol abuse occurs with increased sensitivity; conversely, the possibility of missing people who have an alcohol problem heightens with increased specificity ⁽⁵⁾. Second, in determining the utility of a screening test, knowledge of the test's sensitivity and specificity is not sufficient. The prevalence of the particular condition in the screened population also must be taken into account ⁽⁶⁾. Sensitivity and specificity are functions of a screening test's cutoff score (a value that clinicians use to define a positive result from a screening instrument). If the base rate of a condition in a population is low, most of the cases identified by a sensitive test will be false positives ⁽⁵⁾.

In addition, it is important to note that no "gold standard" exists for evaluating the accuracy of screening instruments. Clinicians compare evidence for alcoholism from medical records and clinical examination with screening results to confirm the accuracy of a particular alcoholism-screening instrument.

The CAGE questionnaire, a mnemonic for attempts to cut down on drinking, annoyance with criticisms about drinking, guilt about drinking, and using alcohol as an eye-opener ^(7,8), is a self-report screening instrument that appears to be suited to a busy medical setting when there is limited time for patient interviews ⁽⁹⁾. The CAGE, which can be self-administered or conducted by a clinician, poses four overt yes-no questions and requires approximately 1 minute to complete. Bush and colleagues ⁽¹⁰⁾ used the CAGE to screen 518 patients in a community teaching hospital At a cutoff score of "2" (in this case, meaning two "yes" answers), the investigators found that the test correctly identified 75 percent of alcoholics (sensitivity) and 96 percent of nonalcoholics (specificity). For routine health screening, the test may identify individuals with alcohol problems that might have been missed otherwise ⁽¹¹⁾.

The Michigan Alcoholism Screening Test (MAST) ⁽¹²⁾ is a formal 25-item questionnaire that requires approximately 25 minutes to complete. The MAST focuses on the consequences of problem drinking and on the subjects' own perceptions of their alcohol problems. Recent studies have reported that a cutoff score of "12" or "13" achieves balanced rates of false positives and false negatives ^(13,14). Two shortened forms of the MAST, a 13-item Short MAST (SMAST) ⁽¹⁵⁾ and a 10-item brief MAST (b-MAST) ⁽¹⁶⁾, have been constructed using items from the original test that are highly discriminating for alcoholism. A cutoff score of "3" is suggested for the SMAST; a cutoff score of "6" is suggested for the b-Mast.

The Self-Administered Alcoholism Screening Test (SMST) ⁽¹⁷⁾ is a 35-item questionnaire or interview with a yes-no format. A score of "10" or greater denotes probable alcoholism. Hurt and colleagues (18) evaluated the use of the test with patients undergoing general examinations and recommended the instrument as an adjunct to a physician interview and an examination. A more recent study reported that the original SAAST and an abbreviated nine-item version are useful for screening medical patients for alcoholism ⁽¹⁹⁾.

The Alcohol Dependence Scale (ADS) ⁽²⁰⁾ is a self-report questionnaire designed to measure elements of the alcohol dependence syndrome described by Edwards and Gross ⁽²¹⁾. The test, which yields an index of severity of alcohol dependence, addresses core features of dependence, including an individual's compulsion to drink excessively, repetitive experiences of withdrawal symptoms, and loss of control overdrinking. Ross and colleagues ⁽¹⁴⁾ compared the merits of the ADS and the MAST as screening tools and determined that the specificity and sensitivity for the two tests were approximately equivalent.

Alcohol is the most widely used drug by young persons between the ages of 12 and 17 years ⁽²²⁾. Routine screening, however, is relatively rare in pediatric practices ⁽²³⁾. Because life problems for adolescents and adults differ, many screening instruments are inappropriate for younger individuals. The Adolescent Drinking Inventory ⁽²⁴⁾ is a self-report instrument developed specifically to screen adolescents. The inventory's 25 questions focus on drinking-related loss of control as well as social, psychological, and physical symptoms of alcohol problems. Allen and colleagues ⁽⁹⁾ reported that the inventory correctly identified 88 percent of adolescents with alcohol problems and 82 percent of those without alcohol problems.

Heavy alcohol intake during pregnancy can have severe adverse effects on a developing fetus; yet, maternal drinking can be difficult to detect. Sokol and colleagues ⁽²⁵⁾ developed the T-ACE questionnaire to identify pregnant women who consume quantities of alcohol that potentially can damage the fetus (defined in this study as daily intake of 1 ounce of absolute alcohol or greater). The questionnaire takes approximately 1 minute to complete and incorporates the C, A, and E items of the CAGE. The G item is replaced with a question that addresses alcohol tolerance (T). The investigators considered a woman tolerant if she needs more than two drinks to feel the effects of alcohol. Perhaps because many individuals do not understand the implications of tolerance, the tolerance question did not appear to trigger psychological denial. In study of 971 pregnant women, the T-ACE correctly identified 69 percent of those women who consumed more than an ounce of alcohol per day.

Clinical laboratory procedures, the second type of screening test, frequently are used to corroborate results of physicians' interviews; and of self-administered questionnaires. Biochemical markers of heavy alcohol consumption can provide objective evidence of problem drinking, especially in patients who deny any drinking problem. However, the sensitivities and specificities of these biological laboratory markers can be modified by nonalcoholic liver injury, by drug use, and by metabolic disorders or individual metabolic differences.

Several clinical tests may be useful in detecting harmful alcohol use. Increased activity of serum gamma-glutamyltransferase (GGT) is a relatively sensitive index of liver damage in alcoholics and heavy drinkers ^(26,27). However, this test lacks diagnostic specificity because all types of liver damage and a variety of diseases may cause elevated serum activity of this enzyme. Results may be more discriminating when interpreted in conjunction with the measure of mean corpuscular volume (MCV) ⁽²⁸⁾. MCV, an index of red blood cell size, increases with excessive alcohol intake. Although MCV has a high correlation with alcohol consumption, the index, alone, is not a useful screening marker ⁽²⁹⁾. The liver enzyme aspartate aminotransferase (AST) can be a useful marker for alcohol abuse: The ratio of levels of mitochondrial AST to total AST has been found effective in differentiating alcoholics from other patients and in detecting chronic excessive drinking ^(30,31,32).

It is important to note that self-report interviews and questionnaires have greater sensitivity and specificity than routine blood tests for biochemical markers (29). Laboratory tests may be used most successfully in conjunction with self-report instruments to enhance objectivity ^(32,33,34).

Conclusion

Untreated alcoholism often results in severe or fatal outcomes and can be the underlying cause of other illnesses. Therefore, screening all patients for alcohol problems particularly in primary health care settings is a medical necessity.

Structured interviews and self-report instruments are useful for screening. Both are rapid, inexpensive, noninvasive, and relatively accurate tools. A screening instrument should be selected on the basis of staff experience and training, available testing time, and characteristics of the patient population and should be used consistently.

Although laboratory tests such as the GGT can provide useful information to supplement knowledge gained through an interview or self-report, laboratory tests are not adequate when used alone to screen for alcohol problems.

Developing objective markers of alcohol use currently is an important goal of alcohol research. An objective marker should testify to the subject's blood alcohol level over a period of several weeks, even if the subject is abstinent at the time of sampling.

References

1. Cleary, P.D.; Miller, M.; Bush, B.T.; Warburg, M.W.; Delbanco, T.L.; and Aronson, M.D. Prevalence and recognition of alcohol abuse in a primary care population American Journal of Medicine 85:466- 471. 1988.

2. Moore, R.D.; Bone, L.R.: Geller, G.; Mamon, J.A.: Stokes, E.J.; and Levine, D.M. Prevalence, detection, and treatment of alcoholism in hospitalized patients. Journal of the American Medical Association 261(3):403-407. 1989.

3. Clement, S. The identification of alcohol-related problems by general practitioners. British Journal of Addiction 81:257-264, 1986

4. Moore, R.D. & Malitz, F.E. Under diagnosis of alcoholism by residents in an ambulatory medical practice. Journal of Medical Education 61( 1 ):46-52, 1986.

5. Rice, J.P. Statistical issues in the interpretation of tests. In: Screening for Alcoholism in Primary Care Settings. Rockville, MD: National Institute on Alcohol Abuse and Alcoholism, 1987. pp. 3-5.

6. Grant, B.F.; Hasin, D.S.; and Hartford, T.C. Screening for major depression among alcoholics: An application of receiver operating characteristic analysis. Drug and Alcohol Dependence 23:123-131, 1989.

7. Mayfield, D.G.; McLeod. G. and Hall, P. The CAGE questionnaire: Validation of a new alcoholism screening instrument. American Journal of Psychiatry 131:1121-1123, 1974.

8. Ewing, J.A. Detecting alcoholism: The CAGE questionnaire. Journal of the American Medical Association 252(14):1905-1907,1984.

9. Allen, J.P.; Eckardt, W.; and Wallen, J. Screening for alcoholism: Techniques and issues. Public Health Reports 103(6):586-592,1988.

10. BUSH, B.;Shaw. S.; Cleary, P.; Delbanco. T.L.; and Aronson, M.D. Screening for alcohol abuse using the CAGE questionnaire. American Journal of Medicine 82:231-23S, 1987.

11. Clark, W.D. Alcoholism: Blocks to diagnosis and treatment. American Journal of Medicine 71 :275- 286, 1981.

12. Selzer, M.L. The Michigan Alcoholism Screening Test: The quest for a new diagnostic instrument. American Journal of Psychiatry 127(12):89-94,1971.

13. Jacobson, G R. & Lindsay, D. Screening for alcohol problems among the unemployed. In: Galanter, M., ed. Currents in Alcoholism: Recent Advances in Research and Treatment. Vol. VlI. New York: Grune and Stratton, 1980. pp. 357-371.

14. Ross, H.E; Gavin, D.R.; and Skinner, H.A. Diagnostic validity of the MAST and the Alcohol Dependence Scale in the assessment of DSM-III alcohol disorders. Journal of Studies on Alcohol, in press.

15. Selzer, M.L.; Vinokur A.; and van Rooijen, L. A self-administered Short Michigan Alcoholism Screening Test (SMAST). Journal of Studies on Alcohol 36(1):117-126, 1975.

16. Pokorny, A.D.; Miller, B.A.; and Kaplan, H.B. The brief MAST: A shortened version of the Michigan Alcoholism Screening Test. American Journal of Psychiatry 129(3):118-121, 1972.

17. Swenson, W.M. & Morse, R.U. The use of a self-administered alcoholism screening test (SAAST) in a medical center. Mayo Clinic Proceedings 50(4):204-208, 1975.

18. Hurt, R.D.; Morse, R.M.; and Swenson, W.M. Diagnosis of alcoholism with a self-administered alcoholism screening test. Mayo Clinic Proceedings 55:365-370, 1980.

19. Davis, L.J., JR.; Hurt, R.D.; Morse, R.M.; and O'Brien, P.C. Discriminate analysis of the self-administered alcoholism screening test. Alcoholism: Clinical and Experimental Research 11(3):269-273, 1987.

20. Skinner, H.A. & Horn, J.L. Alcohol Dependence Scale (ADS) Users Guide. Toronto: Addition Research Foundation,1984.

21. Edwards, G. & Gross, M.M. Alcohol dependence: provisions description of a clinical syndrome. British Medical Journal 1 (6017): 1058-1061, 1976.

22. Forney, P.D.; Forney, M.A.; and Ripley, W.K. Profile of an adolescent problem drinker. Journal of Family Practice 27(1):65-70, 1988.

23. Klizner, U.; Schwartz, R.H.; Gruenewald, P.; and Blasinsky, M. Screening for risk factors for adolescent alcohol and drug use. American Journal of Diseases of Children 141(Jan.):45-49, 1987.

24. Harrell, A V. & Wirtz P.W. Screening for adolescent problem drinking: Validation of a multidimensional instrument for case identification. Psychological Assessment 1:61 -63,1989.

25. Sokol, R.J.; Martier, S.S.; and Ager, J.W. The T-ACE questions: Practical prenatal detection of risk- drinking. American Journal of Obstetrics and Gynecology 160(4) :863-870,1989.

26. Schuckit, M.A. & Griffiths, J.C. Gamma-glutamyltransferase values in nonalcoholic drinking men. American Journal of Psychiatry 139(2):227-228. 1982.

27. Gjerde,H.; Amundsen, A.; Skog, O.-J.; Morland, J.; and Aasland, O.G. Serum gamma-glutamyltransferase: An epidemiological indicator of alcohol consumption? British Journal of Addiction 82:1027-1031,1987.

28. Chick, J.; Kreitman, N.; and Plant, M. Mean cell volume and gammaglutamyl-transferase as markers of drinking in working men. Lancet 1:12491251, 1981.

29. Bernardt, M.W.; Mumford, J.; Taylor, C.; Smith, B.; and Murray, R.M. Comparison of questionnaire and laboratory tests in the detection of excessive drinking and alcoholism. Lancet 1:325-328, 1982.

30. Nalpas, B.; Vassault, A.; LeGuillou, A.; Lesgourgues, B.; Ferry, N.; Lacour, B.; and Berthelot, P. Serum activity of mitochondrial aspartate aminotransferase: A sensitive marker of alcoholism with or without alcoholic hepatitis. Hepatology 4(5):893-896, 1984.

31. Nalpas, B.; Vassault, A.; Charpin, S.; Lacour, B.; and Berthelot, P. Serum mitochondria aspartate aminotransferase as a marker of chronic alcoholism: Diagnostic value and interpretation in a liver unit. Hepatology 6(4):608-614, 1986.

32. Lumeng, L. New diagnostic markers of alcohol abuse. Hepatology 6(4):742-745, 1986.

33. Watson, R.R.; Mohs, M.E.; Eskelson, C.; Sampliner, R.E.; and Hartmann, B. Identification of alcohol abuse and alcoholism with biological parameters. Alcoholism: Clinical and Experimental Research 10(4):364-385, 1986.

34. Yates, D.W.; Hadfield, J.M.; and Peters, K. The detection of problem drinkers in the Accident & Emergency department. British Journal of Addiction 82:163-167, 1987.

Source: National Institute on Alcohol Abuse and Alcoholism (1999)     National Institutes of Health 

v     Moderate Drinking

Definition of Moderate Drinking

Moderate drinking is difficult to define because it means different things to different people. The term is often confused with "social drinking," which refers to drinking patterns that are accepted by the society in which they occur. However, social drinking is not necessarily free of problems. Moderate drinking may be defined as drinking that does not generally cause problems, either for the drinker or for society. Since there are clearly both benefits and risks associated with lower levels of drinking, this chapter will explore potentially positive and adverse effects of "moderate" drinking.

It would be useful if the above definition of moderate drinking were bolstered by numerical estimates of "safe" drinking limits. However, the usefulness of quantitative definitions of moderate drinking is compromised by the likelihood that a given dose of alcohol may affect different people differently. Adding further complexity, the pattern of drinking is also an important determinant of alcohol-related consequences. Thus, while epidemiologic data are often collected in terms of the "average number of drinks per week," one drink taken each day may have different consequences than seven drinks taken on a Saturday night ⁽¹⁾.

Despite the complexity, numerical definitions of moderate drinking do exist. For example, guidelines put forth jointly by the U.S. Department of Agriculture and the U.S. Department of Health and Human Services ⁽²⁾ define moderate drinking as no more than one drink a day for most women, and no more than two drinks a day for most men. A standard drink is generally considered to be 12 ounces of beer, 5 ounces of wine, or 1.5 ounces of 80-proof distilled spirits. Each of these drinks contains roughly the same amount of absolute alcohol approximately 0.5 ounce or 12 grams ⁽³⁾.

These guidelines exclude the following persons, who should not consume alcoholic beverages: women who are pregnant or trying to conceive; people who plan to drive or engage in other activities that require attention or skill; people taking medication, including over-the-counter medications; recovering alcoholics; and persons under the age of 21 ⁽²⁾. Although not specifically addressed by the guidelines, alcohol use also is contraindicated for people with certain medical conditions such as peptic ulcer.

The existence of separate guidelines for men and women reflects research findings that women become more intoxicated than men at an equivalent dose of alcohol ⁽⁴⁾. This results, in part, from the significant difference in activity of an enzyme in stomach tissue of males and females that breaks down alcohol before it reaches the bloodstream. The enzyme is four times more active in males than in females ⁽⁵⁾. Moreover, women have proportionately more fat and less body water than men. Because alcohol is more soluble in water than in fat, a given dose becomes more highly concentrated in a female's body water than in a male's ⁽⁶⁾.

Since the proportion of body fat increases with age, Dufour and colleagues recommend a limit of one drink per day for the elderly ⁽⁷⁾.

Benefits of Moderate Drinking

Psychological benefits of moderate drinking. A review of the literature ⁸ suggests that lower levels of alcohol consumption can reduce stress; promote conviviality and pleasant and carefree feelings; and decrease tension, anxiety, and self-consciousness. In the elderly, moderate drinking has been reported to stimulate appetite, promote regular bowel function, and improve mood ⁷.

Cardiovascular benefits of moderate drinking. There is a considerable body of evidence that lower levels of drinking decrease the risk of death from coronary artery disease (CAD). This effect has been demonstrated in a broad range of older epidemiologic studies ⁹. More recently, Boffetta and Garfinkel ¹⁰ found that white American men who reported in 1959 that they consumed an average of fewer than three drinks per day were less likely to die during the next 12 years than men who reported abstinence. This finding was due primarily to a reduction in CAD. In a similar study using a wide range of ethnic groups, De Labry and colleagues ¹¹ found that rates of overall mortality were lowest for men who consumed fewer than three drinks per day over a 12-year period.

Similar results have been obtained with female subjects. Stampfer and colleagues ¹² analyzed data on middle-aged women and determined that consumption of approximately one drink per day decreases the risks of coronary heart disease. Razay and colleagues ¹³, using a random population sample, found consumption of up to two drinks per day to be associated with lower levels of cardiovascular risk factors in women. In postmenopausal women, the apparent protective effect of alcohol may be explained in part by an alcohol-induced increase in estrogen levels ¹⁴.

Various researchers have suggested that moderate drinking is not protective against CAD, arguing that higher mortality among abstainers results from including among them people who have stopped drinking because of ill health. Higher mortality among these "sick quitters" would explain the comparative longevity of moderate drinkers ^15,16,17. However, studies investigating the "sick quitter" effect do not support that conclusion; including "sick quitters" in the abstinent category cannot completely explain the apparent protective effect of moderate drinking against CAD ^10,18,19,20.

Risks of Moderate Drinking

There are risks that might offset the benefits of moderate drinking. Research shows that adverse consequences may occur at relatively low levels of consumption ¹.

Stroke. A review of epidemiologic evidence concludes that moderate alcohol consumption increases the potential risk of strokes caused by bleeding, although it decreases the risk of strokes caused by blocked blood vessels ²¹.

Motor vehicle crashes. While there is some evidence to suggest that low blood alcohol concentrations (BACs) bear little relationship to road crashes, impairment of driving-related skills by alcohol has been found to begin at 0.05 percent BAC or lower, with rapidly progressing deterioration as the BAC rises ²². A man weighing 140 pounds might attain a BAC of 0.05 percent after two drinks.

Interactions with medications. Alcohol may interact harmfully with more than 100 medications, including some sold over the counter ²³. The effects of alcohol are especially augmented by medications that depress the function of the central nervous system, such as sedatives, sleeping pills, anticonvulsants, antidepressants, antianxiety drugs, and certain painkillers. There is a consequent increased danger of driving an automobile after even moderate drinking if such medications are taken ²⁴. In advanced heart failure, alcohol may not only worsen the disease, but also interfere with the function of medications to treat the disease ²⁵.

Cancer. Although most evidence suggests an increased risk for certain cancers only among the heaviest drinkers, moderate drinking may be weakly related to female breast cancer. In one study ²⁶, breast cancer was approximately 50 percent more likely to develop in women who consumed three to nine drinks per week than in women who drank fewer than three drinks per week. Although evidence concerning large bowel cancer is conflicting, one study suggests the possibility of a weak relation to consumption of one or more drinks per day ²⁷.

Birth defects. Several ongoing studies are exploring the fetal risks associated with low levels of alcohol consumption. In one study ²⁸, children whose mothers reported consuming an average of two to three drinks per day during pregnancy were smaller in weight, length, and head circumference and had an increased number of minor physical anomalies when examined at intervals through the age of 3. In addition, mothers' self-reported consumption of as few as two drinks per day during pregnancy was found to be related to a decrease in IQ scores of 7-year-old children ²⁹.

The question of whether moderate drinking is a risk factor for the fetus is not altogether settled, because mothers' self-reports of alcohol consumption may be underestimates ³⁰. However, animal research provides additional evidence for adverse fetal effects from low levels of drinking. Nervous system abnormalities occurred in monkeys whose mothers were exposed weekly to low doses of alcohol. An effect occurred at a maternal BAC as low as 0.024 percent ³¹. A 120-pound woman might attain this BAC after one drink. Similarly, low prenatal alcohol doses produced biochemical and physiological changes in rat brains ^32,33.

Shift to heavier drinking. Recovering alcoholics, as well as people whose families have alcohol problems, may not be able to maintain moderate drinking habits ². Once a person progresses from moderate to heavier drinking, the risks of social problems (for example, drinking and driving, violence, trauma) and medical problems (for example, liver disease, pancreatitis, brain damage, reproductive failure, cancer) increase greatly ³⁴.

Conclusion

Drinking at "moderate levels" (up to two drinks a day for men and one drink a day for women) has both benefits and risks. Therefore, it should not be surprising that there are questions about what advice to give to individuals about using alcohol.

Research aimed at more clearly defining the circumstances that increase risk and the categories of individuals who are at risk for alcohol-related problems will help individuals and the professionals who advise them to make more informed decisions concerning alcohol use. Better understanding of the biological mechanisms involved in the cardioprotective aspects of moderate alcohol use also could lead researchers to find alternate ways to provide the same protection.

Current advice to individuals should acknowledge that there are trade-offs involved in each decision about drinking: reducing risk of developing coronary artery disease, for example, may be offset by risk of developing another alcohol-related health condition. In general, if an individual is drinking "moderately" and does not fit into one of the special risk categories discussed here, there is no reason to recommend anything different. Similarly, individuals who are not yet drinking (young adults who have recently turned 21, for example), and not at special risk, can be told that "moderate drinking" will probably not be harmful. (Abstinent individuals, however, should not be advised to begin to drink two drinks a day solely to protect against coronary artery disease.) Finally, those who are at higher risk (because of a family history of alcoholism, for example) must be made aware of the trade-offs involved in decisions to drink. 

References

1. Werch, C.E.; Gorman, D.R.; & Marty, P.J. Relationship between alcohol consumption and alcohol problems in young adults. Journal of Drug Education 17(3):261-276, 1987.

2. U.S. Department of Agriculture/U.S. Department of Health and Human Services. Home and Garden Bulletin No. 232. Nutrition and Your Health: Dietary Guidelines for Americans. 3d ed. Washington, DC: Supt. of Docs., U.S. Govt. Print. Off., 1990.

3. Whelan, E.M. To your health. Across the Board, Jan. 1988, pp. 49-53.

4. Jones, B.M., & Jones, M.K. Alcohol effects in women during the menstrual cycle. Annals of the New York Academy of Sciences 273:576-587, 1976.

5. Frezza, M.; Di Padova, C.; Pozzato, G.; Terpin, M.; Baraona, E.; & Lieber, C.S. High blood alcohol levels in women: The role of decreased gastric alcohol dehydrogenase activity and first-pass metabolism. New England Journal of Medicine 322(2):95-99, 1990.

6. Goist, K.C., & Sutker, P.B. Acute alcohol intoxication and body composition in women and men. Biochemistry & Behavior 22:811-814, 1985.

7. Dufour, M.C.; Archer, L.; & Gordis, E. Alcohol and the elderly. Clinics in Geriatric Medicine 8(1):127-141, 1992.

8. Baum-Baicker, C. The psychological benefits of moderate alcohol consumption: A review of the literature. Drug and Alcohol Dependence 15:305-322, 1985.

9. Moore, R.D., & Pearson, T.A. Moderate alcohol consumption and coronary artery disease: A review. Medicine 65(4):242-267, 1986.

10. Boffetta, P., & Garfinkel, L. Alcohol drinking and mortality among men enrolled in an American Cancer Society prospective study. Epidemiology 1(5):342-348, 1990.

11. De Labry, L.O.; Glynn, R.J.; Levenson, M.R.; Hermos, J.A.; LoCastro, J.S.; & Vokonas, P.S. Alcohol consumption and mortality in an American male population: Recovering the U-shaped curve–findings from the normative aging study. Journal of Studies on Alcohol 53(1):25-32, 1992.

12. Stampfer, M.J.; Colditz, G.A.; Willett, W.C.; Speizer, F.E.; & Hennekens, C.H. A prospective study of moderate alcohol consumption and the risk of coronary disease and stroke in women. New England Journal of Medicine 319(5):267-273, 1988.

13. Razay, G.; Heaton, K.W.; Bolton, C.H.; & Hughes, A.O. Alcohol consumption and its relation to cardiovascular risk factors in British women. British Medical Journal 304:80-83, 1992.

14. Gavaler, J.S., & Van Thiel, D.H. The association between moderate alcoholic beverage consumption and serum estradiol and testosterone levels in normal postmenopausal women: Relationship to the literature. Alcoholism: Clinical and Experimental Research 16(1):87-92, 1992.

15. Marmot, M., & Brunner, E. Alcohol and cardiovascular disease: The status of the U shaped curve. British Medical Journal 303:565-568, 1991.

16. Shaper, A.G. Alcohol and mortality: A review of prospective studies. British Journal of Addiction 85:837- 847, 1990.

17. Shaper, A.G.; Wannamethee, G.; & Walker, M. Alcohol and mortality in British men: Explaining the U-shaped curve. Lancet 2(8623):1267-1273, 1988.

18. Klatsky, A.L.; Armstrong, M.A.; & Friedman, G.D. Risk of cardiovascular mortality in alcohol drinkers, ex- drinkers and nondrinkers. American Journal of Cardiology 66:1237-1242, 1990.

19. Jackson, R.; Scragg, R.; & Beaglehole, R. Alcohol consumption and risk of coronary heart disease. British Medical Journal 303:211-216, 1991.

20. Rimm, E.B.; Giovannucci, E.L.; Willett, W.C.; Colditz, G.A.; Ascherio, A.; Rosner, B.; & Stampfer, M.J. Prospective study of alcohol consumption and risk or coronary disease in men. Lancet 338(8765):464- 468, 1991.

21. Camargo, C.A., Jr. Moderate alcohol consumption and stroke: The epidemiologic evidence. Stroke 20(12):1611-1626, 1989.

22. Council on Scientific Affairs. Alcohol and the driver. Journal of the American Medical Association 255(4):522-527,1986.

23. Shinn, A.F., & Shrewsbury, R.P., eds. Evaluations of Drug Interactions. New York: Macmillan, 1988.

24. Gilman, A.G.; Rall, T.W.; Nies, A.S.; & Taylor, P., eds. Goodman and Gilman's the Pharmacological Basis of Therapeutics. New York: Pergamon Press, 1990.

25. Thomas, B.A., & Regan, T.J. Interactions between alcohol and cardiovascular medications. AlcoholHealth & Research World 14(4):333-339, 1990.

26. Willett, W.C.; Stampfer, M.J.; Colditz, G.A.; Rosner, B.A.; Hennekens, C.H.; & Speizer, F.E. Moder- ate alcohol consumption and the risk of breast cancer. New England Journal of Medicine 316:1174- 1180, 1987.

27. Klatsky A.L.; Armstrong, M.A.; Friedman, G.D.; & Hiatt, R.A. The relations of alcoholic beverage use to colon and rectal cancer. American Journal of Epidemiology 128(5):1007-1015, 1988.

28. Day, N.L.; Robles, N.; Richardson, G.; Geva, D.; Taylor, P.; Scher, M.; Stoffer, D.; Cornelius, M.; & Goldschmidt, L. The effects of prenatal alcohol use on the growth of children at three years of age. Alcoholism: Clinical and Experimental Research 15(1):67-71, 1991.

29. Streissgut, A.P.; Barr, H.M.; & Sampson, P.D. Moderate prenatal alcohol exposure: Effects on child IQ and learning problems at age 7 1/2 years. Alcoholism: Clinical and Experimental Research 14(5):662- 669, 1990.

30. Ernhart, C.B.; Morrow-Tlucak, M.; Sokol, R.J.; & Martier, S. Underreporting of alcohol use in pregnancy. Alcoholism: Clinical and Experimental Research 12(4):506-511, 1988.

31. Clarren S.K.; Astley, S.J.; Bowden, D.M.; Lai, H.; Milam, A.H.; Rudeen, P.K.; & Shoemaker, W.J. Neuroanatomic and neurochemical abnormalities in nonhuman primate infants exposed to weekly doses of ethanol during gestation. Alcoholism: Clinical and Experimental Research 14(5):674-683, 1990.

32. Farr, K.L.; Montano, C.Y.; Paxton, L.L.; & Savage, D.D. Prenatal ethanol exposure decreases hippocam pal 3H-glutamate binding in 45-day-old rats. Alcohol 5(2):125-133, 1988.

33. Swartzwelder, H.S.; Farr, K.L.; Wilson, W.A.; & Savage, D.D. Prenatal exposure to ethanol decreases physiological plasticity in the hippocampus of the adult rat. Alcohol 5(2):121-124, 1988.

34. National Institute on Alcohol Abuse and Alcoholism. Seventh Special Report to the U.S. Congress on Alcohol and Health. DHHS Pub. No. (ADM)90-1656. Washington, DC: Supt. of Docs., U.S. Govt. Print. Off., 1990.

Source: National Institute on Alcohol Abuse and Alcoholism. (April 1992) National Institutes of Health 

v Alcohol and Women

Much of our knowledge of alcoholism has been gathered from studies conducted with a predominance of male subjects. Recent studies involving more female subjects reveal that drinking differs between men and women.

Studies in the general population indicate that fewer women than men drink. It is estimated that of the 15.1 million alcohol-abusing or alcohol-dependent individuals in the United States, approximately 4.6 million (nearly one-third) are women ⁽¹⁾. On the whole, women who drink consume less alcohol and have fewer alcohol-related problems and dependence symptoms than men ^(2,3), yet among the heaviest drinkers, women equal or surpass men in the number of problems that result from their drinking ⁽³⁾.

Drinking behavior differs with the age, life role, and marital status of women. In general, a woman's drinking resembles that of her husband, siblings, or close friends ⁽³⁾. Whereas younger women (aged 18-34) report higher rates of drinking-related problems than do older women ^(3,4), the incidence of alcohol dependence is greater among middle-aged women (aged 35-49) ⁽⁵⁾.

Contrary to popular belief, women who have multiple roles (e.g., married women who work outside the home) may have lower rates of alcohol problems than women who do not have multiple roles ⁽⁶⁾. In fact, role deprivation (e.g., loss of role as wife, mother, or worker) may increase a woman's risk for abusing alcohol ⁽⁷⁾. Women who have never married or who are divorced or separated are more likely to drink heavily and experience alcohol-related problems than women who are married or widowed. Unmarried women living with a partner are more likely still to engage in heavy drinking and to develop drinking problems.

Heath and colleagues ⁽⁸⁾ studied drinking behavior among a select sample of female twins to identify possible environmental factors that may modulate drinking behavior. They reported that, among women, marital status appears to modify the effects of genetic factors that influence drinking habits. Marriage or a marriage-like relationship lessens the effect of an inherited liability for drinking.

Several researchers have explored whether drinking patterns and alcohol-related problems vary among women of different racial or ethnic groups. Black women (46 percent) are more likely to abstain from alcohol than white women (34 percent) ^(9,10). Further, although it is commonly assumed that a larger proportion of black women drink heavily, researchers have disproved this assumption: Equal proportions of black and white women drink heavily ^(3,9). Black women report fewer alcohol-related personal and social problems than white women, yet a greater proportion of black women experience alcohol-related health problems ⁽¹¹⁾.

Data from self-report surveys suggest that Hispanic women are infrequent drinkers or abstainers ^(12,13), but this may change as they enter new social and work arenas. Gilbert ⁽¹⁴⁾ found that reports of abstention are greater among Hispanic women who have immigrated to the United States; reports of moderate or heavy drinking are greater among younger, American-born Hispanic women.

The interval between onset of drinking-related problems and entry into treatment appears to be shorter for women than for men ^(15,16). Moreover, studies of women alcoholics in treatment suggest that they often experience greater physiological impairment earlier in their drinking careers, despite having consumed less alcohol than men ^(17,18). These findings suggest that the development of consequences associated with heavy drinking may be accelerated or "telescoped" in women.

In addition to these many psychosocial and epidemiological differences, the sexes also experience different physiological effects of alcohol. Women become intoxicated after drinking smaller quantities of alcohol than are needed to produce intoxication in men ⁽¹⁹⁾. Three possible mechanisms may explain this response.

First, women have lower total body water content than men of comparable size. After alcohol is consumed, it diffuses uniformly into all body water, both inside and outside cells. Because of their smaller quantity of body water, women achieve higher concentrations of alcohol in their blood than men after drinking equivalent amounts of alcohol. More simply, blood alcohol concentration in women may be likened to the result of dropping the same quantity of alcohol into a smaller pail of water.

Second, diminished activity of alcohol dehydrogenase (the primary enzyme involved in the metabolism of alcohol) in the stomach also may contribute to the gender-related differences in blood alcohol concentrations and a woman's heightened vulnerability to the physiological consequences of drinking. Julkunen and colleagues ⁽²⁰⁾ demonstrated in rats that a substantial amount of alcohol is metabolized by gastric alcohol dehydrogenase in the stomach before it enters the systemic circulation. This "first-pass metabolism" of alcohol decreases the availability of alcohol to the system. Frezza and colleagues ⁽²¹⁾ reported that, because of diminished activity of gastric alcohol dehydrogenase, first-pass metabolism was decreased in women compared with men and was virtually nonexistent in alcoholic women.

Third, fluctuations in gonadal hormone levels during the menstrual cycle may affect the rate of alcohol metabolism, making a woman more susceptible to elevated blood alcohol concentrations at different points in the cycle. Research findings to date, however, have been inconsistent ^(22,23,24).

Chronic alcohol abuse exacts a greater physical toll on women than on men. Female alcoholics have death rates 50 to 100 percent higher than those of male alcoholics. Further, a greater percentage of female alcoholics die from suicides, alcohol-related accidents, circulatory disorders, and cirrhosis of the liver ⁽²⁵⁾.

Increasing evidence suggests that the detrimental effects of alcohol on the liver are more severe for women than for men. Women develop alcoholic liver disease, particularly alcoholic cirrhosis and hepatitis, after a comparatively shorter period of heavy drinking and at a lower level of daily drinking than men ^(26,27). Proportionately more alcoholic women die from cirrhosis than do alcoholic men ⁽²⁸⁾.

The exact mechanisms that underlie women's heightened vulnerability to alcohol-induced liver damage are unclear. Differences in body weight and fluid content between men and women may be contributing factors ⁽²⁹⁾. In addition, Johnson and Williams ⁽³⁰⁾ suggested that the combined effect of estrogens and alcohol may augment liver damage. Finally, alcoholic women may be more susceptible to liver damage because of the diminished activity of gastric alcohol dehydrogenase in first-pass metabolism ⁽²¹⁾.

Drinking also may be associated with an increased risk for breast cancer. After reviewing epidemiological data on alcohol consumption and the incidence of breast cancer, Longnecker and colleagues ⁽³¹⁾ reported that risk increases when a woman consumes 1 ounce or more of absolute alcohol daily. Increased risk appears to be related directly to the effects of alcohol ⁽³²⁾. Moreover, risk for breast cancer and lower levels of alcohol consumption are weakly associated. Data from other studies ⁽³³⁾, however, do not concur with these findings, suggesting that more research is needed to explore the relationship between drinking and breast cancer.

Menstrual disorders (e.g., painful menstruation, heavy flow, premenstrual discomfort, and irregular or absent cycles) have been associated with chronic heavy drinking ^{(34, 35)}. These disorders can have adverse effects on fertility ⁽³⁶⁾. Further, continued drinking may lead to early menopause ^(37,38).

Animal studies have provided data that replicate the findings of studies in humans to determine the effects of chronic alcohol consumption on female reproductive function. Studies in rodents and monkeys demonstrated that prolonged alcohol exposure disrupts estrus regularity and increases the incidence of ovulatory failure ^(39,40,41).

Researchers have begun to examine whether women and men require distinct treatment approaches. It has been suggested that women alcoholics may encounter different conditions that facilitate or discourage their entry into treatment.

Women represent 25.4 percent of alcoholism clients in traditional treatment centers in the United States ⁽⁴²⁾. Although it appears that they comprise a small proportion of the treatment population (25 percent women compared with 75 percent men), the proportion of female alcoholics to male alcoholics in treatment is similar to the proportion of all female alcoholics to male alcoholics (30 percent women to 70 percent men). In addition, women drinkers pursue avenues other than traditional alcoholism programs, such as psychiatric services or personal physicians, for treatment ⁽⁴³⁾.

Women alcoholics may encounter motivators and barriers to seeking treatment that differ from those encountered by men. Women are more likely to seek treatment because of family problems ⁽⁴⁴⁾, and they often are encouraged by parents or children to pursue therapy. Men usually are encouraged to pursue therapy by their wives. Fewer women than men reach treatment through the criminal justice system or through employee assistance programs ⁽⁴⁵⁾. Lack of child care is one of the most frequently reported barriers to treatment for alcoholic women ⁽⁴⁶⁾.

Sokolow and colleagues ⁽⁴⁷⁾ attempted to compare treatment outcome between men and women and reported that, among those who completed treatment, abstinence was slightly higher among women than among men. Women had a higher abstinence rate if treated in a medically oriented alcoholism facility, whereas the abstinence rate was higher for men treated in a peer group-oriented facility. Treatment outcome was better for women treated in a facility with a smaller proportion of female clients and better for men in a facility with a larger proportion of female clients. This study provided preliminary data on gender-specific treatment outcome; however, the trials were not controlled. Although the question of whether women should have separate treatment opportunities is an important one, the supporting evidence still has not been found.

Conclusion

The extent of women's participation in alcoholism treatment appears to equal roughly the prevalence of alcohol-related problems among women. Even so, some women may face barriers that limit access to treatment. Limited financial resources may be one barrier. For example, many women do not have access to the employer-paid alcoholism treatment provided by larger industries, where men tend to predominate in the work force. Child-care concerns and the fear that an identified alcohol problem will cause the loss of dependent children also may create barriers to treatment. With regard to treatment, many questions remain to be answered by research, including whether specialized treatment in a women-only program is more effective than treatment in a mixed-gender setting.

Previous concerns about a lack of women as research subjects in alcohol studies are beginning to be addressed. However, there have been recent charges that alcohol research on women is discriminatory ^(48,49). Research on fetal alcohol and drug effects and the fear of discriminatory actions, such as imprisoning pregnant women solely because of their addiction, is central to this controversy. The issue of fetal effects and how to prevent and treat them will not go away simply because discriminatory policies have been suggested. The challenge for alcohol research will be how both sexes can benefit from the fruits of science.

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Source: National Institute on Alcohol Abuse and Alcoholism (1999)     National Institutes of Health

v Are Women More Vulnerable to Alcohol's Effects?

Women appear to be more vulnerable than men to many adverse consequences of alcohol use. Women achieve higher concentrations of alcohol in the blood and become more impaired than men after drinking equivalent amounts of alcohol. Research also suggests that women are more susceptible than men to alcohol-related organ damage and to trauma resulting from traffic crashes and interpersonal violence. This chapter examines gender differences in alcohol's effects and considers some factors that may place women at risk for alcohol-related problems.

Prevalence of Women's Drinking

Household surveys indicate that alcohol use is more prevalent among men than women in the United States ^(1,2). In one survey, 34 percent of women reported consuming at least 12 standard drinks¹ during the previous year compared with 56 percent of men ⁽¹⁾. Among drinkers surveyed, 10 percent of women and 22 percent of men consumed two or more drinks per day on average ⁽¹⁾. Men are also more likely than women to become alcohol dependent ⁽³⁾.

Women's drinking is most common between ages 26 and 34 and among women who are divorced or separated ⁽²⁾. Binge drinking (i.e., consumption of five or more drinks per occasion on 5 or more days in the past month) is most common among women ages 18 to 25 ⁽²⁾. Among racial groups, women's drinking is more prevalent among whites, although black women are more likely to drink heavily ⁽¹⁾.

Metabolism

Women absorb and metabolize alcohol differently than men. In general, women have less body water than men of similar body weight, so that women achieve higher concentrations of alcohol in the blood after drinking equivalent amounts of alcohol ^(5,6). In addition, women appear to eliminate alcohol from the blood faster than men. This finding may be explained by women's higher liver volume per unit lean body mass ^(7,8), because alcohol is metabolized almost entirely in the liver ⁽⁹⁾.

Consequences of Alcohol Use

Research suggests that women are more vulnerable than men to alcohol-related organ damage, trauma, and legal and interpersonal difficulties.

Liver Damage. Compared with men, women develop alcohol-induced liver disease over a shorter period of time and after consuming less alcohol ^(10,11). In addition, women are more likely than men to develop alcoholic hepatitis and to die from cirrhosis ⁽¹²⁾. Animal research suggests that women's increased risk for liver damage may be linked to physiological effects of the female reproductive hormone estrogen ⁽¹³⁾.

Brain Damage. Views of the brain obtained by magnetic resonance imaging (MRI) suggest that women may be more vulnerable than men to alcohol-induced brain damage. Using MRI, researchers found that a brain region involved in coordinating multiple brain functions was significantly smaller among alcoholic women compared with both nonalcoholic women and alcoholic men. These differences remained significant after measurements were adjusted for head size ⁽¹⁴⁾. Conversely, a study measuring metabolic energy utilization in selected brain regions found a significant difference between alcoholic and nonalcoholic men but no significant difference between alcoholic and nonalcoholic women ⁽¹⁵⁾. These results are not consistent with a greater vulnerability to alcoholic brain damage in women. However, the female alcoholics reported less severe alcohol use compared with the male alcoholics studied ⁽¹⁵⁾.

Heart Disease. Men and women who consume one or two alcoholic drinks per day have a lower death rate from coronary heart disease (e.g., heart attacks) than do heavier drinkers and abstainers. Among heavier drinkers, research shows similar rates of alcohol-associated heart muscle disease (i.e., cardiomyopathy) for both men and women, despite women's 60 percent lower lifetime alcohol use ⁽¹⁷⁾.

Breast Cancer. Many studies report that moderate to heavy alcohol consumption increases the risk for breast cancer ⁽¹⁸⁾ , although one recent study found no increased breast cancer risk associated with consumption of up to one drink per day, the maximum drinking level reported by most women ⁽¹⁹⁾.

Violent Victimization. A survey of female college students found a significant relationship between the amount of alcohol the women reported drinking each week and their experiences of sexual victimization ⁽²⁰⁾. Another study found that female high school students who used alcohol in the past year were more likely than nondrinking students to be the victims of dating violence (e.g., shoving, kicking, or punching) ⁽²¹⁾.

A history of heavy premarital drinking by both partners has been found to predict first-year aggression among newlyweds ⁽²²⁾. In some studies, problem drinking by wives has been linked to husband-to-wife aggression regardless of the husbands' drinking levels ⁽²³⁾.

Traffic Crashes. Although women are less likely than men to drive after drinking ^(1,24) and to be involved in fatal alcohol-related crashes ⁽²⁵⁾, women have a higher relative risk of driver fatality than men at similar blood alcohol concentrations ⁽²⁶⁾. Laboratory studies of the effects of alcohol on responding to visual cues and other tasks suggest that there may be gender differences in how alcohol affects the performance of driving tasks ⁽²⁷⁾.

Women's lower rates of drinking and driving may be attributed to their lower tendency toward risk taking compared with men ^(28,29). Women are also less likely to view drinking and driving as acceptable behavior. In a 1990 national household survey, 17 percent of women, compared with 27 percent of men, agreed that it was acceptable for a person to drink one or two drinks before driving ⁽³⁰⁾. Nevertheless, the proportion of female drivers involved in fatal crashes is increasing. In 1996, 16 percent of all drivers involved in alcohol-related fatal crashes were women, compared with 13 percent in 1986 and 12 percent in 1980 ⁽²⁵⁾.

Risk Factors for Women's Alcohol Use

Factors that may increase women's risk for alcohol abuse or dependence include genetic influences, early initiation of drinking, and victimization.

Genetic Factors. The relative contribution of genetic factors to women's risk for alcoholism has been debated. A survey of 2,163 female twins revealed greater similarity between identical twins compared with fraternal twins on measures of alcohol consumption ⁽³¹⁾. Similar studies including more than 12,000 twin pairs from the general population have confirmed that among both male and female twin pairs, identical twins are more likely than fraternal twins to have similar rates of alcohol dependence, alcohol abuse, and heavy alcohol consumption ^(32,33).

Studies of women who had been adopted at birth have shown a significant association between alcoholism in adoptee's and their biological parents ⁽³⁴⁾. In addition, antisocial personality (e.g., aggressiveness) in biological parents may predict alcoholism in both male and female adoptees ⁽³⁵⁾. However, potential interactions between genetic and environmental influences require further study.

Using laboratory animals, researchers are currently attempting to identify gender-specific genetic factors whose interactions might contribute to differential sensitivity to alcohol's effects ⁽³⁶⁾.

Age of Initiating Drinking. Results of a large nationwide survey show that more than 40 percent of persons who initiated drinking before age 15 were diagnosed as alcohol dependent at some point in their lives ⁽³⁷⁾. Rates of lifetime dependence declined to approximately 10 percent among those who began drinking at age 20 or older. The annual rate of this decline was similar for both genders ⁽³⁷⁾. Although in the past women generally started drinking at later ages than men, more recent survey data show that this difference has nearly disappeared ⁽²⁾.

Victimization. Using data collected in a large general population survey, Wilsnack and colleagues ⁽³⁸⁾ found that women who reported being sexually abused in childhood were more likely than other women to have experienced alcohol-related problems (e.g., family discord or household accidents) and to have one or more symptoms of alcohol dependence. Another study found that women in alcoholism treatment were significantly more likely to report childhood sexual abuse and father-to-daughter verbal aggression or physical violence compared with women in the general population ⁽³⁹⁾.

Widom and colleagues ⁽⁴⁰⁾ reached a different conclusion from that of Miller and colleagues. Instead of relying on women's recall of their pasts, Widom and colleagues consulted court records to identify cases of childhood physical or sexual abuse. These researchers found that for women, a history of childhood neglect, but not abuse, significantly predicted the number of alcohol-related symptoms experienced, independent of parental alcohol or other drug (AOD) problems, childhood poverty, race, and age.

Physical abuse during adulthood has also been associated with women's alcohol use and related problems. One study found that significantly more women undergoing alcoholism treatment experienced severe partner violence (e.g., kicking, punching, or threatening with a weapon) compared with other women in the community. In addition, among women in the community group, those with AOD-related problems reported significantly higher rates of severe partner violence than women without such problems. Although the findings indicate that partner violence and AOD problems co-occur among women, the data do not indicate whether the association is causal ⁽⁴¹⁾.

Conclusion

As can be seen by the varied types of information reported here, the alcohol research field has begun to recognize the importance of understanding gender differences in how alcohol is used, in the consequences of alcohol use, and in the development of alcohol dependence. For example, where women and men drink at the same rate, women continue to be at higher risk than are men for certain serious medical consequences of alcohol use, including liver, brain, and heart damage. We know that some of this risk is due to gender differences in metabolism; it also could quite possibly be due to gender-related differences in brain chemistry, in genetic risk factors, or to entirely different factors that are currently unknown. The more science can tell us about gender-related aspects of alcohol-related problems–not only what they are but why–the better job we will be able to do to prevent and treat those problems in all populations.

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30. Greenfield, T.K., and Room, R. Situational norms for drinking and drunkenness: Trends in the US adult population, 1979-1990. Addiction 92(1):33-47, 1997.

31. Prescott, C.A., and Kendler, K.S. Longitudinal stability and change in alcohol consumption among female twins: Contributions of genetics. Development Psychopathology 8(4):849-866, 1996.

32. Kendler, K.S., and Prescott, C.A. Population-based twin study of alcohol abuse and dependence: Mod eling gender differences. Am J Med Genet 74(6):574, 1997.

33. Prescott, C.A.; Aggen, S.H.; and Kendler, K.S. Sex differences in the sources of genetic liability to alcohol abuse and dependence in a population-based sample of U.S. twins. Alcohol Clin Exp Res 23(7):1136-1144, 1999.

34. Bohman, M.; Sigvardsson, S.; and Cloninger, C.R. Maternal inheritance of alcohol abuse: Cross-foster ing analysis of adopted women. Arch Gen Psychiatry 38(9):965-969, 1981.

35. Cadoret, R.J.; Yates, W.R.; Troughton, E.; et al. An adoption study of drug abuse/dependency in fe males. Compr Psychiatry 37(2):88-94, 1996.

36. Fernandez, J.R.; Vogler, G.; Tarantino, L.M.; et al. Sex-specific QTL influences in alcohol-related pheno- types: Analysis of an F2 population. Behav Genet 27(6):589, 1997.

37. Grant, B.F., and Dawson, D.A. Age at onset of alcohol use and its association with DSM-IV alcohol abuse and dependence: Results from the National Longitudinal Alcohol Epidemiologic Survey. J Sub Abuse 9:103-110, 1997.

38. Wilsnack, S.C.; Vogeltanz, N.D.; Klassen, A.D.; et al. Childhood sexual abuse and women's substance abuse: National survey findings. J Stud Alcohol 58(3):264-271, 1997.

39. Miller, B.A.; Downs, W.R.; and Testa, M. Interrelationships between victimization experiences and women's alcohol use. J Stud Alcohol/Suppl 11:109-117, 1993.

40. Widom, C.S.; Ireland, T.; and Glynn, P.J. Alcohol abuse in abuse and neglected children followed-up: Are they at increased risk? J Stud Alcohol 56(2):207-217, 1995.

41. Miller, B.A. Partner violence experiences and women's drug use: Exploring the connections. In: Wetherington, C.L., and Roman, A.B., eds. Drug Addiction Research and the Health of Women. Rockville, MD: National Institute on Drug Abuse, 1998. pp. 407-416.

Source: National Institute on Alcohol Abuse and Alcoholism (1999)  National Institutes of Health 

v Fetal Alcohol Syndrome

In 1973, Jones and Smith ⁽¹⁾ coined the term "fetal alcohol syndrome" (FAS) to describe a pattern of abnormalities observed in children born to alcoholic mothers. It was originally postulated that malnutrition might be responsible for these defects. However, the pattern of malformation associated with FAS is not seen in children born to malnourished women, and alcohol has been found to be acutely toxic to the fetus independently of the effects of malnutrition ^(2,3).

Criteria for defining FAS were standardized by the Fetal Alcohol Study Group of the Research Society on Alcoholism in 1980 ⁽⁴⁾, and modifications were proposed in 1989 by Sokol and Clarren ⁽⁵⁾. The proposed criteria are 1) prenatal and/or postnatal growth retardation (weight and/or length below the 10th percentile); 2) central nervous system involvement, including neurological abnormalities, developmental delays, behavioral dysfunction, intellectual impairment, and skull or brain malformations; and 3) a characteristic face with short palpebral fissures (eye openings), a thin upper lip, and an elongated, flattened midface and philtrum (the groove in the middle of the upper lip).

Sokol and Clarren ⁽⁵⁾ suggested the term "alcohol-related birth defects" (ARBD) to describe anatomic or functional abnormalities attributed to prenatal alcohol exposure. The term "possible fetal alcohol effect(s)" (FAE) indicates that alcohol is being considered as one of the possible causes of a patient's birth defects. In the view of Sokol and Clarren, the frequent use of this term to indicate a birth defect judged milder than FAS is incorrect, although others continue to use it that way ⁽⁵⁾.

Mental handicaps and hyperactivity are probably the most debilitating aspects of FAS ⁽⁶⁾, and prenatal alcohol exposure is one of the leading known causes of mental retardation in the Western World ⁽⁷⁾. Problems with learning, attention, memory, and problem solving are common, along with in coordination, impulsiveness, and speech and hearing impairment ^(8,6). Deficits in learning skills persist even into adolescence and adulthood ^(6,9).

It is generally accepted that the adverse effects of prenatal alcohol exposure exist along a continuum, with the complete FAS syndrome at one end of the spectrum and incomplete features of FAS, including more subtle cognitive-behavioral deficits, on the other. Thus, infants with suboptimal neurobehavioral responses may later exhibit subtle deficits in such aspects of daily life as judgment, problem solving, and memory ⁽⁶⁾.

According to the CDC catchment study, incidences of FAS per 10,000 total births for different ethnic groups were as follows: Asians 0.3, Hispanics 0.8, whites 0.9, blacks 6.0, and Native Americans 29.9 ⁽¹³⁾. In the case of blacks, the risk of FAS remains about sevenfold higher than for whites, even after adjustment for the frequency of maternal alcohol intake, occurrence of chronic alcohol problems, and parity (number of children borne) ⁽¹⁶⁾. This raises the question of some kind of genetic susceptibility, the nature of which is unknown.

Apart from epidemiology, the key questions in FAS research include, How much alcohol is too much? and, When is the fetus at greatest risk? The major problem in addressing these questions is the lack of a specific physiological measure that accurately reflects alcohol consumption. There is no biological marker currently available to measure alcohol intake, and self-reports of alcohol consumption may be unreliable, perhaps especially so during pregnancy ⁽¹⁷⁾. Morrow-Tlucak and colleagues ⁽¹⁸⁾ found that women with more-serious alcohol-related problems are those more likely to underreport their alcohol consumption when interviewed during pregnancy.

While it is apparent that children who meet the criteria for FAS are born only to those mothers who consume large amounts of alcohol during pregnancy, studies have reported neurobehavioral deficits and intrauterine growth retardation in infants born to mothers who reported themselves to be moderate alcohol consumers during pregnancy ^(19,20,21). In a prospective study of 359 newborns, Ernhart and colleagues ⁽²²⁾ found a trend toward increasing head and facial abnormalities with increasing embryonic alcohol exposure. An effect occurred at even the lowest reported levels of alcohol intake, so that a clear threshold (minimum amount of alcohol to produce an effect) could not be defined ⁽²²⁾.

Given the range of defects that result from prenatal alcohol exposure, the search for an overall threshold for fetal risk may be unreasonable. Instead, each abnormal outcome in brain structure and function and growth might have its own dose-response relationship ⁽²³⁾. Animal research has shown that different profiles of alcohol-related birth defects are related to critical periods for specific aspects of fetal development ⁽³⁾. Thus, heavy alcohol consumption throughout pregnancy results in a wide variety of effects characteristic of FAS, while episodic binge drinking at high levels results in partial expression of the syndrome, with the abnormalities being unique to the period of exposure ⁽²⁴⁾. Vulnerability of individual organ systems may be greatest at the time of their most rapid cell division ⁽²⁵⁾.

An important strategy for preventing alcohol-related birth defects is the development of better screening techniques to identify women at high risk for heavy alcohol consumption throughout their pregnancy. Currently available laboratory tests for detecting biochemical markers of heavy drinking are not as sensitive as self-report screening instruments, whereas the latter are complicated by denial ⁽¹²⁾.

Conclusion

From a scientific perspective, the link between moderate drinking and alcohol-related birth defects has not been clearly established. Whether there is a threshold below which alcohol can be consumed without harming the fetus is not known: self-reported data showing a relationship between moderate use and alcohol-related birth defects may often underestimate the true level of drinking. Researchers are working on developing an objective marker for alcohol consumption that will help clarify these questions and assist clinicians in identifying alcohol-abusing patients as a part of routine prenatal care, using, for example, blood samples typically drawn during an initial examination.

Clinicians, however, must offer advice to their patients based upon the best available scientific evidence. Although some clinicians believe that recommending total abstention for pregnant women may subject them to unwarranted guilt about drinking small amounts of alcohol, most accept the need for clinical caution. Because we do not know at what point alcohol damage begins, it is prudent to recommend that pregnant women abstain from alcohol use pending confirmation of alcohol's role vis-à-vis fetal development.

There is good news in recent evidence that the number of women who consume alcohol during pregnancy is declining. However, it also appears that the rates of alcohol consumption among high-risk populations (pregnant smokers, unmarried women, women under the age of 25, and women with the least amount of education) remain virtually unchanged ⁽²⁸⁾. This points to a need to develop better targeted prevention and education efforts to reach high-risk populations and to identify women at high risk through primary health care and other systems traditionally used by high-risk individuals before and during pregnancy.

References

1. Jones, K.L., & Smith, D.W. Recognition of the fetal alcohol syndrome in early infancy. Lancet 2:999-1001, 1973.

2. Phillips, D.K.; Henderson, G.I.; & Schenker, S. Pathogenesis of fetal alcohol syndrome: Overview with emphasis on the possible role of nutrition. Alcohol Health & Research World 13(3):219-227, 1989.

3. Randall, C.L. Alcohol as a teratogen: A decade of research in review. Alcohol and Alcoholism Suppl. 1:125-132, 1987.

4. Rosett, H.L. A clinical perspective of the fetal alcohol syndrome. Alcoholism: Clinical and Experimental Research 4(2):119-122, 1980.

5. Sokol, R.J., & Clarren, S.K. Guidelines for use of terminology describing the impact of prenatal alcohol on the offspring. Alcoholism: Clinical and Experimental Research 13(4):597-598, 1989.

6. Streissguth, A.P.; Sampson, P.D.; & Barr, H.M. Neurobehavioral dose-response effects of prenatal alco hol exposure in humans from infancy to adulthood. Annals of the New York Academy of Sciences 562:145- 158, 1989.

7. Abel, E.L., & Sokol, R.J. Fetal alcohol syndrome is now leading cause of mental retardation. Lancet 2:1222, 19860.

8. Streissguth, A.P., & LaDue, R.A. Psychological and behavioral effects in children prenatally exposed to alcohol. Alcohol Health & Research World 10(1):6-12, 1985.

9. Streissguth, A.P.; Aase, J.M.; Clarren, S.K.; Randels, S.P.; LaDue, R.A.; & Smith, D.F. Fetal alcohol syndrome in adolescents and adults. Journal of the American Medical Association 265(15):1961-1967, 1991.

10. Abel, E.L., & Sokol, R.J. Incidence of fetal alcohol syndrome and economic impact of FAS-related anomalies. Drug and Alcohol Dependence 19:51-70, 1987.

11. Little, B.B.; Snell, L.M.; Rosenfeld, C.R.; Gilstrap, L.C.; & Gant, N.F. Failure to recognize fetal alcohol syndrome in newborn infants. American Journal of Diseases of Children 144(10):1142-1146, 1990.

12. Sokol, R.J.; Martier, S.S.; & Ager, J.W. The T-ACE questions: Practical prenatal detection of risk-drink ing. American Journal of Obstetrics and Gynecology 160(4):863-870, 1989.

13. Chavez, G.F.; Cordero, J.F.; & Becerra, J.E. Leading major congenital malformations among minority groups in the United States, 1981-1986. Journal of the American Medical Association 261(2):205-209, 1989.

14. May, P.A.; Hymbaugh, K.J.; Aase, J.M.; & Samet, J.M. Epidemiology of fetal alcohol syndrome among American Indians of the Southwest. Social Biology 30(4):374-387, 1983.

15. Aase, J.M. The fetal alcohol syndrome in American Indians: A high risk group. Neurobehavioral Toxicol- ogy and Teratology 3(2):153-156, 1981.

16. Sokol, R.J.; Ager, J.; Martier, S.; Debanne, S.; Ernhart, C.; Kuzma, J.; & Miller, S.I. Significant determi nants of susceptibility to alcohol teratogenicity. Annals of the New York Academy of Sciences

17. Ernhart, C.B.; Morrow-Tlucak, M.; Sokol, R.J.; & Martier, S. Underreporting of alcohol use in pregnancy. Alcoholism: Clinical and Experimental Research 12(4):506-511, 1988.

18. Morrow-Tlucak, M.; Ernhart, C.B.; Sokol, R.J.; Martier, S.; & Ager, J. Underreporting of alcohol use in pregnancy: Relationship to alcohol problem history. Alcoholism: Clinical and Experimental Research 13(3):399-401, 1989.

19. Little, R.E.; Asker, R.L.; Sampson, P.D.; & Renwick, J.H. Fetal growth and moderate drinking in early pregnancy. American Journal of Epidemiology 123(2):270-278, 1986.

20. Coles, C.D.; Smith, I.E.; Lancaster, J.S.; & Falek, A. Persistenc e over the first month of neurobehavioral differences in infants exposed to alcohol prenatally. Infant Behavior and Develop ment 10:23-37, 1987.

21. Russell, M. Clinical implications of recent research on the fetal alcohol syndrome. Bulletin of the New York Academy of Medicine 67(3):207-222, 1991.

22. Ernhart, C.B.; Sokol, R.J.; Martier, S.; Moron, P.; Nadler, D.; Ager, J.W.; & Wolf, A. Alcohol teratoge nicity in the human: A detailed assessment of specificity, critical period, and threshold. American Journal of Obstetrics and Gynecology 156(1):33-39, 1987.

23. Clarren, S.K.; Bowden, D.M.; & Astley, S.J. Pregnancy outcomes after weekly oral administration of ethanol during gestation in the pig-tailed macaque (Macaca nemestrina). Teratology 35(3):345-354, 1987.

24. Kotkoskie, L.A., & Norton, S. Cerebral cortical morphology and behavior in rats following acute prenatal ethanol exposure. Alcoholism: Clinical and Experimental Research 13(6):776-781, 1989.

25 Weiner, L., & Morse, B.A. FAS: Clinical perspectives and prevention. In: Chasnoff, I.J., ed. Drugs, Alcohol, Pregnancy and Parenting. Boston: Kluwer Academic Publishers, 1989. pp. 127-148.

26. Robles, N., & Day, N.L. Recall of alcohol consumption during pregnancy. Journal of Studies on Alcohol 51(5):403-407, 1990.

27. Coles, C.D.; Smith, I.; Fernhoff, P.M.; & Falek, A. Neonatal neurobehavioral characteristics as corre lates of maternal alcohol use during gestation. Alcoholism: Clinical and Experimental Re search 9(5):454-460, 1985.

28. Serdula, M.; Williamson, D.F.; Kendrick, J.S.; Anda, R.F.; & Byers, T. Trends in alcohol consumption by pregnant women: 1985 through 1988. Journal of the American Medical Association 265(7):876-879, 1991

Source: National Institute on Alcohol Abuse and Alcoholism (1999)  National Institutes of Health

v Children of Alcoholics

Children of Alcoholics: Important Facts

1. Alcoholism affects the entire family.

Living with a non-recovering alcoholic in the family can contribute to stress for all members of the family. Each member may be affected differently. Not all alcoholic families experience or react to this stress in the same way. The level of dysfunction or resiliency of the non-alcoholic spouse is a key factor in the effects of problems impacting children.

Children raised in alcoholic families have different life experiences than children raised in non-alcoholic families. Children raised in other types of dysfunctional families may have similar developmental losses and stressors as do children raised in alcoholic families.

Children living with a non-recovering alcoholic score lower on measures of family cohesion, intellectual-cultural orientation, active-recreational orientation, and independence. They also usually experience higher levels of conflict within the family.

Many children of alcoholics (COAs) experience other family members as distant and non-communicative.

Children of alcoholics may be hampered by their inability to grow in developmentally healthy ways.

2. Many people report being exposed to alcoholism in their families.

Seventy six million Americans, about 43% of the U.S. adult population, have been exposed to alcoholism in the family.

Almost one in five adult Americans (18%) lived with an alcoholic while growing up.

Roughly one in eight American adult drinkers is alcoholic or experiences problems due to the use of alcohol. The cost to society is estimated at in excess of $166 billion each year.

There are an estimated 26.8 million COAs in the United States. Preliminary research suggests that over 11 million are under the age of 18.

3. There is strong, scientific evidence that alcoholism tends to run in families.  Children of alcoholics are more at risk for alcoholism and other drug abuse than children of non-alcoholics.

Children of alcoholics are four times more likely than non-COAs to develop alcoholism.

Genetic factors play a major role in the development of alcoholism. There is an expanding base of literature which strongly supports a heritable basis for alcoholism and a range of family influences that may direct the development of children of alcoholics.

Children's perceptions of parental drinking quantity and circumstances appear to influence their own drinking frequency.

Children's alcohol expectancies reflect recognition of alcohol-related norms and a cognizance of parental drinking patterns by a very early age.

Alcohol expectancies appear to be one of the mechanisms explaining the relationship between paternal alcoholism and heavy drinking among offspring during college.

Parental alcoholism and other drug dependencies have an impact upon children's early learning about alcohol and other drugs.

Family interaction patterns also may influence the COA's risk for alcohol abuse. It has been found that families with an alcoholic parent displayed more negative family inter action during problem-solving discussions than in non-alcoholic families.

Almost one-third of any sample of alcoholics has at least one parent who also was or is an alcoholic.

Children of alcoholics are more likely than non-COAs to marry into families in which alcoholism is prevalent.

Parental alcoholism influences adolescent substance use through several different pathways including stress, negative affect and decreased parental monitoring. Negative affect and impaired parental monitoring are associated with adolescent's joining in a peer network that supports drug use behavior.

After drinking alcohol, sons of alcoholics experience more of the physiological changes associated with pleasurable effects compared with sons of non-alcoholics, although ` only immediately after drinking.

4. Alcoholism usually has strong negative effects on marital relationships.

Separated and divorced men and women were three times as likely as married men and women to say they had been married to an alcoholic or problem drinker.

Almost two-thirds of separated and divorced women, and almost half of separated or divorced men, under age 46, have been exposed to alcoholism in the family at some time.

5. Alcohol is associated with a substantial proportion of human violence, and perpetrators are often under the influence of alcohol.

Alcohol is a key factor in 68% of manslaughters, 62% of assaults, 54% of murders and attempted murders, 48% of robberies, and 44% of burglaries.

Studies of family violence frequently document high rates of alcohol and other drug involvement.

COAs may be more likely to be the targets of physical abuse and to witness family violence.

Compared with non-alcoholic families, alcoholic families demonstrate poorer problem- solving abilities, both among the parents and within the family as a whole. These poor communication and problem-solving skills may be mechanisms through which lack of cohesion and increased conflict develop and escalate in alcoholic families.

COAs are more at risk for disruptive behavioral problems and are more likely than non-COAs to be sensation seeking, aggressive, and impulsive.

6. Based on clinical observations and preliminary research, a relationship between parental alcoholism and child abuse is indicated in a large proportion of child abuse cases.

A significant number of children in this country are being raised by addicted parents. With more than one million children confirmed each year as victims of child abuse and neglect by state child protective service agencies, state welfare records have indicated that substance abuse is one of the top two problems exhibited by families in 81% of the reported cases.

Studies suggest an increased prevalence of alcoholism among parents who abuse children.

Existing research suggests alcoholism is more strongly related to child abuse than are other disorders, such as parental depression.

Although several studies report very high rates of alcoholism among the parents of incest victims, much additional research is needed in this area.

7. Children of alcoholics exhibit symptoms of depression and anxiety more than children of non-alcoholics.

In general, COAs appear to have lower self-esteem than non-COAs in childhood, adolescence and young adulthood.

Children of alcoholics exhibit elevated rates of psychopathology. Anxiety, depression, and externalizing behavior disorders are more common among COAs than among children of non-alcoholics.

Young COAs often show symptoms of depression and anxiety such as crying, bed wetting, not having friends, being afraid to go to school, or having nightmares. Older youth may stay in their rooms for long periods of time and not relate to other children claiming they "have no one to talk to." Teens may show depressive symptoms by being perfectionistic in their endeavors, hoarding, staying by themselves, and being excessively self-conscious. Teenage COAs may begin to develop phobias.

8. Children of alcoholics experience greater physical and mental health problems and higher health care costs than children from non-alcoholic families.

Inpatient admission rates for substance abuse are triple that of other children.

Inpatient admission rates for mental disorders are almost double that of other children.

Injuries are more than one and one-half times greater than those of other children.

The rate of total health care costs for children of alcoholics is 32% greater than children from non-alcoholic families.

9. Children of alcoholics score lower on tests measuring verbal ability.

COAs tend to score lower on tests that measure cognitive and verbal skills. Their ability to express themselves may be impaired, which can impede their school performance, peer relationships, ability to develop and sustain intimate relationships, and hamper performance on job interviews.

Low verbal scores, however, should not imply that COAs are intellectually impaired.

10. Children of alcoholics often have difficulties in school.

COAs often believe that they will be failures even if they do well academically. They often do not view themselves as successful.

Children of alcoholics are more likely to be raised by parents with poorer cognitive abilities and in an environment lacking stimulation. A lack of stimulation in the rearing environment may account in part for the pattern of failure found in COAs compared with non-COAs.

Pre-school aged COAs exhibited poorer language and reasoning skills than did non- COAs, and poorer performance among the COAs was predicted by the lower quality of stimulation present in the home.

COAs are more likely to be truant, drop out of school, repeat grades, or be referred to a school counselor, or psychologist. This may have little to do with academic ability; rather, COAs may have difficulty bonding with teachers, other students and school; they may experience anxiety related to performance; or they may be afraid of failure. The actual reasons have yet to be determined.

There is an increasing body of scientific evidence indicating that risk for later problems, and even alcoholic outcomes is detectable early in the life course and, in some in stances, before school entry.

11. Children of alcoholics have greater difficulty with abstraction and conceptual reasoning.

Abstraction and conceptual reasoning play an important role in problem solving, whether the problems are academic or are situation related to the problems of life. Therefore, children of alcoholics might require very concrete explanations and instruc tions.

12. Children of alcoholics may benefit from adult efforts which help them to:

Develop autonomy and independence.

Develop a strong social orientation and social skills.

Engage in acts of "required helpfulness."

Develop a close bond with a care-giver.

Cope successfully with emotionally hazardous experiences.

Perceive their experiences constructively, even if those experiences cause pain or suffering, and gain, early in life, other people's positive attention.

Develop day-to-day coping strategies.

13. Children can be protected from many problems associated with growing up in an alcoholic family.

If healthy family rituals or traditions, such as vacations, mealtimes or holidays, are highly valued and maintained, if the active alcoholic is confronted with his or her problem, if there are consistent significant others in the life of the child or children, and if there is moderate to high religious observance, children can be protected from many of the consequences of parental alcoholism.

14. Maternal alcohol consumption during any time of pregnancy can cause alcohol- related birth defects or alcohol-related neurological deficits.

 The rate of drinking during pregnancy appears to be increasing.

Prenatal alcohol effects have been detected at moderate levels of alcohol consumption by non-alcoholic women. Even though a mother is not an alcoholic, her child may not be spared the effects of prenatal alcohol exposure.

Cognitive performance is less affected by alcohol exposure in infants and children whose mothers stopped drinking in early pregnancy, despite the mothers' resumption of alcohol use after giving birth.

One analysis of 6-year olds, with demonstrated effects of second-trimester alcohol exposure, had lower academic achievement and problems with reading, spelling, and mathematical skills.

Approximately 6 percent of the offspring of alcoholic women have Fetal Alcohol Syndrome (FAS); the FAS risk for offspring born after an FAS sibling, is as high as 70 percent.

Those diagnosed as having Fetal Alcohol Syndrome had IQ scores ranging from 20- 105 with a mean of 68. Subjects also demonstrated poor concentration and attention.

People with FAS demonstrate growth deficits, morphologic abnormalities, mental retardation, and behavioral difficulties. Secondary effects of FAS among adolescents and adults include mental health problems, disrupted schooling (dropping out or being suspended or expelled), trouble with the law, dependent living as an adult, and problems with employment.

COA Resources Information

National Association for Children of Alcoholics (NACoA)
11426 Rockville Pike, Suite 100
Rockville, MD 20852
(888) 55-4COAS
www.health.org/nacoa/
nacoa@erols.com

National Association for Native American Children of Alcoholics (NANACoA)
130 Andover Park East, Suite 210
Seattle, WA 98188
(800) 322-5601
www.nanacoa.org
nanacoa@nanacoa.org

National Black Alcoholism Council (NBAC)
1629 K Street NW, Suite 802
Washington, DC 20006
(202) 296-2696

National Council on Alcoholism and Drug Dependence (NCADD)
12 West 21st Street, 7th Floor
New York, NY 10017
(800) NCA-CALL
www.ncadd.org

Self-help groups for COAs:

Al-Anon Family Group Headquarters, Inc.,
1600 Corporate Landing Parkway
Virginia Beach, VA. 23454-5617
1-888-4AL-ANON
www.al-anon.org

Adult Children of Alcoholics (ACA/ACoA)
P.O. Box 3216
Torrance, CA 90510
(310) 534-1815
www.adultchildren.org

Alcohol/other drug prevention information for volunteers, professionals, and the general public:

Children of Alcoholics Foundation
164 West 74th Street
New York, NY 10023
(212) 595-5810 ext. 7760
Fax (212) 595-2553
www.coaf.org

National Clearinghouse for Alcohol and Drug Information (NCADI)
P.O. Box 2345
Rockville, MD 20847-2345
(800) 729-6686

Children of Alcoholics: Are They Different?

An estimated 6.6 million children under the age of 18 years live in households with at least one alcoholic parent ⁽¹⁾. Current research findings suggest that these children are at risk for a range of cognitive, emotional, and behavioral problems. In addition, genetic studies indicate that alcoholism tends to run in families and that a genetic vulnerability for alcoholism exists (2,3,4). Yet, some investigators also report that many children from alcoholic homes develop neither psychopathology nor alcoholism.

While research findings suggest that some children suffer negative consequences due to parental alcoholism, a larger proportion of COAs function well and do not develop serious problems. These resilient children shared several characteristics that contributed to their success, including the ability to obtain positive attention from other people, adequate communication skills, average intelligence, a caring attitude, a desire to achieve, and a belief in self-help.

Studies comparing COAs and nonCOAs have suggested that, although the two groups differ in a variety of psychosocial areas, differences in cognitive performance are observed most frequently. School-aged children of alcoholic parents often have academic problems. Academic performance may be a better measure than IQ of the effect of living with an alcoholic parent.

School records indicate that COAs experience such academic difficulties as repeating grades, failing to graduate from high school, and requiring referrals to school psychologists ^(10,11). Although cognitive deficits in COAs may account, in part, for their poor academic performance, motivational difficulties or the stress of the home environment also may contribute to their problems in school.

Studies comparing COAs with nonCOAs also have found that parental alcoholism is linked to a number of psychological disorders in children. Divorce, parental anxiety or affective disorders, or undesirable changes in the family or in life situations can add to the negative effect of parental alcoholism on children's emotional functioning ^(12,13).

The results of several studies have shown that children from alcoholic families report higher levels of depression and anxiety and exhibit more symptoms of generalized stress (i.e., low self-esteem) than do children from nonalcoholic families (12,13,14,15). In addition, COAs often express a feeling of lack of control over their environment.

Finally, children from homes with alcoholic parents often demonstrate behavioral problems. Study findings suggest that these children exhibit such problems as lying, stealing, fighting, truancy, and school behavior problems, and they often are diagnosed as having conduct disorders ⁽¹⁷⁾. Teachers have rated COAs as significantly more overactive and impulsive than nonCOAs. COAs also appear to be at greater risk for delinquency and school truancy (12,19,20). Several investigators have reported an association between the incidence of diagnosed conduct disorders and parental alcohol abuse (21 ,22,23). However, other problems associated with alcoholism (e.g., depression among the alcoholic parents and divorce) also may contribute to conduct problems and disorders among COAs.

The alcoholic family's home environment and the manner in which family members interact may contribute to the risk for the problems observed among COAs. Although alcoholic families are a heterogeneous group, common characteristics have been identified. Families of alcoholics have lower levels of family cohesion, expressiveness, independence, and intellectual orientation and higher levels of conflict compared with nonalcoholic families (13,24,25,26). Some characteristics, however, are not specific to alcoholic families: Impaired problem-solving ability and hostile communication are observed both in alcoholic families and in families with problems other than alcohol ⁽²⁷⁾. Moreover, the characteristics of families with recovering alcoholic members and of families with no alcoholic members do not differ significantly, suggesting that a parent's continued drinking may be responsible for the disruption of family life in an alcoholic home ⁽¹³⁾.

The family environment also may affect transmission of alcoholism to COAs. Children with alcoholic parents are less likely to become alcoholics as adults when their parents consistently set and follow through on plans and maintain such rituals as holidays and regular mealtimes ⁽²⁸⁾. 

Source: National Institute on Alcohol Abuse and Alcoholism (1999)                                                   National Institutes of Health

v Alcohol and Minorities

Do blacks, Hispanics, American Indians, and Asians and Pacific Islanders in the United States drink more or less than whites drink? Do they have more alcohol-related medical problems? Do they receive treatment in proportion to their problems? In 1990, 68.3 percent of whites, 64.5 percent of Hispanics, and 55.6 percent of blacks used alcohol ⁽¹⁾. Although these percentages appear similar, different patterns of use and abuse and varying prevalence of alcohol-related problems underlie the numbers (2-9). This chapter considers why some minorities have more medical problems than others and whether minorities receive adequate treatment and prevention services. It examines genetic and environmental factors that may put minorities at risk for or protect them from alcohol problems. It also reviews research on screening to identify those at risk for alcoholism or alcohol abuse.

Medical Consequences and Alcohol-Related Trauma

Given major underreporting of alcohol-related diagnoses, minimum estimates from one survey of non-Federal, short-stay hospitals in 1991 found 54.5 patient discharges for alcohol-related diagnoses for every 10,000 people in the United States over age 15 ⁽¹⁰⁾. The rate for whites was 48.2 per 10,000; however, the rate for blacks was 102.9 per 10,000 population ⁽¹⁰⁾. Because it is not known whether the rates of underreporting are equal among ethnic groups, it is difficult to interpret the meaning of such reported differences.

A study of alcohol-related mortality in California showed that blacks and Hispanics had higher rates of mortality from alcoholic cirrhosis than did whites or Asian-Americans. Nationwide, death rates attributed to alcohol dependence syndrome also were highest for blacks, although a higher percentage of blacks than whites abstain from using alcohol (5,11). The high rates of medical problems seen in blacks thus occur among a smaller percentage of the black population when compared with whites.

The California study suggests that for many alcohol-related causes of death such as alcohol dependence syndrome and alcoholic hepatitis, Hispanics had either similar or lower mortality rates compared with whites. However, the mortality rate among Hispanics from alcohol-related motor vehicle crashes was 9.16 per 100,000, significantly higher than the rates for whites (8.15) or blacks (8.02) ⁽¹¹⁾.

The group identified as "Asian/Other" in the California study had lower rates of alcohol-related mortality than any other group for most causes of death. Their mortality rate from motor vehicle crashes, for example, was 5.39 per 100,000 ⁽¹¹⁾. Asians tend to have lower rates of drinking and alcohol abuse than whites ⁽²⁾.

Although highly variable among tribes, alcohol abuse is a factor in five leading causes of death for American Indians, including motor vehicle crashes, alcoholism, cirrhosis, suicide, and homicide. Mortality rates for crashes and alcoholism are 5.5 and 3.8 times higher, respectively, among American Indians than among the general population. Among tribes with high rates of alcoholism, reports estimate that 75 percent of all accidents, the leading cause of death among American Indians, are alcohol related ⁽⁷⁾.

Fetal Alcohol Syndrome (FAS)

The prevalence of FAS among select groups of Navajo, Pueblo, and Southwestern Plains Indians has been studied. Among two populations of Southwestern Plains Indians ages newborn to 14 years, 10.7 of every 1,000 children were born with FAS. This was compared with 2.2 per 1,000 for Pueblo Indians and 1.6 for Navajo ⁽¹²⁾. Overall rates for FAS in the United States range from 1 to 3 per 1,000 ⁽¹⁵⁾. Cultural influences, patterns of alcohol consumption, nutrition, and differing rates of alcohol metabolism or other innate physiological differences may account for the varying FAS rates among Indian communities ⁽¹³⁾.

The incidence of FAS among blacks appears to be about seven times higher than among whites, although more blacks than whites abstain from drinking (5,14,15). The reasons for this difference in FAS rates are not yet known ^(14,15). Paradoxically, one study has found that black women believe drinking is acceptable in fewer social situations than do white women ⁽⁶⁾. Ten percent of black compared with 23 percent of white women surveyed said that drinking more than one or two drinks at a bar with friends is acceptable ⁽⁶⁾. This attitudinal difference could help to explain why fewer black women are frequent, high-quantity drinkers than are white women ⁽⁶⁾. Nevertheless, FAS seems to be more prevalent among blacks than among whites.

Genetic Influences

Certain minority groups may possess genetic traits that either predispose them to or protect them from becoming alcoholic. Few such traits have so far been discovered. However, the flushing reaction, found in the highest concentrations among people of Asian ancestry, is one example.

Flushing has been linked to variants of genes for enzymes involved in alcohol metabolism. It involves a reddening of the face and neck due to increased blood flow to those areas and can be accompanied by headaches, nausea, and other symptoms. Flushing can occur when even small amounts of alcohol are consumed ⁽¹⁶⁾.

Japanese-Americans living in Los Angeles have been studied. Among those with quick flushing responses (flushing occurs after one drink or less), fewer consumed alcohol than did those with no or with slow flushing responses (flushing occurs after two or more drinks)⁽¹⁷⁾. In another group of Japanese-American students in Los Angeles, flushing was far less correlated with abstention from alcohol than it was in the first group ⁽¹⁷⁾. Thus, although flushing appears to deter alcohol use, people with the trait may nevertheless consume alcohol.

Another genetic difference between ethnic groups occurs among other enzymes involved in metabolizing alcohol in the liver. Variations have been observed between the structures and activity levels of the enzymes prevalent among Asians, blacks, and whites ⁽¹⁸⁾. One enzyme found in Japanese, for example, has been associated with faster elimination of alcohol from the body when compared with whites ⁽¹⁹⁾. Interesting leads relating these varying rates of alcohol metabolism among minorities to medical complications of alcoholism, such as liver disease, are now being followed.

Influence of Acculturation

Acculturation has a dramatic effect on drinking patterns among immigrants to the United States and successive generations. Comparisons of drinking among immigrant and second and third generation Mexican-American women reveal that drinking rates of successive generations approach those of the general population of American women. Seventy-five percent of Mexican immigrant women in one study abstained from alcohol; only 38 percent of third generation Mexican-American women abstained. This rate is close to the 36-percent abstention rate for women in the general U.S. population ⁽²⁰⁾. Rates of alcohol-related problems also may be affected by acculturation. A study has found that Hispanic women who are at least second generation Americans have higher rates of social and personal problems than either foreign born or first generation Hispanic women ⁽³⁾. Studies of Asian-Americans have suggested that their drinking rates conform to those of the U.S. population as acculturation occurs ^(17,21).

Identification and Treatment

Do screening instruments for alcohol-related problems, validated in primarily white populations, accurately detect alcohol problems among minorities? One study evaluated the Self-Administered Alcoholism Screening Test (SAAST), translated into Spanish, in Mexico City and the original English version in Rochester, MN. The Spanish translation identified alcoholics and nonalcoholics at rates comparable to those of the English version. The study found that the questions that best predicted alcoholism were the same in both versions ⁽²²⁾. This study suggests that translations or other revisions of screening tools may be just as accurate as the original instruments, but more studies are needed before firm conclusions can be drawn.

It is not known whether all treatment programs are effective for members of minority groups. Among minority patients who enter treatment programs for the general population, success rates are equal to those of whites in the same programs ^(23,24). Also, despite the existence of programs designed to treat specific minority groups, no evidence exists that either supports or denies their ability to produce improved outcomes ^(25,26).

Do minorities have the same access to alcoholism treatment as do whites? Access to treatment for minorities has not been assessed widely, but several factors have been studied. There is evidence that not everyone in these groups who needs treatment receives it. For example, Hispanics and blacks are less likely to have health insurance and more likely to be below the poverty level than whites, factors that may decrease their access to treatment (24,27,28).

No studies focus on access to alcoholism treatment for the U.S. Hispanic population as a whole ⁽²⁸⁾. Some culturally sensitive programs exist for Hispanics and are often aimed at specific cultures within this group, such as Puerto Ricans. These programs have not been evaluated ^(24,28).

Prevention

Prevention efforts that work among the general population have been shown to be effective among some minorities ⁽²⁹⁾. However, it is unclear whether interventions designed for specific minorities also would be beneficial. For example, programs incorporating peer counseling, enhancing adolescents' coping skills, and alcohol education appear to be effective among American Indians. One study has demonstrated that specific populations of American Indian adolescents who completed such a program used less alcohol when compared with their peers 6 months after completion of the program ⁽²⁹⁾. A second study showed that American Indian participants in another program decreased their own use of alcohol when evaluated 12 months after the program's completion ⁽³⁰⁾.

The effectiveness of warning labels on alcoholic beverage containers has been evaluated in a group of black women ⁽³¹⁾. A study showed that 6 months after the label was mandated by law, pregnant black women who were light drinkers slightly reduced their drinking during pregnancy, whereas black women who were heavier drinkers did not change their drinking habits ⁽³¹⁾.

Conclusion

The increasing number of studies of alcohol problems among minorities has produced both important findings and new questions to answer. Higher abstention rates among African-Americans coexist with higher cirrhosis mortality. Native American groups vary greatly in their drinking practices, but the specific contributions of social, cultural, and genetic influences to these variations are not yet known. We need to understand why acculturation seems to increase drinking among successive generations of Hispanics and diminishes the "protective" effect of the flushing reaction among succeeding generations of Asian-Americans. Finally, we need to know more about disparities in access to treatment and prevention among minority groups and whether culturally relevant treatment appr oaches improve treatment outcome.

References

1. National Institute on Drug Abuse. National Household Survey on Drug Abuse: Main Findings 1990. DHHS Pub. No. (ADM)91-1788. Washington, DC: Supt. of Docs., U.S. Govt. Print. Off., 1991.
2. Ahern, F.M. Alcohol use and abuse among four ethnic groups in Hawaii: Native Hawaiians, Japanese, Filipinos and Caucasians. In: Alcohol Use Among U.S. Ethnic Minorities. National Institute on Alcohol Abuse and Alcoholism Research Monograph No. 18. DHHS Pub. No. (ADM)89-1435. Washington, DC: Supt. of Docs., U.S. Govt. Print. Off., 1989. pp. 315-328.
3. Caetano, R. Drinking patterns and alcohol problems in a national sample of U.S. Hispanics. In: Alcohol Use Among U.S. Ethnic Minorities. National Institute on Alcohol Abuse and Alcoholism Research Monograph No. 18. DHHS Pub. No. (ADM)89-1435. Washington, DC: Supt. of Docs., U.S. Govt. Print. Off., 1989. pp. 147-162. ⁽⁴⁾ Herd, D. Subgroup differences in drinking patterns among black and white men: Results from a national survey. Journal of Studies on Alcohol 51(3):221-232, 1990.
4. Herd, D. The epidemiology of drinking patterns and alcohol-related problems among U.S. blacks. In: Alcohol Use Among U.S. Ethnic Minorities. National Institute on Alcohol Abuse and Alcoholism Research Monograph No. 18. DHHS Pub. No. (ADM)89-1435. Washington, DC: Supt. of Docs., U.S. Govt. Print. Off., 1989. pp. 3-50.
5. Herd, D. An analysis of alcohol-related problems in black and white women drinkers. Addiction Research 1(3):181-198, 1993.
6. Manson, S.M.; Shore, J.H.; Baron, A.E.; Ackerson, L.; & Neligh, G. Alcohol abuse and dependence among American Indians. In: Helzer, J.E., and Canino, G.J., eds. Alcoholism in North America, Europe, and Asia. New York: Oxford University Press, 1992. pp. 113-130.
7. Manson, S.M.; Shore, J.H.; Bloom, J.D.; Keepers, G.; & Neligh, G. Alcohol abuse and major affective disorders: Advances in epidemiologic research among American Indians. In: Alcohol Use Among U.S. Ethnic Minorities. National Institute on Alcohol Abuse and Alcoholism Research Monograph No. 18. DHHS Pub. No. (ADM)89-1435. Washington, DC: Supt. of Docs., U.S. Govt. Print. Off., 1989. pp. 291- 300.
8. Windle, M. Alcohol use and abuse: Some findings from the National Adolescent Student Health Survey. Alcohol Health & Research World 15(1):5-10, 1991.
9. Caces, M.F., & Dufour, M.C. Surveillance Report #28: Trends in Alcohol-Related Morbidity Among Short-Stay Community Hospital Discharges, United States: 1979-91. National Institute on Alcohol Abuse and Alcoholism. Division of Biometry and Epidemiology. Dec. 1993.
10. Sutocky, J.W.; Shultz, J.M.; & Kizer, K.W. Alcohol-related mortality in California, 1980 to 1989. American Journal of Public Health 83(6):817-823, 1993.
11. May, P.A. Fetal alcohol effects among North American Indians: Evidence and implications for society. Alcohol Health & Research World 15(3):239-248, 1991.
12. Aase, J.M. The fetal alcohol syndrome in American Indians: A high risk group. Neurobehavioral Toxicology and Teratology 3(2):153-156, 1981.
13. Chávez, G.F.; Cordero, J.F.; & Becerra, J.E. Leading major congenital malformations among minority groups in the United States, 1981-1986. Journal of the American Medical Association 261(2):205-209, 1989.
14. Sokol, R.J.; Ager, J.; & Martier, S. Significant determinants of susceptibility to alcohol teratogenicity. Annals of the New York Academy of Sciences 477:87-102, 1986.
15. Thomasson, H.R., & Li, T.-K. How alcohol and aldehyde dehydrogenase genes modify alcohol drinking, alcohol flushing, and the risk for alcoholism. Alcohol Health & Research World 17(2):167- 172, 1993.
16. Nakawatase, T.V.; Yamamoto, J.; & Toshiaki, S. The association between fast-flushing response and alcohol use among Japanese Americans. Journal of Studies on Alcohol 54(1):48-53, 1993.
17. Burnell, J.C., & Bosron, W.F. Genetic polymorphism of human liver alcohol dehydrogenase and kinetic properties of the isoenzymes. In: Crow, K.E., and Batt, R.D., eds. Human Metabolism of Alcohol: Volume 2. Regulation, Enzymology, and Metabolites of Ethanol. Boca Raton, FL: CRC Press, 1989. pp. 65-75.
18. Meier-Tackmann, D.; Leonhardt, R.A.; Agarwal, D.P.; & Goedde, H.W. Effect of acute ethanol drinking on alcohol metabolism in subjects with different ADH and ALDH genotypes. Alcohol 7(5):413-418, 1990.
19. Gilbert, M.J. Acculturation and changes in drinking patterns among Mexican-American women. Alcohol Health & Research World 15(3):234-238, 1991.
20. Johnson, R.C., & Nagoshi, C.T. Asians, Asian-Americans and alcohol. Journal of Psychoactive Drugs 22(1):45-52, 1990.
21. Davis, L.J., Jr.; de la Fuente, J.-R.; Morse, R.M.; Landa, E.; & O'Brien, P.C. Self-Administered Alcohol ism Screening Test (SAAST): Comparison of classificatory accuracy in two cultures. Alcoholism: Clinical and Experimental Research 13(2):224-228, 1989.
22. Gilbert, M.J., & Cervantes, R.C. Alcohol services for Mexican Americans: A review of utilization patterns, treatment considerations and prevention activities. Hispanic Journal of Behavioral Sciences 8(3):191-223, 1986.
23. Institute of Medicine. Populations defined by structural characteristics. In: Broadening the Base of Treatment for Alcohol Problems. Washington, DC: National Academy Press, 1990. pp. 356-380.
24. Institute of Medicine. Patient-treatment matching and outcome improvement in alcohol rehabilitation. In: Prevention and Treatment of Alcohol Problems: Research Opportunities. Washington, DC: National Academy Press, 1989. pp. 231-246.
25. Westermeyer, J. Alcoholism and services for ethnic populations. In: Pattison, E., and Kaufman, E., eds. Encyclopedic Handbook of Alcoholism. New York: Gardner Press, 1982. pp. 709-717.
26. Anderson, R.M.; Giachello, A.L.; & Aday, L.A. Access of Hispanics to health care and cuts in services: A state-of-the-art overview. Public Health Reports 101(3):238-252, 1986.
27. Caetano, R. Priorities for alcohol treatment research among U.S. Hispanics. Journal of Psychoactive Drugs 25(1):53-60, 1993.
28. Gilchrist, L.D.; Schinke, S.P.; Trimble, J.E.; & Cvetkovich, G.T. Skills enhancement to prevent sub stance abuse among American Indian adolescents. International Journal of the Addictions 22(9):869- 879, 1987.
29. Carpenter, R.A.; Lyons, C.A.; & Miller, W.R. Peer-managed self-control program for prevention of alcohol abuse in American Indian high school students: A pilot evaluation study. International Journal of the Addictions 20(2):299-310, 1985.
30. Hankin, J.R.; Firestone, I.J.; Sloan, J.J.; Ager, J.W.; Goodman, A.C.; Sokol, R.J.; & Martier, S.S. The impact of the alcohol warning label on drinking during pregnancy. Journal of Public Policy & Marketing 12(1):10-18, 1993.

Source: National Institute on Alcohol Abuse and Alcoholism (Jan. 1994) National Institutes of Health

v Alcohol and the Workplace

Drinking among U.S. workers can threaten public safety, impair job performance, and result in costly medical, social, and other problems affecting employees and employers alike. Productivity losses attributed to alcohol were estimated at $119 billion for 1995 ⁽¹⁾. As this chapter explains, several factors contribute to problem drinking in the workplace.

Employers are in a unique position to mitigate some of these factors and to motivate employees to seek help for alcohol problems.

Factors Contributing to Employee Drinking

Drinking rates vary among occupations, but alcohol-related problems are not characteristic of any social segment, industry, or occupation. Drinking is associated with the workplace culture and acceptance of drinking, workplace alienation, the availability of alcohol, and the existence and enforcement of workplace alcohol policies (2,3).

Workplace Culture. The culture of the workplace may either accept and encourage drinking or discourage and inhibit drinking. A workplace's tolerance of drinking is partly influenced by the gender mix of its workers. Studies of male-dominated occupations have described heavy drinking cultures in which workers use drinking to build solidarity and show conformity to the group (4,5). Some male-dominated occupations therefore tend to have high rates of heavy drinking and alcohol-related problems (6,7). In predominantly female occupations both male and female employees are less likely to drink and to have alcohol-related problems than employees of both sexes in male-dominated occupations ⁽⁸⁾.

Workplace Alienation. Work that is boring, stressful, or isolating can contribute to employees' drinking ⁽²⁾. Employee drinking has been associated with low job autonomy ⁽⁹⁾, lack of job complexity, lack of control over work conditions and products ^(10,11), boredom ⁽¹²⁾, sexual harassment, verbal and physical aggression, and disrespectful behavior ⁽¹³⁾.

Alcohol Availability. The availability and accessibility of alcohol may influence employee drinking. More than two-thirds of the 984 workers surveyed at a large manufacturing plant said it was "easy" or "very easy" to bring alcohol into the workplace, to drink at work stations, and to drink during breaks ⁽¹⁴⁾. Twenty-four percent reported any drinking at work at least once during the year before the survey ⁽¹⁵⁾. In a survey of 6,540 employees at 16 worksites representing a range of industries, 23 percent of upper-level managers reported any drinking during working hours in the previous month ⁽¹⁶⁾.

Restricting workers' access to alcohol may reduce their drinking. The cultural prohibition against alcohol in the Middle East, making alcohol less available, may explain the reduction in drinking among U.S. military personnel serving in Operations Desert Shield and Desert Storm. An estimated 80 percent of the military personnel surveyed reported decreased drinking while serving in those operations ⁽¹⁷⁾.

Supervision. Limited work supervision, often a problem on evening shifts, has been associated with employee alcohol problems (2,18). In one study of 832 workers at a large manufacturing plant, workers on evening shifts, during which supervision was reduced, were more likely than those on other shifts to report drinking at work ⁽¹⁵⁾.

Alcohol Policies. There is wide variation in the existence of alcohol policies, in employees' awareness of them, and in their enforcement in workplaces across the country. Researchers found that most managers and supervisors in one large manufacturing plant had little knowledge of the company's alcohol policy. In addition, supervisors were under constant pressure to keep production moving and were motivated to discipline employees for drinking only if the drinking was compromising production or jeopardizing safety. Workers' knowledge that policies were rarely enforced seemed to encourage drinking ⁽¹⁴⁾.

Effects of Employee Drinking

Alcohol-related job performance problems are caused not only by on-the-job drinking but also by heavy drinking outside of work ^(15,19). Ames and colleagues ⁽¹⁵⁾ found a positive relationship between the frequency of being "hungover" at work and the frequency of feeling sick at work, sleeping on the job, and having problems with job tasks or co-workers. The hangover effect was demonstrated among pilots whose performance was tested in flight simulators. Yesavage and Leirer ⁽²⁰⁾ found evidence of impairment 14 hours after pilots reached blood alcohol concentrations (BACs) of between 0.10 percent and 0.12 percent. Morrow and colleagues ⁽²¹⁾ found that pilots were still significantly impaired 8 hours after reaching a BAC of 0.10 percent. Drinking at work, problem drinking, and frequency of getting "drunk" in the past 30 days were positively associated with frequency of absenteeism, arriving late to work or leaving early, doing poor work, doing less work, and arguing with co-workers ⁽¹⁹⁾.

Conclusion

Researchers have begun to look not just at the effectiveness of workplace alcohol programs in intervening in drinking problems but also at the culture of the workplace itself as a determinant in both drinking and nondrinking behavior of employees. This research is providing management with a powerful tool for preventing drinking problems as well as in identifying those who are at risk for alcohol problems.

References

1. Harwood, H.; Fountain, D.; and Livermore, G. The Economic Costs of Alcohol and Drug Abuse in the United States 1992. Rockville, MD: National Institute on Drug Abuse, 1998.

2. Ames, G.M., and Janes, C. A cultural approach to conceptualizing alcohol and the workplace. Alcohol Health & Research World 16(2):112-119, 1992.

3. Trice, H.M., and Sonnenstuhl, W.J. Drinking behavior and risk factors related to the work place: Implications for research and prevention. Journal of Applied Behavioral Science 24(4):327-346, 1988.

4. Trice, H.M. Work-related risk factors associated with alcohol abuse. Alcohol Health & Research World 16(2):106-111, 1992.

5. Sonnenstuhl, W.J. Working Sober: The Transformation of an Occupational Drinking Culture. Ithaca, NY: Cornell University Press, 1996.

6. Hoffman, J.P.; Larison, C.; and Sanderson, A. An Analysis of Worker Drug Use and Workplace Policies and Programs. Rockville, MD: Substance Abuse and Mental Health Services Administration, 1997.

7. Mandell, W.; Eaton, W.W.; Anthony, J.C.; and Garrison, R. Alcoholism and occupations: A review and analysis of 104 occupations. Alcoholism: Clinical and Experimental Research 16(4):734-746, 1992.

8. Kraft, J.M.; Blum, T.C.; Martin, J.K.; and Roman, P.M. Drinking patterns and the gender mix of occupations: Evidence from a national survey of American workers. Journal of Substance Abuse 5(2):157-174, 1993.

9. Greenberg, E.S., and Grunberg, L. Work alienation and problem alcohol behavior. Journal of Health and Social Behavior 36(1):83-102, 1995.

10. Parker, D.A., and Brody, J.A. Risk factors for alcoholism and alcohol problems among employed women and men. In: Occupational Alcoholism: A Review of Research Issues. National Institute on Alcohol Abuse and Alcoholism Research Monograph No. 8. DHHS Pub No. (ADM)82-1184. Rockville, MD: the Institute, 1982. pp. 99-127.

11. Kohn, M.L., and Schooler, C. The reciprocal effects of substantive complexity of work and intellectual flexibility: A longitudinal assessment. American Journal of Sociology 84:24-52, 1978.

12. Hingson, R.; Mangione, T.; and Barrett, J. Job characteristics and drinking practices in the Boston metropolitan area. Journal of Studies on Alcohol 42(9):725-738, 1981.

13. Richman, J.A.; Rospenda, K.M.; Nawyn, S.J.; Flaherty, J.A.; Fendrich, M.; Drum, M.L.; and Johnson, T.P. Sexual harassment and generalized workplace abuse among university employees: Prevalence and mental health correlates. American Journal of Public Health 89:358-363, 1999.

14. Ames, G.; Delaney, W., and Janes, C. Obstacles to effective alcohol policy in the workplace: A case study. British Journal of Addiction 87(7):1055-1069, 1992.

15. Ames, G.M.; Grube, J.W.; and Moore, R.S. The relationship of drinking and hangovers to workplace problems: An empirical study. Journal of Studies on Alcohol 58(1):37-47, 1997.

16. Mangione, T.W.; Howland, J.; and Lee, M. New Perspectives for Worksite Alcohol Strategies: Results From a Corporate Drinking Study. Boston, MA: JSI Research and Training Institute, 1998.

17. Bray, R.M.; Kroutil, L.A.; Luckey, J.W.; Wheeless, S.C.; Iannacchione, V.G.; Anderson, D.W.; Marsden, M.E.; and Dunteman, G.H. Highlights 1992 Worldwide Survey of Substance Abuse and Health Behaviors Among Military Personnel. Research Triangle Park, NC: Research Triangle Institute, 1992.

18. Roman, P., and Trice, H.M. The development of deviant drinking behavior. Archives of Environmental Health 20:424-435, 1970.

19. Mangione, T.W.; Howland, J.; Amick, B.; Cote, J.; Lee, M.; Bell, N.; and Levine, S. Employee drinking practices and work performance. Journal of Studies on Alcohol 60(2):261-270, 1999.

20. Yesavage, J.A., and Leirer, V.O. Hangover effects on aircraft pilots 14 hours after alcohol ingestion: A preliminary report. American Journal of Psychiatry 143(12):1546-1550, 1986.

21. Morrow, D.; Leirer, V.; and Yesavage, J. The influence of alcohol and aging on radio communication during flight. Aviation, Space, and Environmental Medicine 61(1):12-20, 1990.

22. Vicary, J.R. Primary prevention and the workplace. Journal of Primary Prevention 15(2):99-103, 1994.

23. Shain, M; Suurvali, H.; and Boutilier, M. Healthier Workers: Health Promotion and Employee Assis tance Programs. Lexington, MA: Lexington Books, 1986.

24. Snow, D.L., and Kline, M.L. Preventive interventions in the workplace to reduce negative psychiatric consequences of work and family stress. In: Mazure, C.M., ed. Does Stress Cause Psychiatric Illness? Washington, DC: American Psychiatric Press, 1995. pp. 221-270.

25. Bacharach, S.B.; Bamberger, P.A.; and Sonnenstuhl, W.J. MAPs: Labor-based peer assistance in the workplace. Industrial Relations 35(2):261-275, 1996.

26. Scanlon, W.F. Alcoholism and Drug Abuse in the Workplace: Managing Care and Costs Through Employment Assistance Programs. 2d ed. New York: Praeger, 1991.

27. Leong, D.M., and Every, D.K. Internal and external EAPs: Is one better than the other? Employee Assistance Quarterly 12(3):47-62, 1997. (28) Blum, T.C., and Roman, P.M. A description of clients using employee assistance programs. Alcohol Health & Research World 16(2):120-128, 1992.

29. Normand, J.; Lempert, R.O.; and O'Brien, C.P., eds. Under the Influence? Drugs and the American Work Force. Washington, DC: National Academy Press, 1994.

30. French, M.T.; Zarkin, G.A.; Bray, J.W.; and Hartwell, T.D. Costs of employee assistance programs: Findings from a national survey. American Journal of Health Promotion 11(3):219-222, 1997.

31. Kenkel, D.S. Self-insurance and worksite alcohol programs: An econometric analysis. Journal of Studies on Alcohol 58(2):211-219, 1997.

32. Googins, B. EAPs and early intervention: Maximizing the opportunities. In: Roman, P.M., ed. Alcohol Problem Intervention in the Workplace: Employee Assistance Programs and Strategic Alternatives. Westport, CT: Quorum Books, 1990. pp. 191-202.

33. Flynn, C.F.; Sturges, M.S.; Swarsen, R.J.; and Kohn, G.M. Alcoholism and treatment in airline aviators: One company's results. Aviation, Space, and Environmental Medicine 64(4):314-318, 1993.

34. Walsh, D.C.; Hingson, R.W.; Merrigan, D.M.; Levenson, S.M.; Cupples, L.A.; Heeren, T.; Coffman, G.A.; Becker, C.A.; Barker, T.A.; Hamilton, S.K.; McGuire, T.G.; and Kelly, C.A. A randomized trial of treatment options for alcohol-abusing workers. New England Journal of Medicine 325(11):775-782, 1991.

35. Foote, A., and Erfurt, J.C. Effects of EAP follow-up on prevention of relapse among substance abuse clients. Journal of Studies on Alcohol 52(3):241-248, 1991.

Source: National Institute on Alcohol Abuse. (July 1999)                                                                National Institutes of Health

v Alcohol and Tobacco

Extensive research supports the popular observation that "smokers drink and drinkers smoke." Moreover, the heaviest alcohol consumers are also the heaviest consumers of tobacco. Concurrent use of these drugs poses a significant public health threat. A survey of persons treated for alcoholism and other drug addictions revealed that 222 of 845 subjects had died over a 12-year period; one-third of these deaths were attributed to alcohol-related causes, and one-half were related to smoking ⁽¹⁾. This chapter explores the association between alcohol and tobacco use, possible mechanisms of their combined health effects, and some implications for alcoholism treatment.

The Co-occurrence of Alcoholism and Smoking

Between 80 and 95 percent of alcoholics smoke cigarettes ⁽²⁾, a rate that is three times higher than among the population as a whole. Approximately 70 percent of alcoholics are heavy smokers (i.e., smoke more than one pack of cigarettes per day), compared with 10 percent of the general population ⁽³⁾. Drinking influences smoking more than smoking influences drinking. Nevertheless, smokers are 1.32 times as likely to consume alcohol as are nonsmokers ⁽⁴⁾.

Most adult users of alcohol or tobacco first tried these drugs during their early teens ⁽⁵⁾. Among smoking alcoholics, the initiation of regular cigarette smoking typically precedes the onset of alcoholism by many years, although data are inconsistent ⁽⁶⁾. Adolescents who begin smoking are 3 times more likely to begin using alcohol ⁽⁷⁾, and smokers are 10 times more likely to develop alcoholism than are nonsmokers ⁽⁶⁾.

Why Are Alcohol and Tobacco Used Together?

Postulated mechanisms for the concurrent use of alcohol and tobacco fall into two broad, nonexclusive categories: Either drug may increase the desired (rewarding) effects of the other, or either may decrease the toxic or unpleasant (aversive) effects of the other. These interactions involve processes of reinforcement or tolerance, as described below. (A third possibility that one drug may alter the metabolism of the other, thereby affecting its absorption, distribution, or elimination from the body has not been convincingly established [8].)

Reinforcement. Reinforcement refers to the physiological processes by which a behaviorsuch as consumption of a drug becomes habitual. A key process in reinforcement for some drugs occurs when nerve cells release the chemical messenger dopamine into a small area of the brain called the nucleus accumbens following consumption of the drug ⁽⁹⁾. Nicotine is the primary ingredient of tobacco that triggers reinforcement. After reaching the brain, nicotine activates a group of proteins called nicotinic receptors. These proteins, located on the surface of certain brain cells, normally regulate a host of physiological functions, some of which may contribute to aspects of reinforcement. Ultimately, nicotine brings about the release of dopamine in the nucleus accumbens ⁽⁵⁾. Alcohol consumption also leads to dopamine release, although the mechanism by which alcohol produces this effect is incompletely understood ^(10,11).

Tolerance. Tolerance is decreased sensitivity to a given effect of a drug such that increased doses are needed to achieve the same effect. Long-term administration of nicotine in animals can induce tolerance to some of alcohol's reinforcing effects, and chronic alcohol administration induces tolerance to some effects of nicotine ⁽⁸⁾. Such cross-tolerance might lead to increased consumption of both drugs in an attempt to regain former levels of reward. In addition, cross-tolerance can develop to the aversive effects of drugs. For example, smokers may reduce their tobacco intake when they begin to feel its aversive effects (e.g., increased heart rate, "nervousness"). Alcohol's sedating effects may mitigate these effects of nicotine, facilitating continued tobacco use ⁽¹²⁾. Conversely, nicotine's stimulating effects can mitigate alcohol-induced loss of mental alertness ⁽⁸⁾.

Animal studies provide support for these interactions. For example, alcohol appears to induce loss of physical coordination in mice by inhibiting nicotinic receptors in the cerebellum, a part of the brain that is active in coordinating movement and balance. Administration of nicotine appears to remove this inhibition and restore coordination ^(13,14). In addition, alcohol interferes with the normal functioning of the chemical messenger vasopressin, which may play a role in memory processes. Vasopressin is also associated with the development of tolerance to alcohol ⁽¹⁵⁾. Nicotine helps normalize vasopressin function in the brain, reducing alcohol-induced impairment of memory and other intellectual abilities ⁽¹¹⁾.

What Is the Risk of Cancer From Alcohol and Tobacco?

Smoking and excessive alcohol use are risk factors for cardiovascular and lung diseases and for some forms of cancer. The risks of cancer of the mouth, throat, or esophagus for the smoking drinker are more than the sum of the risks posed by these drugs individually ⁽²⁾. For example, compared with the risk for nonsmoking nondrinkers, the approximate relative risks for developing mouth and throat cancer are 7 times greater for those who use tobacco, 6 times greater for those who use alcohol, and 38 times greater for those who use both tobacco and alcohol ⁽¹⁶⁾.

How Do Alcohol and Tobacco Increase Cancer Risk?

Approximately 4,000 chemical substances are generated by the chemical reactions that occur in the intense heat of a burning cigarette ⁽¹⁷⁾. A group of these chemicals, collectively known as tar, is carried into the lungs on inhaled smoke. The bloodstream then distributes the components of tar throughout the body. Certain enzymes found mainly in the liver (i.e., microsomal enzymes) convert some ingredients of tar into chemicals that can cause cancer. Long-term alcohol consumption can activate some such microsomal enzymes, greatly increasing their activity and contributing to smoking-related cancers ^(18,19).

Microsomal enzymes are found not only in the liver but also in the lungs and digestive tract, which are major portals of entry for tobacco smoke. The esophagus may be particularly susceptible, because it lacks an efficient mechanism for removing toxic substances produced by activated microsomal enzymes ⁽²⁰⁾. Consistent with these observations, alcohol has been shown to promote esophageal tumors in laboratory animals exposed simultaneously to specific components of tar ^(18,19).

Finally, alcoholics frequently exhibit deficiencies of zinc and vitamin A, substances that confer some protection against cancer ⁽²⁰⁾.

Addictions Treatment for Smoking Alcoholics

Until recently, alcoholism treatment professionals have generally not addressed the issue of smoking cessation, largely because of the belief that the added stress of quitting smoking would jeopardize an alcoholic's recovery ⁽²¹⁾.

Research has not confirmed this belief. One study evaluated the progress of residents in an alcoholism treatment facility who were concurrently undergoing a standard smoking cessation program (i.e., experimental group) ⁽⁶⁾. A comparison group of smoking alcoholics participated in the same alcoholism program but without undergoing the smoking cessation program. One year after treatment, results indicated that the smoking cessation program had no effect on abstinence from alcohol or other drugs. In addition, 12 percent of the subjects in the experimental group, but none of the subjects in the comparison group, had stopped smoking.

Some data suggest that alcoholism recovery may facilitate nicotine abstinence. In one study, patients participating in concurrent treatment for nicotine addiction during residential treatment for alcohol and other drug abuse achieved at least a temporary reduction in smoking and an increased motivation to quit smoking ⁽²²⁾. Similarly, persons who achieve abstinence from alcohol without formal treatment often stop smoking at the same time (6,23).

Following the lead of other health facilities, many addictions treatment facilities are becoming smoke-free, providing a "natural experiment" on the effectiveness of dual recovery programs. Initial evaluations suggest that no-smoking policies are feasible in this setting ⁽²⁴⁾. However, no outcome studies have been performed, and additional research is needed.

Problems encountered in smoke-free alcoholism treatment programs include surreptitious smoking by patients as well as by staff. Further, researchers have suggested modifying smoking cessation programs to conform with the structure and language of concurrent alcoholism programs (e.g., use of a 12-step approach) ⁽²⁾. Nicotine patch therapy for smoking alcoholics may require higher doses of nicotine than are usually applied, because of alcohol-induced tolerance to some of nicotine's effects ^(25,26).

Smoking alcoholics with a history of depressive disorders are generally less successful at smoking cessation than are subjects without such a history ⁽²⁷⁾. Smoking may diminish the chances of recurring depression in some people, and a major depressive episode may follow smoking cessation in these subjects ⁽²⁸⁾. An additional clinical consideration is that activation of microsomal enzymes by alcohol and tobacco tar may reduce the effectiveness of antidepressant medications ⁽¹⁷⁾. Therefore, medication levels should be carefully monitored in patients undergoing treatment for depression and addiction to alcohol and tobacco ⁽⁵⁾.

Conclusion

Alcohol and tobacco are frequently used together, may share certain brain pathways underlying dependence, and because of their numerous social and health-related consequences, are a continuing source of national public policy debate.

Many alcoholism treatment professionals have not actively pursued smoking cessation among their patients based on the belief that the stress of quitting smoking while undergoing alcoholism treatment might cause relapse. As a physician who has seen the ravages caused by both alcoholism and smoking, I am pleased that we now have research evidence showing that both can be treated simultaneously without endangering alcoholism recovery. As basic science learns more about how alcohol and nicotine act singly and together within the brain, new treatments for alcohol and nicotine dependence will follow.

Finally, society has attempted to minimize the consequences of using both alcohol and tobacco through public policy actions, including health warning labels, restrictions on advertising, and age restrictions on use. Unlike tobacco, however, moderate use of alcohol has certain health benefits.

References

1. Hurt, R.D.; Offord, K.P.; Croghan, I.T.; et al. Mortality following inpatient addictions treatment: Role of tobacco use in a community-based cohort. JAMA 275(14):1097-1103, 1996.

2. Patten, C.A.; Martin, J.E.; and Owen, N. Can psychiatric and chemical dependency treatment units be smoke free? J Subst Abuse Treat 13(2):107-118, 1996.

3. Collins, A.C., and Marks, M.J. Animal models of alcohol-nicotine interactions. In: Fertig, J.B., and Allen, J.P. Alcohol and Tobacco: From Basic Science to Clinical Practice. NIAAA Research Monograph No. 30. NIH Pub. No. 95-3931. Washington, DC: Supt. of Docs., U.S. Govt. Print. Off., 1995. pp. 129-144.

4. Shiffman, S., and Balabanis, M. Associations between alcohol and tobacco. In: Fertig, J.B., and Allen, J.P. Alcohol and Tobacco: From Basic Science to Clinical Practice. NIAAA Research Monograph No. 30. NIH Pub. No. 95-3931. Washington, DC: Supt. of Docs., U.S. Govt. Print. Off., 1995. pp. 17-36.

5. Jarvik, M.E., and Schneider, N.G. Nicotine. In: Lowinson, J.H.; Ruiz, P.; and Millman, R.B. Substance Abuse: A Comprehensive Textbook. 2nd ed. Baltimore: Williams & Wilkins, 1992. pp. 334-356.

6. Hurt, R.D.; Eberman, K.M.; Croghan, I.T.; et al. Nicotine dependence treatment during inpatient treat ment for other addictions: A prospective intervention trial. Alcohol Clin Exp Res 18(4):867-872, 1994.

7. Hughes, J.R. Clinical implications of the association between smoking and alcoholism. In: Fertig, J.B., and Allen, J.P. Alcohol and Tobacco: From Basic Science to Clinical Practice. NIAAA Research Mono graph No. 30. NIH Pub. No. 95-3931. Washington, DC: Supt. of Docs., U.S. Govt. Print. Off., 1995. pp. 171- 185.

8. Zacny, J.P. Behavioral aspects of alcohol-tobacco interactions. In: Galanter, M., ed. Recent Develop ments in Alcoholism. Vol. 8. New York: Plenum Press, 1990. pp. 205-219.

9. Di Chiara, G., and Imperato, A. Drugs abused by humans preferentially increase synaptic dopamine concentrations in the mesolimbic system of freely moving rats. Proc Natl Acad Sci U S A 85(14):5274- 5278, 1988.

10. Dar, M.S.; Li, C.; and Bowman, E.R. Central behavioral interactions between ethanol, (-)-nicotine, and (-)-cotinine in mice. Brain Res Bull, 32(1):23-28, 1993.

11. Pomerleau, O.F. Neurobiological interactions of alcohol and nicotine. In: Fertig, J.B., and Allen, J.P. Alcohol and Tobacco: From Basic Science to Clinical Practice. NIAAA Research Monograph No. 30. NIH Pub. No. 95-3931. Washington, DC: Supt. of Docs., U.S. Govt. Print. Off., 1995. pp. 145-158.

12. Collins, A.C. The nicotinic cholinergic receptor as a potential site of ethanol action. In: Deitrich, R.A., and Erwin, V.G. Pharmacological Effects of Ethanol on the Nervous System. Boca Raton: CRC Press, 1996. pp. 95-115.

13. Dar, M.S.; Bowman, E.R.; and Li, C. Intracerebellar nicotinic-cholinergic participation in the cerebellar adenosinergic modulation of ethanol-induced motor coordination in mice. Brain Res 644(1):117-127, 1994.

14. Yu, D.; Zhang, L.; Eiselé, J.-L.; et al. Ethanol inhibition of nicotinic acetylcholine type alpha 7 recep tors involves the amino-terminal domain of the receptor. Mol Pharmacol 50:1010-1016, 1996.

15. Hoffman, P. Neuroadaptive functions of the neuropeptide arginine vasopressin: Ethanol tolerance. Ann N Y Acad Sci 739:168-175, 1994.

16. Blot, W.J. Alcohol and cancer. Cancer Res (supp.) 52:2119s-2123s, 1992.

17. Hardman, J.G.; Limbird, L.E.; Molinoff, P.B.; et al., eds. Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York: McGraw-Hill, 1995.

18. U.S. Department of Health and Human Services. The Health Consequences of Smoking: Cancer, a Report of the Surgeon General. DHHS (PHS) No. 82-50179. Washington, DC: Supt. of Docs., U.S. Govt. Print. Off., 1982.

19. Garro, A.J.; Espina, N.; and Lieber, C.S. Alcohol and cancer. Alcohol Health Res World 16(1):81-86, 1992.

20. Seitz, H.K., and Osswald, B. Effect of ethanol on procarcinogen activation. In: Watson, R.R., ed. Alcohol and Cancer. Boca Raton: CRC Press, 1992. pp. 55-72. (21) Burling, T.A.; Marshall, G.D.; and Seidner, A.L. Smoking cessation for substance abuse inpatients. J Subst Abuse 3(3):269-276, 1991.

22. Joseph, A.M.; Nichol, K.L.; Willenbring, M.L.; et al. Beneficial effects of treatment of nicotine depen- dence during an inpatient substance abuse treatment program. JAMA 263(22):3043-3046, 1990.

23. Sobell, L.C.; Cunningham, J.A.; and Sobell, M.B. Recovery from alcohol problems with and without treatment: Prevalence in two population surveys. Am J Public Health 86(7):966-972, 1996.

24. Martin, J.E.; Calfas, K.J.; Patten, C.A.; et al. Prospective evaluation of three smoking interventions in 205 recovering alcoholics: One-year results of Project SCRAP—Tobacco. J Consult Clin Psychol 65(1):190-194, 1997.

25. Abrams, D.B.; Monti, P.M.; Niaura, R.S.; et al. Interventions for alcoholics who smoke. Alcohol Health Res World 20(2):111-117, 1996.

26. Hurt, R.D.; Dale, L.C.; Offord, K.P.; et al. Nicotine patch therapy for smoking cessation in recovering alcoholics. Addiction 90(11):1541-1546, 1995.

27. Covey, L.S.; Glassman, A.H.; Stetner, F.; et al. Effect of history of alcoholism or major depression on smoking cessation. Am J Psychiatry 150(10):1546-1547, 1993.

28. Glassman, A.H.; Helzer, J.E.; Covey, L.S.; et al. Smoking, smoking cessation, and major depression. JAMA 264(12):1546-1549, 1990.

Source: National Institute on Alcohol Abuse. (July 1999)                                                                National Institutes of Health

v Alcoholism and Co-occurring Disorders

The term "comorbidity" refers to the presence of any two or more illnesses in the same person. These illnesses can be medical or psychiatric conditions, as well as drug use disorders, including alcoholism. Comorbid illnesses may occur simultaneously or sequentially. The fact that two illnesses are comorbid, however, does not necessarily imply that one is the cause of the other, even if one occurs first.

An understanding of comorbidity is essential in developing effective treatment and prevention efforts. For example, since alcoholism causes liver disease, measures to decrease alcohol consumption will help reduce the incidence of liver disease. With respect to treatment, persons exhibiting comorbid alcohol-related and medical or psychiatric disorders often fall through the cracks of the health care system because of administrative distinctions among addiction, medical, and mental health-related services. Patients are often forced to choose between clinical settings, often resulting in neglect of one condition ⁽¹⁾.

Alcoholism and other disorders might be related in a number of ways, including the following (2,3): 1) Alcoholism and a second disorder can co-occur, either sequentially or simultaneously, by coincidence. 2) Alcoholism can cause various medical and psychiatric conditions or increase their severity. 3) Comorbid disorders might cause alcoholism or increase its severity. 4) Both alcoholism and the comorbid disorder may be caused, separately, by some third condition. 5) Alcohol use or alcohol withdrawal can produce symptoms that mimic those of an independent psychiatric disorder.

Research on the nature of the relationship between comorbid disorders generally relies on surveys of either the clinical population (persons in treatment) or the general population. Most studies of comorbidity are based on clinical samples. This may result in inflated estimates of comorbidity, since persons with multiple ailments may be more likely to seek treatment (Berkson's fallacy) ⁽⁴⁾. This trend may be countered to some extent by the reluctance of some alcoholism treatment centers to admit persons exhibiting serious psychiatric problems. Thus, the prevalence of comorbid psychiatric disorders among alcoholics in treatment does not reflect the actual prevalence of such comorbidity in the community ⁽³⁾.

Additional methodological difficulties complicate both clinical and general population investigations. For example, estimates of comorbidity will also vary depending on how alcohol use disorders are defined. Definitions of alcoholism have included 1) formal definitions of abuse and dependence appearing in psychi atric classification systems such as the DSM-III-R; 2) alcohol-related symptom ratings; 3) serious manifestations of physiological dependence (i.e., tolerance and withdrawal); and 4) various levels of heavy alcohol consumption. Since alcohol use, alcohol withdrawal, and alcohol abuse and dependence may each relate to comorbid conditions in an entirely different way, it is essential when evaluating comorbidity to clarify which aspects of alcohol use are involved ⁽⁵⁾. Similar considerations apply to the evaluation of comorbid disorders. For example, when evaluating depression, it is important to distinguish among sadness, grief, and major depressive disorder ⁽²⁾.

An important source of comorbidity data is the Epidemiologic Catchment Area (ECA) program of the National Institute of Mental Health ⁽⁶⁾. The ECA surveyed more than 20,000 respondents residing in households, group homes, and long-term institutions in five sites across the United States ⁽⁷⁾ to provide data about the prevalence and incidence of psychiatric disorders, as well as issues related to treatment. (Prevalence is the number of existing cases; incidence is the number of new cases.)

Conclusions about causal relationships between alcohol use disorders and comorbid psychiatric disorders based on ECA data are problematic, since sequencing criteria consisted of age at first symptom of the alcohol use disorder, rather than age at onset of the syndrome ⁽⁸⁾. Moreover, the ECA program defined alcohol use disorders as the occurrence of enough symptoms to meet the associated diagnostic criteria over the life course. The sporadic occurrence of isolated symptoms, perhaps years apart, provides an insufficient basis for testing competing hypotheses related to comorbidity.

Because the term "comorbidity" is often not applied to medical conditions, a number of medical conditions that are often comorbid with alcoholism are mentioned below. A discussion of comorbidity with psychiatric disorders will follow.

Medical Conditions

Alcohol has been shown to be directly toxic to the liver. Approximately 90 to 100 percent of heavy drinkers show evidence of fatty liver, an estimated 10 to 35 percent develop alcoholic hepatitis, and 10 to 20 percent develop cirrhosis ⁽⁹⁾. Fatty liver is reversible with abstinence, alcoholic hepatitis is usually reversible upon abstinence, and while alcoholic cirrhosis is often progressive and fatal, it can stabilize with abstinence ⁽¹⁰⁾. In addition to liver disease, heavy alcohol consumption causes chronic pancreatitis ⁽¹¹⁾ and malabsorption of nutrients ⁽¹²⁾.

The prevalence of alcoholic cardiomyopathy (heart muscle disease) is unknown. Alcohol-induced heart damage appears to increase with lifetime dose of alcohol ⁽¹³⁾.

Alcohol can damage the brain in many ways. The most serious effect is Korsakoff's syndrome, characterized in part by an inability to remember recent events or to learn new information. The incidence of alcohol-related brain damage is approximately 10 percent of adult dementias in the United States ⁽¹⁴⁾. Milder attention and memory deficits may improve gradually with abstinence ⁽¹⁵⁾.

Additional diseases strongly linked to alcohol consumption include failure of reproductive function ⁽¹⁰⁾ and cancers of the mouth, larynx, and esophagus ⁽¹⁶⁾. Hospitalized alcoholics have also been found to have an increased prevalence of dental problems, compared with nonalcoholic psychiatric patients, including missing teeth and nonrestorable teeth ⁽¹⁷⁾.

Psychiatric disorders. Despite the study's shortcomings, data from the ECA provide a starting point for assessing the prevalence of some comorbidities (on a lifetime basis). Based on ECA data, alcoholics are 21.0 times more likely to also have a diagnosis of antisocial personality disorder compared with nonalcoholics. Similar "odds ratios" for some other psychiatric comorbidities are as follows: drug abuse, 3.9 times; mania, 6.2 times; and schizophrenia, 4.0 times. There is only a mild increase in major depressive disorder among alcoholics (odds ratio 1.7), and essentially no increase in anxiety disorders ⁽¹⁸⁾.

Antisocial personality disorder. The strongest correlate of alcoholism documented in the ECA is antisocial personality disorder (ASPD) ⁽¹⁸⁾. Determining the chronological relationships between the two disorders is complicated by the following factors (3,19,20): 1) both disorders typically begin early in life, thus requiring retrospective reporting from adults; 2) there is considerable overlap in the symptoms of the two disorders; 3) alcohol or other drug abuse is itself one of the diagnostic criteria for ASPD; and 4) intoxication leads to behavioral disinhibition, thus lowering the threshold for antisocial behavior ⁽²⁰⁾.

Comorbid ASPD has prognostic and treatment implications for alcoholics. Patients with ASPD have an earlier age of onset of alcohol and other drug abuse and a more rapid and serious course of illness (21,22, 23,24).

Bulimia. Bulimia is an eating disorder in which patients, usually female, binge on sugar- and fat-rich meals, and purge regularly, as by self-induced vomiting. This disorder is characterized by craving, preoccupation with binge eating, loss of control during binges, an emphasis on short-term gratification, and ambivalence about treatment symptoms that resemble those of addictive disorders ^(19,25). Bulimics commonly exhibit multiple drug use disorders and have high rates of alcoholism. Between 33 and 83 percent of bulimics may have a first-degree relative suffering from alcohol abuse or alcoholism ⁽²⁵⁾.

Depression. Although it has been suggested that alcoholism and depression are manifestations of the same underlying illness, the results of family, twin, and adoption studies suggest that alcoholism and mood disorder are probably distinct illnesses with different prognoses and treatments (1,2). However, symptoms of depression are likely to develop during the course of alcoholism, and some patients with mood disorders may increase their drinking when undergoing a mood change, fulfilling criteria for secondary alcoholism. When depressive symptoms are secondary to alcoholism, they are likely to disappear within a few days or weeks of abstinence, as withdrawal symptoms subside (2,15,26,27).

Anxiety . Studies (not using ECA data) indicate that approximately 10 to 30 percent of alcoholics have panic disorder, and about 20 percent of persons with anxiety disorders abuse alcohol ⁽²⁸⁾. Among alcoholics entering treatment, about two-thirds have symptoms that resemble anxiety disorders ⁽²⁹⁾. The relation between major anxiety disorders and alcoholism is unclear ⁽³⁰⁾. Several studies indicate that anxious patients may use alcohol or other drugs to self-medicate, despite the fact that such use may ultimately exacerbate their clinical condition ⁽²⁸⁾.

The strongest correlation between alcoholism and severe anxiety symptoms occurs in the context of alcohol withdrawal ⁽³⁰⁾. The severe tremors, feelings of tension, restlessness, and insomnia associated with withdrawal begin to subside after 4 or 5 days, although a vulnerability to panic attacks and to generalized anxiety may continue for months. Because these symptoms decrease with abstinence, they are unlikely to represent an independent anxiety disorder ⁽³⁰⁾. Interestingly, subjects suffering from both alcoholism and panic disorder are unable to distinguish between a number of symptoms common to both disorders ⁽³¹⁾.

Other drug abuse. Based on ECA data ⁽¹⁸⁾, alcoholics are 35 times more likely than nonalcoholics to also use cocaine. Similar odds ratios for other types of drugs are: sedatives, 17.0 times; opioids, 13.0 times; hallucinogens, 12.0; stimulants, 11.0; and marijuana and related drugs, 6.0. Surveys of both clinical and nonclinical populations indicate that at least 90 percent of alcoholics are nicotine dependent ⁽³²⁾.

Comorbidity affects the course of illness and the response to treatment of both alcoholism and its comorbid illnesses, whether these occur simultaneously or sequentially. Because alcohol-related comorbidity is so common, research is needed to improve the recognition and appropriate management of alcohol abuse and alcoholism occurring in the context of other disorders ⁽¹⁸⁾ .

Conclusion

Treatment for co-occurring illnesses in persons with alcoholism should be a standard part of every alcoholism treatment program. Unfortunately, many patients with such illnesses fall through the cracks; for example, alcoholic patients with psychiatric problems who may be rejected by both alcoholism programs and mental health programs. This situation is unacceptable. In many instances, leadership can help solve this problem. Program directors who are concerned about providing the best care to their patients should work within their ser vice areas to develop comprehensive treatment networks for multiply affected patients. In some cases, this may mean facilitating changes in city, county, or State laws to mandate care for such patients. In other cases, it might mean working to resolve differences in treatment philosophy that make it difficult for patients to be treated for comorbid conditions; for example, the requirement of some alcoholism programs that methadone-maintained individuals be drug free before acceptance for treatment. Patients who are alcoholic and who also suffer from other illnesses deserve the same kind of comprehensive care as a cancer patient with pneumonia, or a diabetic patient with glaucoma.

Researchers interested in the causes of disease will differ on whether studying the patient with co-occurring disease is a promising research strategy. On the one hand, the presence of one illness has been known to modify the course of another for better or worse. Clearly, it would be valuable to understand why. On the other hand, because we barely understand the fundamentals of alcoholism, studying it in the presence of other diseases may introduce complications. For example, diabetes increases an individual's risk for atherosclerosis, but researchers interested in atherosclerosis might not choose to unravel the causes of this disease by studying it primarily in diabetic patients.

Beacause of the increase in the frequency of polydrug abuse, alcoholism treatment programs must be aware of and prepared to deal with this problem in their patients. It should be noted, however, that the most common pattern of abuse in the United States is still alcoholism alone ⁽³³⁾.

References

1. Merikangas, K.R., & Gelernter, C.S. Comorbidity for alcoholism and depression. Psychiatric Clinics of North America 13(4):613-632, 1990.

2. Schuckit, M.A. Genetic and clinical implications of alcoholism and affective disorder. American Journal of Psychiatry 143(2):140-147, 1986.

3. Meyer, R.E. Prospects for a rational pharmacotherapy of alcoholism. Journal of Clinical Psychiatry 50(11):403-412, 1989.

4. Berkson, J. Limitations of the application of the 4-fold table analyses to hospital data. Biometrics 2:47- 53, 1946.

5. Grant, B.F., & Hasin, D.S. The Alcohol Use Disorders and Associated Disabilities Interview Schedule (AUDADIS). Rockville, MD: National Institute on Alcohol Abuse and Alcoholism, 1990.

6. Regier, D.A.; Farmer, M.E.; Rae, D.S.; Locke, B.Z.; Keith, S.J.; Judd, L.L.; & Goodwin, F.K. Comorbidity of mental disorders with alcohol and other drug abuse. Journal of the American Medical Association 264(19):2511-2518, 1990.

7. Regier, D.A.; Myers, J.K.; Kramer, M.; Robins, L.N.; Blazer, D.G.; Hough, R.L.; Eaton, W.W.; & Locke, B.Z. The NIMH Epidemiologic Catchment Area Program. Archives of General Psychiatry 41(10):934- 941, 1984.

8. Grant, B.F., & Towle, L.H. Standardized diagnostic instruments for alcohol research. Alcohol Health & Research World, in press.

9. Grant, B.F.; Dufour, M.C.; & Harford, T.C. Epidemiology of alcoholic liver disease. Seminars in Liver Disease 8(1):12-25, 1988.

10. Rubin, E. How alcohol damages the body. Alcohol Health & Research World 13(4):322-327, 1989.

11. Korsten, M.A. Alcoholism and pancreatitis: Does nutrition play a role? Alcohol Health & Research World 13(3):232-237, 1989.

12. Feinman, L. Absorption and utilization of nutrients in alcoholism. Alcohol Health & Research World 13(3):207-210, 1989.

13. Urbano-Marquez, A.; Estruch, R.; Navarro-Lopez, F.; Grau, J.M.; Mont, L.; & Rubin, E. The effects of alcoholism on skeletal and cardiac muscle. New England Journal of Medicine 320(7):409-415, 1989.

14. Berman, M.O. Severe brain dysfunction: Alcoholic Korsakoff's syndrome. Alcohol Health & Re search World 14(2):120-129, 1990.

15. Desoto, C.B.; O'Donnell, W.E.; & amp; DeSoto, J.L. Long-term recovery in alcoholics. Alcoholism: Clinical and Experimental Research 13(5): 693-697, 1989.

16. Lieber, C.S.; Garro, A.J.; Leo, M.A.; & Worner, T.M. Mechanisms for the interrelationship between alcohol and cancer. Alcohol Health & Research World 10(3):10-17, 48-50, 1986.

17. King, W.H., & Tucker, K.M. Dental problems of alcoholic and nonalcoholic psychiatric patients. Quarterly Journal of Studies on Alcohol 34(4):1208-1211, 1973.

18. Helzer, J.E., & Pryzbeck, T.R. The co-occurrence of alcoholism with other psychiatric disorders in the general population and its impact on treatment. Journal of Studies on Alcohol 49(3):219-224, 1988. 

19. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised. Washington, DC: the Association, 1987.

20. Bukstein, O.G.; Brent, D.A.; & Kaminer, Y. Comorbidity of substance abuse and other psychiatric disorders in adolescents. American Journal of Psychiatry 146(9):1131-1141, 1989.

21. Hesselbrock, M.N.; Hesselbrock, V.M.; Babor, T.F.; Stabenau, J.R.; Meyer, R.E.; & Weidenman, M. Anti social behavior, psychopathology and problem drinking in the natural history of alcoholism. In: Goodwin, D.W. Longitudinal Research in Alcoholism. Boston: Kluwer-Nijhoff Publishing, 1984. pp. 197-214.

22. Hesselbrock, M.N.; Meyer, R.E.; & Keener, J.J. Psychopathology in hospitalized alcoholics. Archives of General Psychiatry 42:1050-1055, 1985.

23. Hesselbrock, V. M.; Hesselbrock, M.N.; & Workman-Daniels, K.L. Effect of major depression and antiso cial personality on alcoholism: Course and motivational patterns. Journal of Studies on Alcohol 47(3):207- 212, 1986.

24. Penick, E.C.; Powell, B.J.; Othmer, E.; Bingham, S.F.; Rice, A.S.; & Liese, B.S. Subtyping alcoholics by coexisting psychiatric syndromes: Course, family history, outcome. In: Goodwin, D.W. Longitudinal Research in Alcoholism. Boston: Kluwer-Nijhoff Publishing, 1984. pp. 167-196.

25. Kaye, W.H.; Gwirtsman, H.E.; George, S.R.; Weiss, S.R.; & Jimerson, D.C. Relationship of mood alter ations to bingeing behaviour in bulimia. British Journal of Psychiatry 149:479-485, 1986.

26. Clark, D.C.; Pisani, V.D.; Aagesen, C.A.; Sellers, D.; & Fawcett, J. Primary affective disorder, drug abuse, and neuropsychological impairment in sober alcoholics. Alcoholism: Clinical and Experimental Re search 8(4):399-404, 1984.

27. Brown, S.A., & Schuckit, M.A. Changes in depression among abstinent alcoholics. Journal of Studies on Alcohol 49(5):412-417, 1988.

28. Cox, B.J.; Norton, G.R.; Swinson, R.P.; & Endler, N.S. Substance abuse and panic-related anxiety: A critical review. Behavior Research and Therapy 28(5):385-393, 1990.

29. Ross, H.E.; Glaser, F.B.; & Germanson, T. The prevalence of psychiatric disorders in patients with alcohol and other drug problems. Archives of General Psychiatry 45:1023-1031, 1988.

30. Schuckit, M.A., & Monteiro, M.G. Alcoholism, anxiety and depression. British Journal of Addiction 83:1373-1380, 1988.

31. George, D.T.; Zerby, A.; Noble, S.; & Nutt, D.J. Panic attacks and alcohol withdrawal: Can subjects differentiate the symptoms? Biological Psychiatry 24:240-243, 1988.

32. Bobo, J.K. Nicotine dependence and alcoholism epidemiology and treatment. Journal of Psychoactive Drugs 21(3):323-329, 1989.

33. National Institute on Drub Abuse. National Household Survey on Drug Abuse: 1990 Findings. DHHS Pub. No. (ADM)91-1732. Washington, DC: Supt. of Docs., U.S. Govt. Print. Off., 1991.

Source: National Institute on Alcohol Abuse. (July 1999)                                                               National Institutes of Health

v Alcohol and Coronary Heart Disease

Heart attacks and other forms of coronary heart disease (CHD) result in approximately 500,000 deaths annually ⁽¹⁾, accounting for 25 percent of the Nation's total mortality ⁽²⁾. Research has revealed an association between moderate alcohol consumption1 and lower risk for CHD. This chapter reviews epidemiologic evidence for this association, explores lifestyle factors and physiological mechanisms that might suggest ways to explain alcohol's apparent protective effects, and presents available data on the balance between alcohol's beneficial and harmful effects on health.

Epidemiologic Evidence

With few exceptions, epidemiologic data from at least 20 countries in North America, Europe, Asia, and Australia demonstrate a 20- to 40-percent lower CHD incidence among drinkers compared with nondrinkers (3,4). Moderate drinkers exhibit lower rates of CHD-related mortality than both heavy drinkers and abstainers (3,4). Such studies range from comparisons of nationwide population data to retrospective analyses of health and drinking patterns within communities.

The most persuasive epidemiologic evidence for alcohol's possible protective effects on CHD comes from prospective studies, in which participants provide information on their drinking habits and health-related practices before the onset of disease. Participants' subsequent health histories are evaluated through a series of follow-up interviews. Large-scale prospective investigations confirm an association between moderate drinking and lower CHD risk. The specific studies described here represent a total population of more than 1 million men and women of different ethnicities. Follow-up periods average 11 years,2 the longest being the 24-year prospective phase of the Framingham CHD mortality study ⁽⁵⁾. The two largest of these studies were conducted by the American Cancer Society, one including 276,800 men ⁽⁶⁾ and the other including 490,000 men and women ⁽⁷⁾.

Other large prospective investigations that associate moderate drinking with lower risk for CHD include a series of studies by Kaiser-Permanente analyzing CHD hospitalization (8,9) and death rates ^(10,11) in both men and women; studies of CHD incidence ⁽¹²⁾ and mortality ⁽¹³⁾ among female nurses; and studies of CHD incidence ^(14,15) and mortality ⁽¹⁶⁾ among male physicians. Results of these American studies are confirmed by data from similar investigations conducted in England ⁽¹⁷⁾, Denmark ⁽¹⁸⁾, China ⁽¹⁹⁾, and other countries (1,4). In addition, a smaller 12-year study found an association between moderate drinking and lower risk of CHD-related death among older persons (average age of 69) with late-onset diabetes, a population at high risk for CHD ⁽²⁰⁾. However, a recent 21-year prospective study from Scotland found no association between moderate drinking and lower risk for CHD among 6,000 working men ages 35 to 64 ⁽²¹⁾.

Is Alcohol's Role Causal or Incidental?

An association between moderate drinking and lower risk for CHD does not necessarily mean that alcohol itself is the cause of the lower risk. For example, a review of population studies indicates that the higher mortality risk among abstainers may be attributable to shared traits other than participants' nonuse of alcohol ⁽²²⁾. Substantial evidence ⁽¹⁾ has discounted speculation that abstainers include a large proportion of former heavy drinkers with preexisting health problems (i.e., "sick quitters"). Nevertheless, health-related life-style factors that correlate consistently with drinking level could account for some of the association between alcohol and lower risk for CHD ⁽⁴⁾. Among the most widely studied of these factors are exercise and diet.

Few studies have adjusted for subjects' levels of physical activity, despite evidence that exercise protects against CHD occurrence and mortality. In a comprehensive review of published studies, Berlin and Colditz ⁽²³⁾ concluded that risk for CHD was proportionately lower at higher exercise levels. Measures of activity level vary among studies. Studies evaluate factors such as job-related physical requirements, frequency of participation in unspecified sports, estimated vigorousness of given activities, calculations of energy expended, and tests of cardiovascular fitness ⁽²³⁾. Results of a community survey indicated that the prevalence of regular exercise was higher among moderate and heavy drinkers than among nondrinkers ⁽²⁴⁾. Regular exercise was defined as any form of nonoccupational physical activity performed at least three times per week. The role of exercise in the alcohol-CHD association requires additional study.

Diet is one of the strongest influences on CHD-related death among men ages 50 to 70 ⁽²⁵⁾. International comparisons, laboratory data, and prospective studies suggest that diets high in saturated fat and cholesterol increase the risk for CHD ⁽²⁶⁾. Epidemiologic data suggest that moderate drinkers may consume less fat and cholesterol than heavier drinkers ⁽¹⁴⁾ and abstainers ⁽²⁷⁾, potentially accounting for a portion of the lower CHD risk associated with alcohol. However, results of other prospective studies indicate that alcohol's association with lower CHD risk is independent of nutritional factors ^(12-14).

The Role of Beverage Choice

Some studies report that wine (particularly red wine) affords more CHD protection than beer or liquor at equivalent levels of alcohol consumption ⁽²⁸⁾. This finding suggests that the association between alcohol consumption and CHD risk may result from the effects of beverage ingredients other than alcohol itself. Epidemiologic and laboratory studies investigating this hypothesis have produced conflicting results.

A comparison of data from 21 developed countries concluded that wine consumption was more strongly correlated with lower CHD risk than was consumption of other alcoholic beverages ⁽²⁹⁾. However, large-scale prospective studies have not found any difference in the incidence of CHD associated with beverage type ^(1,9). Red wine has been shown to contain certain nonalcoholic ingredients that could hypothetically interfere with the progression of CHD ⁽³⁰⁾.

However, research has not yet demonstrated a significant role for these chemicals in arresting CHD development in humans ^(30,31).

Evidence suggests that a preference for wine over other alcoholic beverages is associated with a lifestyle that includes other favorable health-related practices. For example, drinkers who prefer wine tend to smoke less and drink less ^(10,11,32) and have a more healthful diet ⁽³³⁾ than those who prefer beer or liquor.

How Might Alcohol Lower Risk for CHD?

To function normally, the muscle tissue that constitutes the bulk of the heart requires a constant supply of oxygen-containing blood. Blood is delivered to the heart muscle through the coronary arteries. Cholesterol and other fatty substances can accumulate within the coronary arteries, partially impeding the flow of blood. This condition underlies the clinical manifestations of CHD, which may range from episodic chest pain to sudden death. The most common serious manifestation of CHD is the heart attack. Heart attacks are generally triggered by the formation of a blood clot within a constricted coronary artery, obstructing blood flow and depriving a portion of the heart muscle of oxygen. The resulting impairment of the heart's pumping ability may cause permanent disability or death, either immediately or through the progressive development of medical complications ⁽²⁾.

Researchers have investigated several theories to explain how alcohol itself might lower risk for CHD. For example, alcohol may protect the heart by preventing the constriction of the coronary arteries, inhibiting clot formation, and enhancing recovery following a heart attack. Most of the evidence supporting these potential mechanisms is derived from experiments using animals or cells isolated from artery walls and grown in the laboratory. Controlled clinical experiments are needed to confirm that the effects observed in such studies can alter the development or progression of CHD in humans.

Results of laboratory research indicate that alcohol administration may help prevent arterial narrowing in mice ⁽³⁴⁾. Such an effect could stem from changes in the blood concentrations of certain fatty substances that influence the deposition of cholesterol within the coronary arteries ⁽³⁵⁾. However, human ⁽³⁶⁾ and animal ^(34,37) studies indicate that less than one-half of the lower risk for CHD associated with alcohol consumption can be explained by altered blood levels of these fatty substances. Therefore, researchers are investigating additional explanations for alcohol's apparent protective effects.

Alcohol may help prevent clot formation within already narrowed coronary arteries. Clotting occurs partly in response to chemicals released into the blood from the arterial wall. Exposure of these cells to alcohol in the laboratory suppresses the production of substances that promote clotting and stimulates the production and activity of substances that inhibit clotting ⁽³⁸⁾. In addition, analyses of blood samples drawn from human volunteers indicate that alcohol consumption increases blood levels of anticlotting factors ^(39,40) and decreases the "stickiness" of the specialized blood cells (i.e., platelets) that clump together to form clots ⁽⁴¹⁾.

Results of laboratory research suggest that alcohol might help protect against reperfusion injury, a form of damage caused by the sudden restoration of blood flow to heart muscle weakened by previous oxygen deprivation. Alcohol's effects on reperfusion injury have been studied in guinea pigs ⁽⁴²⁾ and rats ⁽⁴³⁾, but not in humans. Heavy alcohol consumption by humans can cause rapid and irregular heartbeat and can impair the heart's pumping ability ⁽⁴¹⁾, two of the major causes of death following a heart attack ⁽⁴⁴⁾. Alcohol may also interact harmfully with medications prescribed to treat heart diseases ⁽⁴⁵⁾. Thus, although alcohol may help protect against CHD, drinking may increase the risk of adverse health effects after a heart attack ⁽⁴⁶⁾.

Risks and Benefits

The apparent benefits of moderate drinking on CHD mortality are offset at higher drinking levels by increasing risk of death from other types of heart disease (5,16,32); cancer; liver cirrhosis; and trauma, including trauma from traffic crashes ⁽⁴⁷⁾. Moderate drinking is not risk free. The trade-offs between risks and benefits can be exemplified by the fact that alcohol's anticlotting ability, potentially protective against heart attack, may increase the risk of hemorrhagic stroke, or bleeding within the brain ⁽¹²⁾.

Conclusion

Research findings continue to confirm an association between moderate drinking and a lower risk for CHD. While there is an association between moderate drinking and lower CHD risk, science has not confirmed that alcohol itself causes the lower risk. It also is plausible that the lower risk might result from some as yet unidentified factor or surrogate associated both with alcohol use and lower CHD risk, such as lifestyle, diet and exercise, or additives to alcoholic beverages. Research is now in progress to answer these questions. The distinction between an association and a cause is important, particularly when considering what advice to give to the public. Further, even if we find that alcohol itself is responsible for the lower risk, still to be considered would be the trade-offs between the benefits and risks, particularly for specific subsets of the population. For example, moderate drinking by older persons may lower CHD but increase risk for other alcohol-related health conditions, such as adverse alcohol-drug interactions; trauma, including falls and automobile crashes; or hemorrhagic stroke.

Until these issues are clarified, we continue to believe that the most prudent advice is the following: ⁽¹⁾ Individuals who are not currently drinking should not be encouraged to drink solely for health reasons, because the basis for health improvements has not yet been established as deriving from alcohol itself; ⁽²⁾ individuals who choose to drink and are not otherwise at risk for alcohol-related problems3 should not exceed the one- to two-drink-per-day limit recommended by the U.S. Dietary Guidelines; and ⁽³⁾ individuals who currently are drinking beyond the U.S. Dietary Guidelines' recommended limits should be advised to lower their daily alcohol intake to these limits.

References

1. Hennekens, C.H. Alcohol and risk of coronary events. In: Zakhari, S., and Wassef, M., eds. Alcohol and the Cardiovascular System. NIAAA Research Monograph No. 31. NIH Pub. No. 96-4133. Washington, DC: U.S. Govt. Print. Off., 1996. pp. 15-24.

2. McKenzie, C.R., and Eisenberg, P.R. Alcohol, coagulation, and arterial thrombosis. In: Zakhari, S., and Wassef, M., eds. Alcohol and the Cardiovascular System. NIAAA Monograph No. 31. NIH Pub. No. 96- 4133. Washington, DC: U.S. Govt. Print. Off., 1996. pp. 413-439.

3. Renaud, S.; Criqui, M.H.; Farchi, G.; et al. Alcohol drinking and coronary heart disease. In: Verschuren, P.M., ed. Health Issues Related to Alcohol Consumption. Washington, DC: ILSI Press, 1993. pp. 81-123.

4. Klatsky, A.L. Epidemiology of coronary heart disease?Influence of alcohol. Alcohol Clin Exp Res 18(1):88-96, 1994.

5. Friedman, L.A., and Kimball, A.W. Coronary heart disease mortality and alcohol consumption in Framingham. Am J Epidemiol 124(3):481-489, 1986.

6. Boffetta, P., and Garfinkel, L. Alcohol drinking and mortality among men enrolled in an American Cancer Society prospective study. Epidemiol 1(5):342-348, 1990.

7. Thun, M.J.; Peto, R.; Lopez, A.D.; et al. Alcohol consumption and mortality among middle-aged and elderly U.S. adults. N Engl J Med 337(24):1705-1714, 1997.

8. Klatsky, A.L.; Armstrong, M.A.; and Friedman, G.D. Relations of alcoholic beverage use to subsequent coronary artery disease hospitalization. Am J Cardiol 58(9):710-714, 1986.

9. Klatsky, A.L.; Armstrong, M.A.; and Friedman, G.D. Red wine, white wine, liquor, beer, and risk for coronary artery disease hospitalization. Am J Cardiol 80(4):416-420, 1997.

10. Klatsky, A.L.; Armstrong, M.A.; and Friedman, G.D. Risk of cardiovascular mortality in alcohol drinkers, ex-drinkers and nondrinkers. Am J Cardiol 66(17):1237-1242, 1990.

11. Klatsky, A.L.; Armstrong, M.A.; and Friedman, G.D. Alcohol and mortality. Ann Intern Med 117(8):646- 654, 1992.

12. Stampfer, M.J.; Colditz, G.A.; Willett, W.C.; et al. A prospective study of moderate alcohol consumption and the risk of coronary disease and stroke in women. N Engl J Med 319(5):267-273, 1988.

13. Fuchs, C.S.; Stampfer, M.J.; Colditz, G.A.; et al. Alcohol consumption and mortality among women. N Engl J Med 332(19):1245-1250, 1995 [erratum N Engl J Med 336(7):523, 1997].

14. Rimm, E.B.; Giovannucci, E.L.; Willett, W.C.; et al. Prospective study of alcohol consumption and risk of coronary disease in men. Lancet 338(8765):464-468, 1991.

15. Camargo, C.A., Jr.; Stampfer, M.J.; Glynn, R.J.; et al. Moderate alcohol consumption and risk for angina pectoris or myocardial infarction in U.S. male physicians. Ann Intern Med 126(5):372-375, 1997.

16. Camargo, C.A., Jr.; Hennekens, C.H.; Gaziano, J.M.; et al. Prospective study of moderate alcohol consumption and mortality in US male physicians. Arch Intern Med 157(1):79-85, 1997.

17. Doll, R.; Peto, R.; Hall, E.; et al. Mortality in relation to consumption of alcohol: 13 years' observations on male British doctors. BMJ 309(6959):911-918, 1994.

18. Grønbæk, M.; Deis, A.; Sørensen, T.I.A.; et al. Mortality associated with moderate intakes of wine, beer, or spirits. BMJ 310(6988):1165-1169, 1995.

19. Yuan, J.-M.; Ross, R.K.; Gao, Y.-T.; et al. Follow up study of moderate alcohol intake and mortality among middle aged men in Shanghai, China. BMJ 314(7073):18-23, 1997.

20. Valmadrid, C.T.; Klein, R.; Moss, S.E.; et al. Alcohol intake and the risk of coronary heart disease mortality in persons with older-onset diabetes mellitus. JAMA 282(3):239-246, 1999.

21. Hart, C.L.; Smith, G.D.; Hole, D.J.; et al. Alcohol consumption and mortality from all causes, coronary heart disease, and stroke: Results from a prospective cohort study of Scottish men with 21 years of follow up. BMJ 318:1725-1729, 1999.

22. Fillmore, K.M.; Golding, J.M.; Graves, K.L.; et al. Alcohol consumption and mortality: I. Characteris tics of drinking groups. Addiction 93(2):183-203, 1998.

23. Berlin, J.A., and Colditz, G.A. A meta-analysis of physical activity in the prevention of coronary heart disease. Am J Epidemiol 132(4):612-628, 1990.

24. Barrett, D.H.; Anda, R.F.; Croft, J.B.; et al. The association between alcohol use and health behaviors related to the risk of cardiovascular disease: The South Carolina Cardiovascular Disease Prevention Project. J Stud Alcohol 56(1):9-15, 1995.

25. Huijbregts, P.; Feskens, E.; Räsänen, L.; et al. Dietary pattern and 20 year mortality in elderly men in Finland, Italy, and the Netherlands: Longitudinal cohort study. BMJ 315(7099):13-17, 1997.

26. Ascherio, A.; Rimm, E.B.; Giovannucci, E.L.; et al. Dietary fat and risk of coronary heart disease in men: Cohort follow up study in the United States. BMJ 313(7049):84-90, 1996.

27. Ashley, M.J. Alcohol consumption and ischemic heart disease: The epidemiologic evidence. In: Smart, R.G.; Cappell, H.D.; Glaser, F.B.; et al. Research Advances in Alcohol and Drug Problems. Vol. 8. New York: Plenum Press, 1984. pp. 99-147.

28. Ruf, J.-C.; Berger, J.-L.; and Renaud, S. Platelet rebound effect on alcohol withdrawal and wine drinking in rats: Relation to tannins and lipid peroxidation. Arteriosclerosis Thromb Vasc Bio 15(1):140-144, 1995.

29. Criqui, M.H., and Ringel, B.L. Does diet or alcohol explain the French paradox? Lancet 344(8939/ 8940):1719-1723, 1994.

30. Reinke, L.A., and McCay, P.B. Interaction between alcohol and antioxidants. In: Zakhari, S., and Wassef, M., eds. Alcohol and the Cardiovascular System. NIAAA Research Monograph No. 31. NIH Pub. No. 96-4133. Washington, DC: U.S. Govt. Print. Off., 1996. pp. 441-457.

31. Pellegrini, N.; Pareti, F.I.; Stabile, F.; et al. Effects of moderate consumption of red wine on platele aggregation and haemostatic variables in healthy volunteers. Eur J Clin Nutr 50(4):209-213, 1996.

32. Kannel, W.B., and Ellison, R.C. Alcohol and coronary heart disease: The evidence for a protective effect. Clinica Chimica Acta 246(1-2):59-76, 1996.

33. Tjønneland, A.; Grønbæk, M.; Stripp, C.; et al. Wine intake and diet in a random sample of 48763 Danish men and women. Am J Clin Nutr 69(1):49-54, 1999.

34. Emeson, E.E.; Manaves, V.; Singer, T.; et al. Chronic alcohol feeding inhibits atherogenesis in C57BL/6 hyperlipidemic mice. Amer J Pathol 147(6):1749-1758, 1995.

35. Dreon, D.M., and Krauss, R.M. Alcohol, lipids, and lipoproteins. In: Zakhari, S., and Wassef, M., eds. Alcohol and the Cardiovascular System. NIAAA Research Monograph No. 31. NIH Pub. No. 96-4133. Washington, DC: U.S. Govt. Print. Off., 1996. pp. 369-391.

36. Aikens, M.L.; Grenett, H.E.; Benza, R.L.; et al. Alcohol-induced upregulation of plasminogen activators and fibrinolytic activity in cultured human endothelial cells. Alcohol Clin Exp Res 22(2):375-381, 1998.

37. Dai, J.; Miller, B.A.; and Lin, R.C. Alcohol feeding impedes early arteriosclerosis in low-density lipo protein receptor knockout mice: Factors in addition to high-density lipoprotein-apolipoprotein A1 are involved. Alcohol Clin Exp Res 21(1):11-18, 1997.

38. Booyse, F.M.; Aikens, M.L.; and Grenett, H.E. Endothelial cell fibrinolysis: Transcriptional regulation of fibrinolytic protein gene expression (t-PA, u-PA, and PAI-1) by low alcohol. Alcohol Clin Exp Res 23(6):1119-1124, 1999.

39. Ridker, P.M.; Vaughan, D.E.; Stampfer, M.J.; et al. Association of moderate alcohol consumption and plasma concentration of endogenous tissue-type plasminogen activator. JAMA 272(12):929-933, 1994.

40. Hendriks, H.F.J.; Veenstra, J.; Wierik, E.J.M.V.; et al. Effect of moderate dose of alcohol with evening meal on fibrinolytic factors. BMJ 308(6935):1003-1006, 1994.

41. Rubin, R. Effect of ethanol on platelet function. Alcohol Clin Exp Res 23(6):1114-1118, 1999.

42. Miyamae, M.; Diamond, I.; Weiner, M.W.; et al. Regular alcohol consumption mimics cardiac precondi- tioning by protecting against ischemia-reperfusion injury. Proc Nat Acad Sci 94(7):3235-3239, 1997.

43. McDonough, K.H. Chronic alcohol consumption causes accelerated myocardial preconditioning to ischemia-reperfusion injury. Alcohol Clin Exp Res 21(5):869-873, 1997.

44. Guyton, A.C. Human Physiology and Mechanisms of Disease. 5th ed. Philadelphia: Saunders, 1992.

45. Thomas, B.A., and Regan, T.J. Interactions between alcohol and cardiovascular medications. Alcohol Health Res World 14(4):333-339, 1990.

46. Wannamethee, G.; Whincup, P.H.; Shaper, A.G.; et al. Factors determining case fatality in myocardial infarction: "Who dies in a heart attack?" BMJ 74:324-331, 1995.

47. NIAAA. Ninth Special Report to the U.S. Congress on Alcohol and Health. NIH Pub. No. 97-4017. Bethesda, MD: the Institute, 1997.

Source: National Institute on Alcohol Abuse. (July 1999)                                                                National Institutes of Health

v Alcohol and the Liver

Alcoholic liver disease is one of the most serious medical consequences of chronic alcohol use. Moreover, chronic excessive alcohol use is the single most important cause of illness and death from liver disease (alcoholic hepatitis and cirrhosis) in the United States ⁽¹⁾.

The Normal Liver

Normal liver function is essential to life. The liver is the largest organ of the body, located in the upper right section of the abdomen. It filters circulating blood, removing and destroying toxic substances; it secretes bile into the small intestine to help digest and absorb fats; and it is involved in many of the metabolic systems of the body. Digested food substances are carried from the intestine directly to the liver for further processing. The liver stores vitamins; synthesizes cholesterol; metabolizes or stores sugars; processes fats; and assembles amino acids into various proteins, some for use within the liver and some for export. The liver controls blood fluidity and regulates blood-clotting mechanisms. It also converts the products of protein metabolism into urea for excretion by the kidneys.

Alcoholic Liver Disease

The three alcohol-induced liver conditions are fatty liver, alcoholic hepatitis, and cirrhosis.

Some degree of fat deposition usually occurs in the liver after short-term excessive use of alcohol. However, fatty liver rarely causes illness ⁽²⁾.

In some heavy drinkers, alcohol consumption leads to severe alcoholic hepatitis, an inflammation of the liver characterized by fever, jaundice, and abdominal pain ⁽³⁾. Severe alcoholic hepatitis can be confused with many serious abdominal conditions, such as cholecystitis (inflammation of the gall bladder), appendicitis, and pancreatitis. It is important to be aware of this potential confusion because some of these other conditions require surgery, and surgery is contraindicated in patients with alcoholic hepatitis. These patients have a high death rate following surgery.

The most advanced form of alcoholic liver injury is alcoholic cirrhosis. This condition is marked by progressive development of scar tissue that chokes off blood vessels and distorts the normal architecture of the liver ⁽²⁾.

A patient may have only one of the three alcohol-induced conditions or any combination of them. Traditionally, they have been considered sequentially related, progressing from fatty liver to alcoholic hepatitis to cirrhosis. However, some studies have demonstrated that alcoholics may progress to cirrhosis without passing through any visible stage resembling hepatitis. Thus, alcoholic cirrhosis can appear insidiously, with little warning ⁽⁴⁾.

Fatty liver is reversible with abstinence. Alcoholic hepatitis may be fatal but can be reversible with abstinence ⁽⁵⁾. While alcoholic cirrhosis is often progressive and fatal, it can stabilize with abstinence ⁽³⁾.

Complications of advanced liver disease include severe bleeding from distended veins in the esophagus, brain disorders (hepatic encephalopathy), accumulation of fluid in the abdomen (ascites), and kidney failure ⁽⁶⁾.

Not all liver disease that may occur in alcoholics is caused by alcohol. In addition, when alcohol-induced liver disease does occur, it may be accompanied by other conditions, not related to alcohol, that also can cause liver failure. These include nonalcoholic hepatitis and exposure to drugs and occupational chemicals (see below).

Extent of the Problem

Alcohol-related cirrhosis is know n to be underreported. However, about 44 percent of all deaths caused by cirrhosis in North America are reportedly alcohol related ⁽⁷⁾.

Up to 100 percent of heavy drinkers show evidence of fatty liver, an estimated 10 to 35 percent develop alcoholic hepatitis, and 10 to 20 percent develop cirrhosis ⁽¹⁾.

Daily drinkers are at a higher risk of developing alcoholic cirrhosis than are binge drinkers ⁽⁸⁾. In general, patients with alcoholic cirrhosis have been drinking heavily for 10 to 20 years (8-10).

Mortality from cirrhosis in the United States varies significantly with gender, race, and age. In 1988, the highest mortality from cirrhosis occurred in nonwhite males, followed by white males, nonwhite females, and white females ⁽¹¹⁾. Most of the deaths from alcoholic cirrhosis occur in people ages 40-65 ⁽¹¹⁾. Thus, alcoholic cirrhosis kills people in what should be their most productive years.

How Does Alcohol Damage the Liver?

Normal liver function is essential to life. Alcohol-induced liver damage disrupts the body's metabolism, eventually impairing the function of other organs. Multiple physiological mechanisms, discussed in the following sections, interact to influence the progression of ALD. Medications that affect these mechanisms may help prevent some of the medical complications of ALD or reduce the severity of the illness.

Alcohol Metabolism. Most of the alcohol a person drinks is eventually broken down by the liver. However, some products generated during alcohol metabolism (e.g., acetaldehyde) are more toxic than alcohol itself. In addition, a group of metabolic products called free radicals can damage liver cells and promote inflammation, impairing vital functions such as energy production. The body's natural defenses against free radicals (e.g., antioxidants) can be inhibited by alcohol consumption, leading to increased liver damage ⁽³⁾.

The Inflammatory Response. Inflammation is the body's response to local tissue damage or infection. Inflammation prevents the spread of injury and mobilizes the defense mechanisms of the immune system. One such defense mechanism is the generation of free radicals that can destroy disease-causing microorganisms. Long-term alcohol consumption prolongs the inflammatory process, leading to excessive production of free radicals, which can destroy healthy liver tissue.

Bacteria that live in the human intestine play a key role in the initiation of ALD. Alcohol consumption increases the passage of a noxious bacterial product called endotoxin through the intestinal wall into the bloodstream. Upon reaching the liver, endotoxin activates specialized cells (i.e., Kupffer cells) that monitor the blood for signs of infection. These cells respond to the presence of endotoxin by releasing substances called cytokines that regulate the inflammatory process (4-6).

Cytokines. Cytokines are produced by cells of the liver and immune system in response to infection or cell damage. Alcohol consumption increases cytokine levels, and cytokines in humans produce symptoms similar to those of alcoholic hepatitis ⁽⁷⁾. Recent studies implicate cytokines in scar formation and in the depletion of oxygen within liver cells, processes that are associated with cirrhosis ⁽⁷⁾. Each of the disease mechanisms described above contributes to the death of liver cells. The presence of damaged cells triggers the body's defensive responses, including the release of additional cytokines, resulting in a vicious cycle of inflammation, cell death, and scarring.

Scar Formation. Normal scar formation is part of the wound-healing process. Alcohol-induced cell death and inflammation can result in scarring that distorts the liver's internal structure and impairs its function. This scarring is the hallmark of cirrhosis. The process by which cirrhosis develops involves the interaction of certain cytokines and specialized liver cells (i.e., stellate cells). In the normal liver, stellate cells function as storage depots for vitamin A. Upon activation by cytokines, stellate cells proliferate, lose their vitamin A stores, and begin to produce scar tissue. In addition, activated stellate cells constrict blood vessels, impeding the delivery of oxygen to liver cells (6,8).

Acetaldehyde may activate stellate cells directly, promoting liver scarring in the absence of inflammation (9,10). This finding is consistent with the observation that heavy drinkers can develop cirrhosis insidiously, without preexisting hepatitis.

Factors That Influence Vulnerability to ALD

Susceptibility to ALD differs considerably among individuals, so that even among people drinking similar amounts of alcohol, only some develop cirrhosis. Understanding the mechanisms of these differences may help clinicians identify and treat patients at increased risk for advanced liver damage.

Genetic Factors. Structural or functional variability in any of the cell types and biochemical substances discussed above could influence a person's susceptibility to ALD. Researchers are seeking genetic factors that may underlie this variability. Results of this research may provide the basis for future gene-based therapies.

Dietary Factors. Nutritional factors influence the progression of ALD ⁽¹¹⁾. For example, a high-fat, low-carbohydrate diet promotes liver damage in alcohol-fed rats ^(12,13), and high amounts of polyunsaturated fats may promote the development of cirrhosis in animals ^(14,15).

Gender. Women develop ALD after consuming lower levels of alcohol over a shorter period of time compared with men ⁽¹⁶⁾. In addition, women have a higher incidence of alcoholic hepatitis and a higher mortality rate from cirrhosis than men ⁽¹⁷⁾. The mechanisms that underlie gender-related differences are unknown.

Hepatitis C . Many patients with ALD are infected with hepatitis C virus (HCV), which causes a chronic, potentially fatal liver disease ^(18,19). The presence of HCV may increase a person's susceptibility to ALD and influence the severity of alcoholic cirrhosis. For example, alcohol-dependent patients infected with HCV develop liver injury at a younger age and after consuming a lower cumulative dose of alcohol than do those without HCV ⁽²⁰⁾. Patients with HCV are often treated with an antiviral substance called interferon. However, interferon is less effective in patients with chronic HCV who are heavy drinkers, compared with those who are not ⁽²¹⁾.

Treatment Effectiveness

Abstinence is the cornerstone of ALD therapy. With abstinence, fatty liver and alcoholic hepatitis are frequently reversible, and survival is improved among patients with ALD, including those with cirrhosis ⁽¹⁾. For terminally ill patients, liver transplantation remains the only effective treatment. Research has established the effectiveness of liver transplantation in patients with alcoholic cirrhosis ⁽¹⁾. More recently, Belle and colleagues ⁽²²⁾ summarized followup medical data on all persons who received liver transplants in the United States between 1988 and 1995. Deaths among these subjects were not alcohol related. That is, alcohol-dependent patients died from the same conditions that caused deaths among patients without alcoholism (e.g., infection, cancer, or heart disease). Recurrences of liver disease among alcohol-dependent patients are rare ⁽²³⁾.

Hepatitis C infection in patients with ALD does not appear to affect survival after liver transplantation, despite the continued presence of the virus in the bloodstream ⁽²⁴⁾.

Medication Interactions. Chronic alcohol consumption may increase the adverse side effects of medications used to treat conditions other than ALD. In particular, excessive use of the widely used pain killer acetaminophen has been associated with liver damage in people drinking heavily ⁽²⁵⁾.

Prospects for Future Treatment

The multiple mechanisms of ALD development provide several potential targets for medical intervention. Some promising lines of inquiry are summarized below.

The role of endotoxin in the inflammatory response suggests the possibility of inhibiting ALD development at its earliest stages. For example, suppression of endotoxin-producing intestinal bacteria reduced signs of liver damage in alcohol-fed rats (4,26).

An adequate daily supply of total carbohydrates is important in treating ALD ^(13,27). In addition, researchers are investigating certain nutritional supplements for patients with ALD. One such supplement is polyunsaturated lecithin (PUL), a mixture of fatty substances extracted from soybeans. PUL protected against liver scarring in alcohol-fed baboons (9,28). Another dietary factor, S-adenosyl-l-methionine (SAM), can reduce liver cell damage in animals that is induced by alcohol or other toxic substances ⁽²⁹⁾. The safety and effectiveness of these supplements for treating human ALD are under investigation.

Finally, an important goal of ALD research is to develop medications that can moderate the toxic effects of inflammatory cytokines while sparing their essential defensive functions. In one study, administration of antibodies designed to recognize and inactivate key inflammatory cytokines markedly decreased liver injury in rats ⁽³⁰⁾.

Conclusion

Abstinence from alcohol is the single most important component of treatmen t for alcoholic liver disease. Continued drinking will worsen the condition of patients with this disease and greatly increase their risk for death. Physicians who treat alcoholic liver disease, no matter how competently, and who do not address their patients' drinking are practicing bad medicine, akin to treating an iron-deficiency anemia and disregarding the colon cancer that is causing it.

Because many alcohol abusers and most alcoholics require some form of treatment to remain abstinent, simply giving advice to "quit" drinking often is not sufficient. Physicians who choose not to manage their patients' alcohol problems may refer these patients to specialized alcohol treatment providers for evaluation and appropriate treatment. In referring a patient to appropriate alcohol treatment, physicians should keep informed of their patients' progress, as relapse may further complicate management of the alcoholic liver disease.

References

1. Grant, B.F.; Dufour, M.C.; & Harford, T.C. Epidemiology of alcoholic liver disease. Seminars in Liver Disease 8(1):12-25, 1988.

2. Rothschild M.A.; Oratz, M.; & Schreiber, S.S. Alcohol-induced liver disease: Does nutrition play a role? Alcohol Health & Research World 13(3):229-231, 1989.

3. Crabb. D.W., & Lumeng, L. Alcoholic liver diseases. In: Kelley, W.N. Textbook of Internal Medicine. Philadelphia: Lippincott, 1989. pp. 592-602.

4. Maddrey, W.C. Alcoholic hepatitis: Clinicopathologic features and therapy. Seminars in Liver Disease 8(1):91-102, 1988.

5. Galambos, J.T. Natural history of alcoholic hepatitis. III. Histological changes. Gastroenterology 63(6):1026- 1035, 1972. (6)Rubin, M. How alcohol damages the body. Alcohol Health & Research World 13(4):322- 327, 1989.

6. Smart, R.G., & Mann, R.E. Alcohol and the epidemiology of liver cirrhosis. Alcohol Health & Research World 16(3):217-222, 1991.

7. Parrish, K.M.; Higuchi, S.; & Dufour, M.C. Alcohol consumption and the risk of developing liver cirrho sis: Implications for future research. Journal of Substance Abuse 3(3):325-335, 1991.

8. Lelbach, W.K. Epidemiology of alcoholic liver disease. Progress in Liver Disease 5:494-513, 1976.

9. Pequignot, G.; Tuyns, A.J.; & Berta, J.L. Ascitic cirrhosis in relation to alcohol consumption. Interna tional Journal of Epidemiology 7(2):113-120, 1978.

10. Grant, B.F.; DeBakey, S.; & Zobeck, T.S. Surveillance Report No. 18. Liver Cirrhosis Mortality in the United States, 1973-1988. Rockville, MD: National Institute on Alcohol Abuse and Alcoholism, Division of Biometry and Epidemiology, 1991.

11. Lieber, C.S. Alcohol and nutrition: An overview. Alcohol Health & Research World 13(3):197-205, 1989.

12. Annoni, G.; Weiner, F.R.; Colombo, M.; Czaja, M.J.; & Zern, M.A. Albumin and collagen gene regulation in alcohol- and virus-induced human liver disease. Gastroenterology 98(1):197-202, 1990.

13. Lieber, C.S.; Casini, A.; DeCarli, L.M.; Kim, C.; Lowe, N.; Sasaki, R.; & Leo, M.A. S-adenosyl-L- methionine attenuates alcohol-induced liver injury in the baboon. Hepatology 11(2):165-172, 1990.

14. Kawase, T.; Kato, S.; & Lieber, C.S. Lipid peroxidation and antioxidant defense systems in rat liver after chronic ethanol feeding. Hepatology 10(5):815-821, 1989.

15. French, S.W. The mechanism of organ injury in alcoholics: Implications for therapy. In: Kalant, H.; Khanna, J.M.; and Israel, Y., eds. Advances in Biomedical Alcohol Research. Oxford: Pergamon Press, 1991. pp. 57-63.

16. Lieber, C.S. Hepatic, metabolic and toxic effects of ethanol: 1991 update. Alcoholism: Clinical and Experimental Research 15(4):573-592, 1991.

17. Tuma, D.J.; Casey, C.A.; & Sorrell, M.F. Effects of ethanol on hepatic protein trafficking: Impairment of receptor-mediated endocytosis. Alcohol and Alcoholism 25(2-3):117-125, 1990.

18. Lumeng, L. Genetic aspects and risk factors in alcoholism and alcoholic liver disease. In: American Association for the Study of Liver Diseases. Postgraduate Course: Newer Aspects on Alcohol, Nutrition and Hepatic Encephalopathy. Thorofare, NJ: the Association, 1992. pp. 6-34.

19. Mendenhall, C.L.; Seeff, L.; Diehl, A.M.; Ghosn, S.J.; French, S.W.; Gartside, P.S.; Rouster, S.D.; Buskell- Bales, Z.; Grossman, C.J.; Roselle, G.A.; Weesner, R.E.; Garcia-Pont, P.; Goldberg, S.J.; Kiernan, T.W.; Tamburro, C.H.; Zetterman, R.; Chedid, A.; Chen, T.; Rabin, L.; & the VA Cooperative Study Group. Antibodies to hepatitis B virus and hepatitis C virus in alcoholic hepatitis and cirrhosis: Their preva lence and clinical relevance. Hepatology 14(4, pt. 1):581-589, 1991.

20. Schiff, E.R. Non-alcoholic liver disease in the alcoholic. In: American Association for the Study of Liver Diseases. Postgraduate Course: Newer Aspects on Alcohol, Nutrition and Hepatic Encephalopathy. Thorofare, NJ: the Association, 1992. pp. 349-360.

21. Nishiguchi, S.; Kuroki, T.; Yabusako, T.; Seki, S.; Kobayashi, K.; Monna, T.; Otani, S.; Sakurai, M.; Shikata, T.; & Yamamoto, S. Detection of hepatitis C virus antibodies and hepatitis C virus RNA in patients with alcoholic liver disease. Hepatology 14(6):985-989, 1991.

22. Fleisher, J.H.; Lung, C.C.; Meinke, G.C.; & Pinnas, J.L. Acetaldehyde-albumin adduct formation: Possible relevance to an immunologic mechanism in alcoholism. Alcohol and Alcoholism 23(2):133-141, 1988.

23. Zetterman, R.K., & Sorrell, M.F. Immunologic aspects of alcoholic liver disease. Gastroenterology 81:616- 624, 1981.

24. Israel, Y.; Orrego, H.; & Niemelä, O. Immune responses to alcohol metabolites: Pathogenic and diagnostic implications. Seminars in Liver Disease 8(1):81-90, 1988.

25. Maddrey, W.C. Alcoholic hepatitis: Pathogenesis and approaches to treatment. Scandinavian Journal of Gastroenterology 25(Suppl. 175):118-130, 1990.

26. Paronetto, F. Immunologic reactions in alcoholic liver disease. Seminars in Liver Disease, in press.

27. Israel, Y.; Videla, L.; & Bernstein, J. Liver hypermetabolic state after chronic ethanol consumption. Federation Proceedings 34:2052-2059, 1975.

28. Lieber, C.S. Interaction of alcohol with other drugs and nutrients: Implication for the therapy of alcoholic liver disease. Drugs 40(Suppl. 3):23-44, 1990.

29. Lieber, C.S. Interaction of ethanol with drugs, hepatotoxic agents, carcinogens and vitamins. Alcohol and Alcoholism 25(2/3):157-176, 1990.

30. Seeff, L.B.; Cuccherini, B.A.; Zimmerman, H.J.; Adler, E.; & Benjamin, S.B. Acetaminophen hepatotoxic ity in alcoholics: A therapeutic misadventure. Annals of Internal Medicine 104(3):399-404, 1986.

31. Maddrey, W.C. Hepatic effects of acetaminophen: Enhanced effects in alcoholics. Journal of Clinical Gastrology 9:180-185, 1987.

32. Leo, M.A., & Lieber, C.S. Alcohol and vitamin A. Alcohol Health & Research World 13(3):250-254, 1989.

33. Helman, R.A.; Temko, M.H.; & Nye, S.W. Alcoholic hepatitis: Natural history and evaluation of prednisolone therapy. Annals of Internal Medicine 74:311-321, 1971.

34. Maddrey, W.C.; Boitnott, J.K.; Bedine, M.S.; Weber, F.W.; Mezey, E.; & White, R.L. Corticosteroid therapy of alcoholic hepatitis. Gastroenterology 75(2):193-199, 1978.

35. Mendenhall, C.L.; Anderson, S.; Garcia-Pont, P.; Goldberg, S.; Kiernan, T.; Seeff, L.B.; Sorrell, M.; Tamburro, C.; Weesner, R.; Zetterman, R.; Chedid, A.; Chen, T.; Rabin, L.; & the Veterans Administration Cooperative Study on Alcoholic Hepatitis. Short-term and long-term survival in patients with alcoholic hepatitis treated with oxandrolone and prednisolone. New England Journal of Medicine 311(23):1464- 1470, 1984 .

36. Carithers, R.L.; Herlong, H.; & Diehl, A.M. Methyl prednisolone therapy in patients with severe alco holic hepatitis: A randomized multi-center trial. Annals of Internal Medicine 110:685-690, 1989.

37. Maddrey, W.C. Alcoholic hepatitis: Approaches to therapy. In: American Association for the Study of Liver Diseases. Postgraduate Course: Newer Aspects on Alcohol, Nutrition and Hepatic Encephalopa thy. Thorofare, NJ: the Association, 1992. pp. 160-174.

38. Mezey, E.; Caballería, J.; Mitchell, M.C.; Parés, A.; Franklin Herlong, H.; & Rodés, J. Effect of parenteral amino acid supplementation on short-term and long-term outcomes in severe alcoholic hepatitis: A randomized controlled trial. Hepatology 14(6):1090-1096, 1991.

39. Orrego, H.; Blake, J.E.; Blendis, L.M.; Compton, K.V.; & Israel, Y. Long-term treatment of alcoholic liver disease with propylthiouracil. New England Journal of Medicine 317(23):1421-1427, 1987.

40. Hallé, P.; Paré, P.; Kaptein, E.; Kanel, G.; Redeker, A.G.; & Reynolds, T.B. Double-blind, controlled trial of propylthiouracil in patients with severe acute alcoholic hepatitis. Gastroenterology 82(5, pt. 1):925-931, 1982.

41. Kaplowitz, N. Propylthiouracil treatment for alcoholic hepatitis: Should it and does it work? Gastroenter ology 82(6):1468-1471, 1982.

42. Alexander, J.F.; Lischuer, M.W.; & Galambos, J.T. Natural history of alcoholic hepatitis. II. The long-term prognosis. American Journal of Gastroenterology 56:515-525, 1971.

43. Van Thiel, D.H.; Carr, B.; Iwatsuki, S.; Tzakis, A.; Fung, J.J.; & Starzl, T.E. Liver transplantation for alcoholic liver disease, viral hepatitis, and hepatic neoplasms. Transplantation Proceedings 23(3):1917- 1921, 1991.

44. Lieber, C.S.; DeCarli, L.M.; Mak, K.M.; Kim, C.; & Leo, M.A. Attenuation of alcohol-induced hepatic fibrosis by polyunsaturated lecithin. Hepatology 12(6):1390-1398, 1990.

Source: National Institute on Alcohol Abuse (July 1999)        National Institutes of Health

v Alcohol and Cancer

Cancer kills an estimated 526,000 Americans yearly, second only to heart disease ⁽¹⁾. Cancers of the lung, large bowel, and breast are the most common in the United States. Considerable evidence suggests a connection between heavy alcohol consumption and increased risk for cancer, with an estimated 2 to 4 percent of all cancer cases thought to be caused either directly or indirectly by alcohol ⁽²⁾.

A strong association exists between alcohol use and cancers of the esophagus, pharynx, and mouth, whereas a more controversial association links alcohol with liver, breast, and colorectal cancers. Together, these cancers kill more than 125,000 people annually in the United States ⁽¹⁾. The following sections discuss alcohol's role in these cancers.

What Is Cancer?

Cancer is a group of diseases characterized by cells that grow out of control; in many cases, they form masses of cells, or tumors, that infiltrate, crowd out, and destroy normal tissue. Although the body strictly regulates normal cells to grow within the confines of tissues, cancer cells reproduce independently, uninhibited by tissue boundaries. Cancer develops in three stages: initiation, promotion, and progression. Cancer-causing agents, known as carcinogens, can contribute to the first two stages.

Cancer initiation occurs when a cell's DNA (the substance that genes are made of) is irreversibly changed so that, once triggered to divide, the cell will reproduce indefinitely. The "change" involves mutations to the cell's genes that can occur spontaneously or can be induced by a carcinogen. In some cancers, it has been shown that the mutations occur in oncogenes, genes that normally promote cell division, or in suppressor genes, genes that normally suppress cell division. Thus, it is believed that cancer-causing mutations result in overpromotion or undersuppression of cell reproduction. During cancer promotion, the initiated cell is stimulated to divide. The stimulus can be natural, as when tissue damage requires proliferation of new cells, or it can be caused by a carcinogen. During cancer progression, tumors produced by the replicating mass of cells metastasize, or spread, from the initial or primary tumor to other parts of the body, forming secondary
cancers.

Alcohol's Link to Cancer

Two types of research link alcohol and cancer. Epidemiologic research has shown a dose-dependent association between alcohol consumption and certain types of cancer; as alcohol consumption increases, so does risk of developing certain cancers. More tenuous results have come from research into the mechanism by which alcohol could contribute to cancer development.

Epidemiologic Research

The strongest link between alcohol and cancer involves cancers of the upper digestive tract, including the esophagus, the mouth, the pharynx, and the larynx ⁽³⁾. Less consistent data link alcohol consumption and cancers of the liver, breast, and colon ⁽³⁾.

Upper digestive tract. Chronic heavy drinkers have a higher incidence of esophageal cancer than does the general population. The risk appears to increase as alcohol consumption increases (4-6). An estimated 75 percent of esophageal cancers in the United States are attributable to chronic, excessive alcohol consumption ⁽⁷⁾.

Nearly 50 percent of cancers of the mouth, pharynx, and larynx are associated with heavy drinking ⁽⁷⁾. People who drink large quantities of alcohol over time have an increased risk of these cancers as compared with abstainers (8,9). If they drink and smoke , the increase in risk is even more dramatic (5,6).

Liver. Prolonged, heavy drinking has been associated in many cases with primary liver cancer. However, it is liver cirrhosis, whether caused by alcohol or another factor, that is thought to induce the cancer ^(10,11). In areas of Africa and Asia, liver cancer afflicts 50 or more people per 100,000 per year, usually associated with cirrhosis caused by hepatitis viruses. In the United States, liver cancer is relatively uncommon, afflicting approximately 2 people per 100,000, but excessive alcohol consumption is linked to as many as 36 percent of these cases by some investigators (2,12).

The association between alcohol use and liver cancer is difficult to interpret, because liver cirrhosis and hepatitis B and C virus infections often confound data ⁽¹³⁾. Studies of the interactions between alcohol, hepatitis viruses, and cirrhosis will help clarify these associations with liver cancer (see below).

Breast. Chronic alcohol consumption has been associated with a small (averaging 10 percent) increase in a woman's risk of breast cancer (14-17). According to these studies, the risk appears to increase as the quantity and duration of alcohol consumption increases. Other studies, however, have found no evidence of such a link (18-20).

The inconsistency and weakness of epidemiologic findings suggest that a third confounding factor, such as nutrition, may be responsible for the link between alcohol and breast cancer ⁽¹⁵⁾. However, studies that adjusted for dietary factors such as fat intake found that the association between alcohol and breast cancer remained (14,21,22).

Recent studies suggest that alcohol may play an indirect role in the development of breast cancer. These studies indicate that alcohol increases estrogen levels in premenopausal women, which, in turn, may promote breast cancer ⁽²³⁾.

Colon. Epidemiologic studies have found a small but consistent dose-dependent association between alcohol consumption and colorectal cancer ^(15,24), even when controlling for fiber and other dietary factors (15,25,26). Despite the large number of studies, however, causality cannot be determined from the available data.

Other cancers. A few studies have linked chronic heavy drinking with cancers of the stomach, pancreas, and lungs ⁽³⁾. However, the association is consistently weak and the majority of studies have found no association ⁽³⁾.

Mechanisms of Alcohol-Related Cancers

The epidemiologic data provide little insight into whether or how alcohol increases the risk for various cancers. For some cancers, such as mouth and esophageal, alcohol is thought to play a direct causal role. For others, such as liver and breast cancers, alcohol is thought to play an indirect role by enhancing mechanisms that may cause cancer. Studies looking at these direct and indirect mechanisms may shed light on alcohol's role in developing cancers.

Oncogenes. Preliminary studies show that alcohol may affect cancer development at the genetic level by affecting oncogenes at the initiation and promotion stages of cancer. It has been suggested that acetaldehyde, a product of alcohol metabolism, impairs a cell's natural ability to repair its DNA, resulting in a greater likelihood that mutations causing cancer initiation will occur ⁽²⁷⁾. It has recently been suggested that alcohol exposure may result in overexpression of certain oncogenes in human cells and, thereby, trigger cancer promotion ⁽²⁸⁾.

Alcohol as a cocarcinogen. Although there is no evidence that alcohol itself is a carcinogen, alcohol may act as a cocarcinogen by enhancing the carcinogenic effects of other chemicals. For example, studies indicate that alcohol enhances tobacco's ability to stimulate tumor formation in rats ⁽²⁹⁾. In humans, the risk for mouth, tracheal, and esophageal cancer is 35 times greater for people who both smoke and drink than for people who neither smoke nor drink ⁽³⁰⁾, implying cocarcinogenic interaction between alcohol and tobacco-related carcinogens ⁽²⁹⁾.

Alcohol's cocarcinogenic effect may be explained by its interaction with certain enzymes. Some enzymes that normally help to detoxify substances that enter the body can also increase the toxicity of some carcinogens. One of these enzymes is called cytochrome P-450 ^(31,32). Dietary alcohol is able to induce cytochrome P-450 in the liver, lungs, esophagus, and intestines ^(29,33), where alcohol-associated cancers occur. Subsequently, carcinogens such as those from tobacco and diet can become more potent as they, too, pass through the esophagus, lungs, intestines, and liver and encounter the activated enzyme ^(29,33).

Nutrition. Chronic alcohol abuse may result in abnormalities in the way the body processes nutrients and may subsequently promote certain types of cancer. Reduced levels of iron, zinc, vitamin E, and some of the B vitamins, common in heavy drinkers, have been experimentally associated with some cancers ⁽²⁹⁾. Also, levels of vitamin A, hypothesized to have anticancer properties ⁽³⁴⁾, are severely depressed in the liver and esophagus of rats during chronic alcohol consumption (35-37).

A recent study indicates that as few as two drinks per day negates any beneficial effects of a

"correct" diet on decreasing risk of colon cancer ⁽³⁸⁾. Although the study suggests that a diet high in folic acid, a B vitamin found in fresh fruits and vegetables, decreases the risk for colon cancer, it also warns that alcohol consumption may counter this protective action and increase the risk for colon cancer by reducing folic acid levels.

Mechanisms of liver cancer. The possible role of alcohol in the development of liver cancer is incompletely understood. In Asia and Africa, hepatitis B virus infection is thought to cause most liver cancer; the association is less frequent in the United States. Eighty percent of patients with liver cancer also have cirrhosis ⁽³⁹⁾, and between 27 and 80 percent test positive for hepatitis B or C infection ⁽⁴⁰⁾. The chronic heavy drinking that causes liver cirrhosis might exacerbate cirrhosis caused independently by the hepatitis B or C viruses. Some studies indicate that alcohol consumption hastens the development of liver cancer in patients with hepatitis C infection ⁽⁴¹⁾, whereas others indicate that alcohol has no compounding effect in such patients ⁽⁴²⁾.

Suppression of immune response. Alcoholism has been associated with suppression of the human immune system. Immune suppression makes chronic alcohol abusers more susceptible to various infectious diseases and, theoretically, to cancer ⁽⁴³⁾.

Summary

Although epidemiologic studies have found a clear association between alcohol consumption and development of certain types of cancer, study findings are often inconsistent and may vary by country and by type of cancer. The key to understanding the association lies in research designed to decipher how alcohol may promote cancer. Such studies examine alcohol's metabolic effects at the cellular and genetic levels. Research examining the ways in which alcohol may induce cancers has found some potential mechanisms, the most promising of which implicates oncogenes.

Conclusion

As can be seen from this Alcohol Alert, the evidence for alcohol's role in promoting some cancers (e.g., cancers of the mouth and throat) is stronger than the evidence linking alcohol use to other cancers, such as breast cancer. Public health policy should reflect the strength of the evidence of alcohol's role in promoting various cancers. Convincing evidence of alcohol's effects on common cancers—even when these effects are minor—has important public health implications. However, it is equally important that the public not be subjected to undue alarm when evidence for an increased risk for cancer due to alcohol use is weak or inconclusive.

References

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18. Chu, S.Y.; Lee, N.C.; Wingo, P.A.; and Webster, L.A. Alcohol consumption and the risk of breast cancer. American Journal of Epidemiology 130(5):867-877, 1989.
19. Schatzkin, A.; Piantadosi, S.; Miccozzi, M.; and Bartee, D. Alcohol consumption and breast cancer: A cross-national correlation study. International Journal of Epidemiology 18(1):28-31, 1989.
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22. Schatzkin, A.; Jones, D.Y.; Hoover, R.N.; Taylor, P.R.; Brinton, L.A.; Ziegler, R.G.; Harvey, E.B.; Carter, C.L.; Licitra, L.M.; Dufour, M.C.; and Larson, D.B. Alcohol consumption and breast cancer in the Epidemiologic Follow-up Study of the First National Health and Nutrition Examination Survey. New England Journal of Medicine 316(19):1169-1173, 1987.
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24. Longnecker, M.P.; Orza, M.J.; Adams, M.E.; Vioque, J.; and Chalmers, T.C. A meta-analysis of alcoholic beverage consumption in relation to risk of colorectal cancer. Cancer Causes and Control 1(1):59-68, 1990.
25. Kune, S.; Kune, G.A.; and Watson, L.F. Case-control study of alcoholic beverages as etiological factors: The Melbourne Colorectal Cancer Study. Nutrition and Cancer 9(1):43-56, 1987.
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28. Kharbanda, S.; Nakamura, T.; and Kufe, D. Induction of the c-jun proto-oncogene by a protein kinase C- dependent mechanism during exposure of human epidermal keratinocytes to ethanol. Biochemical Pharmacology 45(3):675-681, 1993.
29. Garro, A.J., and Lieber, C.S. Alcohol and cancer. Annual Review of Pharmacology and Toxicology 30:219-249, 1990.
30. Blot, W.J.; McLaughlin, J.K.; Winn, D.M.; Austin, D.F.; Greenberg, R.S.; Preston-Martin, S.; Bernstein, L.; Schoenberg, J.B.; Stemhagen, A.; and Fraumeni, J.F. Smoking and drinking in relation to oral and pharyngeal cancer. Cancer Research 48(11):3282-3287, 1988.
31. Seitz, H.K., and Osswald, B. Effect of ethanol on procarcinogen activation. In: Watson, R.R., ed. Alcohol and Cancer. Boca Raton, FL: CRC Press, 1992. pp. 55-72.
32. Garro, A.J.; Espina, N.; and Lieber, C.S. Alcohol and cancer. Alcohol Health & Research World 16(1):81- 86, 1992.
33. Farinati, F.; Lieber, C.S.; and Garro, A.J. Effects of chronic ethanol consumption on carcinogen activating and detoxifying systems in rat upper alimentary tract tissue. Alcoholism: Clinical and Experimental Research 13(3):357-360, 1989.
34. Leo, M.A.; Kim, C.; and Lieber, C.S. Increased vitamin A in esophagus and other extrahepatic tissues after chronic ethanol consumption in the rat. Alcoholism: Clinical and Experimental Research 10(5):487-492, 1986.
35. Mobarhan, S.; Layden, T.J.; Friedman, H.; Kunigk, A.; and Donahue, P. Depletion of liver and esophageal epithelium vitamin A after chronic moderate ethanol consumption in rats: Inverse relation to zinc nutriture. Hepatology 6(4):615-621, 1986.
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38. Giovannucci, E.; Stampfer, M.J.; Colditz, G.A .; Rimm, E.B.; Trichopoulos, D.; Rosner, B.A.; Speizer, F.E.; and Willett, W.C. Folate, methionine, and alcohol intake and risk of colorectal adenoma. Journal of the National Cancer Institute 85(11):875-884, 1993.
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Source: National Institute on Alcohol Abuse (July 1999)  National Institutes of Health

v Alcohol and AIDS

There are two reasons to investigate connections between alcohol, HIV infection, and AIDS: alcohol may adversely affect the immune system, and alcohol may influence high-risk sexual behavior.

Human immunodeficiency virus (HIV) is the agent that causes acquired immunodeficiency syndrome (AIDS). HIV is transmitted through sexual contact with an infected individual, through exchange of infected blood or blood products, or to the newborn from an infected mother. HIV-infected persons may harbor the virus for many years with no clinical signs of disease. Eventually, HIV destroys the body's immune system, mainly by impairing a class of white blood cells whose regulatory activities are essential for immune protection. As a result, people who have AIDS are prone to lung infections, brain abscesses, and a variety of other infections caused by microorganisms that usually do not produce disease in healthy people. Those who have AIDS also are prone to cancers such as Kaposi's sarcoma, a skin cancer rarely seen in non-HIV-infected populations. The diagnosis of AIDS depends in part on the presence of one or a number of these infections and cancers ⁽¹⁾.

One million people in the United States are estimated to be infected with HIV ⁽²⁾. At least 40,000 new HIV infections are thought to occur among adults and adolescents, and an estimated 1,500 to 2,000 new HIV infections are thought to occur among newborns each year. Currently, 8 to 10 million people worldwide are estimated to be infected with HIV ⁽³⁾. Of these, 50 percent are expected to develop AIDS within 10 years, and 90 percent may develop AIDS within 20 years of initial infection ⁽⁴⁾. The prognosis for persons with AIDS is grim: AIDS-associated mortality may approach 85 percent within 5 years of diagnosis ⁽⁵⁾.

Alcohol and the Immune System

Alcohol can impair normal immune responses that protect the body from disease (6,7,8). Chronic alcohol consumption has been shown to reduce the number of infection-fighting white blood cells in laboratory animals (9,10,11) and in humans ^(12,13). Chronic alcohol ingestion or alcohol dependence can depress antibody production and other immune responses in animals (10,9) and in humans ^(14,15).

Alcohol can suppress activities of certain immune system cells, called macrophages, that help keep the lungs free from infection ^(16,17). In addition, alcoholics appear to be more susceptible to bacterial infections and cancer than are nonalcoholics ^(18,19). Studies in animals and in humans indicate that consuming alcohol during pregnancy can decrease immune resistance in the offspring (20,21,22).

Alcohol's generally immunosuppressive effects could mean that 1) drinking may increase vulnerability to HIV infection among people exposed to the virus, and that 2) among people who are already HIV infected, alcohol-induced immunosuppression might add to HIV-induced immunosuppression, and speed the onset or exacerbate the pathology of AIDS-related illness. These are complex ideas and areas of intense investigation, but so far only a few studies have been published. Researchers have learned that alcohol can impair white blood cell responses to HIV ⁽²³⁾.

A provocative study that warrants replication found that a single drinking episode depressed certain immune responses of white blood cells taken from healthy volunteers ⁽²⁴⁾. In addition, white blood cells isolated after this drinking episode were more susceptible to HIV infection than were cells isolated from subjects who did not drink, hinting that even occasional alcohol consumption may increase the likelihood of infection upon exposure to HIV. Whether alcohol use influences the progression of AIDS in persons already infected with HIV has been explored in a recent study of homosexual men ⁽²⁵⁾. While these researchers found that neither alcohol nor other drugs seem to influence the progression of HIV infection or the development of AIDS, their results await confirmation. Clearly, more research is needed to understand alcohol's role in HIV infection and the course of ensuing disease.

Alcohol and Sexual Behavior

Sexual practices considered to be high risk for acquiring HIV from an infected individual include vaginal or anal intercourse without a condom; other sexual practices that facilitate exchange of blood, semen, or other body secretions; and unprotected sexual activities with multiple partners. The frequency with which sexual partners engage in such practices also influences the risk for exposure to HIV.

Alcohol's relationship to high-risk sexual behavior may be explained in two ways. First, alcohol use may be a marker for a risk-taking temperament: those who drink alcohol may also engage in a variety of high-risk activities, including unsafe sexual practices, as a part of a "problem behavior syndrome" ^(26,27). Second, alcohol may influence high-risk behaviors at specific sexual encounters by affecting judgment and disinhibiting socially learned restraints ^(28,29). These are not mutually exclusive interpretations.

In addition, these two explanations have different implications for the prevention of high-risk sexual behavior. Among people who have a risk-taking temperament, reducing alcohol consumption may not reduce high-risk sexual behavior. However, among those who are more likely to take sexual risks when they are drinking than when they are not, reducing alcohol consumption should also reduce high-risk sexual behavior.

There are two approaches to studying alcohol's relationship to sexual behavior that may result in HIV infection ⁽³⁰⁾. One approach examines whether alcohol use in general is correlated with sexual risk-taking behavior in general. In this approach, an observed association between drinking and high-risk sexual activity could imply that these two behaviors are part of a larger risk-taking tendency, or that alcohol itself influences sexual risk-taking, or both. Another approach examines the consequences of alcohol use during specific sexual encounters. An observed connection between alcohol use and sexual risk-taking during specific encounters suggests a direct influence of alcohol on such behavior.

A number of studies have identified associations between drinking and high-risk sexual activity. These studies also have found that an absence of or a reduction in alcohol use is associated with a decrease in high-risk sexual behavior. A study of heterosexual drinking habits and sexual behavior found that women and men who frequently combined alcohol use with sexual encounters were generally less likely to use condoms during intercourse ⁽³¹⁾.

Similarly, a study of homosexual men found alcohol or other drug use combined with sexual activity to be strongly associated with high-risk sexual behavior: even those who drank only occasionally at the time of sexual encounters were twice as likely to be categorized as "high risk," based on the frequency of involvement in a range of sexual practices within nonmonogamous relationships, than were those who did not drink ⁽³²⁾. Further, those men who did not drink during sexual encounters were three times more likely to be classified in a "no risk" category than were men who combined drinking with sexual activity. Recently, a reduction in alcohol use among homosexual men has been associated with a reduction in high-risk sexual behavior ⁽³³⁾.

Other studies that examine the consequences of alcohol use at specific sexual encounters also have demonstrated a connection between alcohol use and high-risk sexual behavior. Scottish adolescents who drank at the time of first intercourse were less likely to have used a condom than those who did not drink ⁽³⁴⁾. A survey of adolescents in Massachusetts revealed that teens were less likely to use condoms if sexual activity followed drinking or other drug use ⁽³⁵⁾. Similarly, adult homosexual men and heterosexual women (but not heterosexual men) reported that they were less likely to use a condom during those sexual encounters in which they felt intoxicated ⁽³⁶⁾. These reports of simultaneous alcohol use and high-risk sexual behavior suggest that alcohol can directly influence sexual risk-taking. However, these combined behaviors may still reflect a risk-taking tendency in some individuals.

Further research is needed to define conditions under which alcohol use is linked to high-risk sexual activity. Information generated from such studies will be vital for developing and improving programs to prevent HIV transmission.

Conclusion

Science has made remarkable progress in our understanding of HIV and AIDS. Yet we know very little about the role of alcohol in the transmission and acquisition of HIV or in the progression of HIV infection to AIDS. Such knowledge would enhance efforts to prevent HIV exposure and decrease the number of new AIDS cases.

We know that alcohol affects the immune system. This suggests that alcohol could affect the course of HIV infection and AIDS, which is a disease of the immune system. For example, alcohol might affect the body's ability to defend against HIV infection upon exposure to the virus; alcohol might alter the course of infection to the development of AIDS; or alcohol might affect the severity or duration of the special infections, known as opportunistic infections, that characterize AIDS. So far, the research findings in this area are hard to reconcile. On one hand, laboratory evidence shows clearly that alcohol impairs the ability of white blood cells to defend against the human immunodeficiency virus. On the other hand, studies involving human populations have found that neither alcohol nor other drugs modify the course of HIV infection or AIDS. Given the complexity of the human immune system, the contradictions presented by these findings, while puzzling, are not unexpected. One key to solving this puzzle will be more attention, in long-term studies of human populations, to objective evidence of drinking and to laboratory evidence of immune function status.

We know also that alcohol is associated with high-risk sexual activity that potentially can result in exposure to HIV. Some people may be more likely to engage in certain sexual behaviors when drinking as a result of alcohol's disinhibiting effects. (In others, alcohol use and unsafe sexual practices seem to be a part of a "risk-taking temperament," in which unsafe sexual practices may occur whether or not alcohol is consumed.)

Prevention efforts that address the link between alcohol consumption and unsafe sex are being evaluated for their effectiveness in reducing high-risk sexual activity. In addition, researchers are investigating various settings, such as bars and alcohol treatment programs, and certain groups, such as teenagers, where intervention strategies could be employed to decrease alcohol-related high-risk sexual activity. It is hoped that these findings will help target HIV-related prevention strategies in a way that will help to reduce the incidence of new cases of HIV infection, and ultimately reduce the number of persons with AIDS.

References

1. Centers for Disease Control. Revision of the CDC surveillance case definition for acquired immunodefi ciency syndrome. Morbidity and Mortality Weekly Report 36(1S):15-155, 1987.

2. Centers for Disease Control. HIV prevalence estimates and AIDS case projections for the United States: Report based upon a workshop. Morbidity and Mortality Weekly Report: Recommendations and Re ports 39(RR-16):1-31, 1990.

3. World Health Organization. In Point of Fact. Geneva: World Hea lth Organization, May 1991 (No. 74).

4. Chin, J., & Lwanga, S.K. Estimation and projection of adult AIDS cases: A simple epidemiological model. Bulletin of the World Health Organization 69(4):399-406, 1991.

5. Rothernberg, R.; Woelfel, M.; Stoneburner, R.; Milberg, J.; & Parker, R. Survival with the acquired immunodeficiency syndrome: Experience with 5833 cases in New York City. New England Journal of Medicine 317(21):1297-1302, 1987.

6. MacGregor, R.R. Alcohol and drugs as co-factors for AIDS. Advances in Alcohol and Substance Abuse 7(2):47-71, 1988.

7. PLANT, M.A. Alcohol, sex and AIDS. Alcohol & Alcoholism 25(2/3):293-301, 1990.

8. Pillai, R., & Watson, R.R. Response to: `Alcohol, Sex and AIDS.' Alcohol & Alcoholism 25(6):711-713, 1990.

9. Tennenbaum, J.I.; Rupert, R.D.; St. Pierre, R.L.G.; & Greenberger, N.J. The effect of chronic alcohol administration on the immune responsiveness of rats. Journal of Allergy 44:272-281, 1969.

10. Jerrells, T.R.; Marietta, C.A.; Eckardt, M.J.; Majchrowicz, E.; & Weight, F.F. Effects of ethanol adminis- tration on parameters of immunocompetency in rats. Journal of Leukocyte Biology 39(5):499-501, 1986.

11. Saad, A.J., & Jerrells, T.R. Flow cytometric and immunohistochemical evaluation of ethanol-induced changes in splenic and thymic lymphoid cell populations. Alcoholism: Clinical and Experimental Re search 15(5):796-803, 1991.

12. Liu, Y.K. Effects of alcohol on granulocytes and lymphocytes. Seminars in Hematology 17:130-136, 1980.

13. McFarland, W., & Libre, E.P. Abnormal leukocyte response in alcoholism. Annals of Internal Medicine 59:865-877, 1963.

14. Gluckman, S.J.; Dvorak, V.C.; & MacGregor, R.R. Host defenses during prolonged alcohol consumption in a controlled environment. Archives of Internal Medicine 137:1539-1543, 1977.

15. Mutchnick, M.G., & Lee, H.H. Impaired lymphocyte proliferative response to mitogen in alcoholic patients: Absence of a relation to liver disease activity. Alcoholism: Clinical and Experimental Re search 12(1):155-158, 1988.

16. Guarneri, J.J., & Laurenzi, G.A. Effect of alcohol on the mobilization of alveolar macrophages. Journal of Laboratory and Clinical Medicine 72:40-51, 1968.

17. Rimland, D. Mechanisms of ethanol-induced defects of alveolar macrophage function. Alcoholism: Clinical and Experimental Research 8(1):73-76, 1983.

18. MacGregor, R.R. Alcohol and immune defense. Journal of the American Medical Association 256(11):1474-1479, 1986.

19. Mufti, S.I.; Darban H.R.; & Watson, R.R. Alcohol, cancer, and immunomodulation. Critical Reviews in Oncology/Hematology 9(3):243-261, 1989.

20. Redei, E.; Clark, W.R.; & McGivern, R.F. Alcohol exposure in utero results in diminished T-cell function and alterations in brain corticotropin-releasing factor and ACTH content. Alcoholism: Clinical and Experimental Research 13(3):439-443, 1989.

21. Johnson, S.; Knight, R.; Marmier, D.J.; & Steele, R.W. Immunodeficiency in fetal alcohol syndrome. Pediatric Research 15(6):908-911, 1981.

22. Ewald, S.J. T lymphocyte populations in fetal alcohol syndrome. Alcoholism: Clinical and Experimental Research 13(4):485-489, 1989.

23. Nair, M.P.N.; Schwartz, S.A.; Kronfol, Z.A.; Heimer, E.P.; Pottathil, R.; & Greden, J.F. Immunoregulatory effects of alcohol on lymphocyte responses to human immunodeficiency virus proteins. Progress in Clinical and Biological Research 325:221-230, 1990.

24. Bagasra, O.; Kajdacsy-Balla, A.; & Lischner, H.W. Effects of alcohol ingestion on in vitro susceptibil ity of peripheral blood mononuclear cells to infection with HIV and of selected T-cell functions. Alcoholism: Clinical and Experimental Research 13(5):636-643, 1989.

25. Kaslow, R.A.; Blackwelder, W.C.; Ostrow, D.G.; Yerg, D.; Palenicek, J.; Coulson, A.H.; & Valdiserri, R.O. No evidence for a role of alcohol or other psychoactive drugs in acc elerating immunodeficiency in HIV-1-positive individuals: A report from the Multicenter AIDS Cohort Study. Journal of the American Medical Association 261(23):3424, 1989.

26. Donovan, J.E., & Jessor, R. Structure of problem behavior in adolescence and young adulthood. Journal of Consulting and Clinical Psychology 53(6):890-904, 1985.

27. Biglan, A.; Metzler, C.W.; Wirt, R.; Ary, D.; Noell, J.; Ochs, L.; French, C.; & Hood, D. Social and behavioral factors associated with high-risk sexual behavior among adolescents. Journal of Behav ioral Medicine 13(3):245-261, 1990.

28. Steelen, C.M., & Josephs, R.A. Alcohol myopia: Its prized and dangerous effects. American Psycholo gist 45(8):921-933, 1990.

29. Crown, L.C., & George, W.H. Alcohol and human sexuality: Review and integration. Psychological Bulletin 105(3):374-386, 1989.

30. Leigh, B.C. Alcohol and unsafe sex: An overview of research and theory. Progress in Clinical and Biological Research. Alcohol, Immunomodulation, and AIDS. Vol. 325. New York: Alan R. Liss, Inc., 1990. pp.35-46.

31. Bagnall. G.; Plant, M.; & Warwick, W. Alcohol, drugs and AIDS-related risks: Results from a prospec tive study. AIDS Care 2(4):309-317, 1990.

32. Stall, R.; McKusick, L.; Wiley, J.; Coates, T.J.; & Ostrowe, D.G. Alcohol and drug use during sexual activity and compliance with safe sex guidelines for AIDS: The AIDS Behavioral Research Project. Health Education Quarterly 13(4):359-371, 1986.

33. McCusker, J.; Westenhouse, J.; Stoddard, A.M.; Zapka, J.G.; Zorn, M.W.; & Mayer, K.H. Use of drugs and alcohol by homosexually active men in relation to sexual practices. Journal of Acquired Immune Deficiency Syndromes 3(7):729-736, 1990.

34. Robertson, J.A., & Plant, M.A. Alcohol, sex and risks of HIV infection. Drug and Alcohol Dependence 22(1,2):75-78, 1988.

35. Hingson, R.W.; Strunin, L.; Berlin, B.M.; & Heeren, T. Beliefs about AIDS, use of alcohol and drugs, and unprotected sex among Massachusetts adolescents. American Journal of Public Health 80(3):295-299, 1990.

36. Trocki, K.F., & Leigh, B.C. Alcohol consumption and unsafe sex: A comparison of heterosexuals and homosexual men. Journal of Acquired Immune Deficiency Syndromes 4(10):981-986, 1991.

Source: National Institute on Alcohol Abuse (July 1999)                                                                 National Institutes of Health 

v Alcohol and Tolerance

Alcohol consumption interferes with many bodily functions and affects behavior. However, after chronic alcohol consumption, the drinker often develops tolerance to at least some of alcohol's effects. Tolerance means that after continued drinking, consumption of a constant amount of alcohol produces a lesser effect or increasing amounts of alcohol are necessary to produce the same effect ⁽¹⁾. Despite this uncomplicated definition, scientists distinguish between several types of tolerance that are produced by different mechanisms.

Tolerance to alcohol's effects influences drinking behavior and drinking consequences in several ways. This chapter describes how tolerance may encourage alcohol consumption, contributing to alcohol dependence and organ damage; affect the performance of tasks, such as driving, while under the influence of alcohol; contribute to the ineffectiveness or toxicity of other drugs and medications; and may contribute to the risk for alcoholism.

Functional Tolerance

Humans and animals develop tolerance when their brain functions adapt to compensate for the disruption caused by alcohol in both their behavior and their bodily functions. This adaptation is called functional tolerance ⁽²⁾. Chronic heavy drinkers display functional tolerance when they show few obvious signs of intoxication even at high blood alcohol concentrations (BAC's), which in others would be incapacitating or even fatal ⁽³⁾. Because the drinker does not experience significant behavioral impairment as a result of drinking, tolerance may facilitate the consumption of increasing amounts of alcohol. This can result in physical dependence and alcohol-related organ damage.

However, functional tolerance does not develop at the same rate for all alcohol effects (4-6). Consequently, a person may be able to perform some tasks after consuming alcohol while being impaired in performing others. In one study, young men developed tolerance more quickly when conducting a task requiring mental functions, such as taking a test, than when conducting a task requiring eye-hand coordination ⁽⁴⁾, such as driving a car. Development of tolerance to different alcohol effects at different rates also can influence how much a person drinks. Rapid development of tolerance to unpleasant, but not to pleasurable, alcohol effects could promote increased alcohol consumption ⁽⁷⁾.

Different types of functional tolerance and the factors influencing their development are described below. During repeated exposure to low levels of alcohol, environmental cues and processes related to memory and learning can facilitate tolerance development; during exposure to high levels of alcohol, tolerance may develop independently of environmental influences.

Acute tolerance. Although tolerance to most alcohol effects develops over time and over several drinking sessions, it also has been observed within a single drinking session. This phenomenon is called acute tolerance ⁽²⁾. It means that alcohol-induced impairment is greater when measured soon after beginning alcohol consumption than when measured later in the drinking session, even if the BAC is the same at both times (8-10).

Acute tolerance does not develop to all effects of alcohol but does develop to the feeling of intoxication experienced after alcohol consumption ⁽⁴⁾. This may prompt the drinker to consume more alcohol, which in turn can impair performance or bodily functions that do not develop acute tolerance.

Environment-dependent tolerance. The development of tolerance to alcohol's effects over several drinking sessions is accelerated if alcohol is always administered in the same environment or is accompanied by the same cues. This effect has been called environment-dependent tolerance. Rats that regularly received alcohol in one room and a placebo in a different room demonstrated tolerance to the sedative and temperature-lowering effects of alcohol only in the alcohol-specific environment ⁽¹¹⁾. Similar results were found when an alcohol-induced increase in heart rate was studied in humans ⁽¹²⁾. When the study subjects always received alcohol in the same room, their heart rate increased to a lesser extent after drinking in that room than in a new environment.

Environment-dependent tolerance develops even in "social" drinkers in response to alcohol-associated cues. In a study analyzing alcohol's effects on the performance of an eye-hand coordination task, a group of men classified as social drinkers received alcohol either in an office or in a room resembling a bar. Most subjects performed the task better (i.e., were more tolerant) when drinking in the barlike environment ⁽¹³⁾. This suggests that for many people, a bar contains cues that are associated with alcohol consumption and promote environment-dependent tolerance.

Learned tolerance. The development of tolerance also can be accelerated by practicing a task while under the influence of alcohol. This phenomenon is called behaviorally augmented (i.e., learned) tolerance. It first was observed in rats that were trained to navigate a maze while under the influence of alcohol ⁽¹⁴⁾. One group of rats received alcohol before their training sessions; the other group received the same amount of alcohol after their training sessions. Rats that practiced the task while under the influence of alcohol developed tolerance more quickly than rats practicing without prior alcohol administration.

Humans also develop tolerance more rapidly and at lower alcohol doses if they practice a task while under the influence of alcohol. When being tested on a task requiring eye-hand coordination while under the influence of alcohol, people who had practiced after ingesting alcohol performed better than people who had practiced before ingesting alcohol ⁽¹⁵⁾. Even subjects who only mentally rehearsed the task after drinking alcohol showed the same level of tolerance as those who actually practiced the task while under the influence of alcohol ⁽¹⁵⁾.

The expectation of a positive outcome or reward after successful task performance is an important component of the practice effect on tolerance development. When human subjects knew they would receive money or another reward for successful task performance while under the influence of alcohol, they developed tolerance more quickly than if they did not expect a reward ⁽¹⁶⁾. The motivation to perform better contributes to the development of learned tolerance.

Learned and environment-dependent tolerance have important consequences for situations such as drinking and driving. Repeated practice of a task while under the influence of low levels of alcohol, such as driving a particular route, could lead to the development of tolerance, which in turn could reduce alcohol-induced impairment ⁽¹⁶⁾. However, the tolerance acquired for a specific task or in a specific environment is not readily transferable to new conditions ^(17,18). A driver encountering a new environment or an unexpected situation could instantly lose any previously acquired tolerance to alcohol's impairing effects on driving performance.

Environment-independent tolerance. Exposure to large quantities of alcohol can lead to the development of functional tolerance independent of environmental influences. This was demonstrated in rats that inhaled alcohol vapors ⁽¹⁹⁾. In another study, mice demonstrated tolerance in environments different from the one in which the alcohol was administered ⁽²⁰⁾. Significantly larger alcohol doses were necessary to establish this environment-independent tolerance than to establish environment-dependent tolerance. ⁽²⁰⁾

Metabolic Tolerance

Tolerance that results from a more rapid elimination of alcohol from the body is called metabolic tolerance ⁽²⁾. It is associated with a specific group of liver enzymes that metabolize alcohol and that are activated after chronic drinking ^(21,22). Enzyme activation increases alcohol degradation and reduces the time during which alcohol is active in the body ⁽²⁾, thereby reducing the duration of alcohol's intoxicating effects.

However, certain of these enzymes also increase the metabolism of some other drugs and medications, causing a variety of harmful effects on the drinker. For example, rapid degradation of sedatives (e.g., barbiturates) ⁽²³⁾ can cause tolerance to them and increase the risk for their use and abuse. Increased metabolism of some prescription medications, such as those used to prevent blood clotting and to treat diabetes, reduces their effectiveness in chronic drinkers or even in recovering alcoholics ⁽²⁴⁾. Increased degradation of the common painkiller acetaminophen produces substances that are toxic to the liver ⁽²⁵⁾ and that can contribute to liver damage in chronic drinkers.

Tolerance and the Predisposition to Alcoholism

Animal studies indicate that some aspects of tolerance are genetically determined. Tolerance development was analyzed in rats that were bred to prefer or not prefer alcohol over water ^(26,27). The alcohol-preferring rats developed acute tolerance to some alcohol effects more rapidly and/or to a greater extent than the nonpreferring rats ⁽²⁶⁾. In addition, only the alcohol-preferring rats developed tolerance to alcohol's effects when tested over several drinking sessions ⁽²⁷⁾. These differences suggest that the potential to develop tolerance is genetically determined and may contribute to increased alcohol consumption.

In humans, genetically determined differences in tolerance that may affect drinking behavior were investigated by comparing sons of alcoholic fathers (SOA's) with sons of nonalcoholic fathers (SONA's). Several studies found that SOA's were less impaired by alcohol than SONA's ^(28,29). Other studies found that, compared with SONA's, SOA's were affected more strongly by alcohol early in the drinking session but developed more tolerance later in the drinking session ⁽³⁰⁾. These studies suggest that at the start of drinking, when alcohol's pleasurable effects prevail, SOA's experience these strongly; later in the drinking session, when impairing effects prevail, SOA's do not experience these as strongly because they have developed tolerance ⁽³⁰⁾. This predisposition could contribute to increased drinking and the risk for alcoholism in SOA's.

Conclusion

Tolerance can be a useful clue for clinicians in identifying patients who may be at risk for developing alcohol-related problems. For example, younger patients who are early in their drinking histories and who report that they can "hold their liquor well" may be drinking at rates that will place them at risk for medical complications from alcohol use, including alcoholism. The fact that tolerance to all of alcohol's effects does not develop simultaneously is also important; people who are mildly tolerant may exhibit more symptoms of impairment when faced with unfamiliar activities, such as driving in an unknown area, than when they are engaged in routine actions, such as driving home from work. Lastly, although we know that initial sensitivity to alcohol may play a role in the development of alcoholism, the role of tolerance in maintaining addiction to alcohol needs further exploration.

References

1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edi tion. Washington, DC: the Association, 1994.

2. Tabakoff, B.; Cornell, N.; & Hoffman, P.L. Alcohol tolerance. Annals of Emergency Medicine 15(9):1005- 1012, 1986.

3. Chesher, G., & Greeley, J. Tolerance to the effects of alcohol. Alcohol, Drugs and Driving 8(2):93-106, 1992.

4. Vogel-Sprott, M.D. Acute recovery and tolerance to low doses of alcohol: Differences in cognitive and motor skill performance. Psychopharmacology 61(3):287-291, 1979.

5. Pohorecky, L.A.; Brick, J.; & Carpenter, J.A. Assessment of the development of tolerance to ethanol using multiple measures. Alcoholism: Clinical and Experimental Research 10(6):616-622, 1986.

6. Tabakoff, B., & Kiianmaa, K. Does tolerance develop to the activating, as well as the depressant, effects of ethanol? Pharmacology Biochemistry & Behavior 17(5):1073-1076, 1982.

7. Tabakoff, B., & Hoffman, P.L. Tolerance and the etiology of alcoholism: Hypothesis and mechanism. Alcoholism: Clinical and Experimental Research 12(1):184-186, 1988.

8. Beirness, D., & Vogel-Sprott, M. The development of alcohol tolerance: Acute recovery as a predictor. Psychopharmacology 84(3):398-401, 1984.

9. Bennett, R.H.; Cherek, D.R.; & Spiga, R. Acute and chronic alcohol tolerance in humans: Effects of dose and consecutive days of exposure. Alcoholism: Clinical and Experimental Research 17(4):740-745, 1993.

10 Hiltunen, A.J., & Järbe, T.U.C. Acute tolerance to ethanol using drug discrimination and open-field procedures in rats. Psychopharmacology 102(2):207-212, 1990.

11. Mansfield, J.G., & Cunningham, C.L. Conditioning and extinction of tolerance to the hypothermic effect of ethanol in rats. Journal of Comparative and Physiological Psychology 94(5):962-969, 1980.

12. Dafters, R., & Anderson, G. Conditioned tolerance to the tachycardia effect of ethanol in humans. Psychopharmacology 78(4):365-367, 1982.

13. McCusker, C.G., & Brown, K. Alcohol-predictive cues enhance tolerance to and precipitate "craving" for alcohol in social drinkers. Journal of Studies on Alcohol 51(6):494-499, 1990.

14. LeBlanc, A.E.; Gibbins, R.J.; & Kalant, H. Behavioral augmentation of tolerance to ethanol in the rat. Psychopharmacologia 30:117-122, 1973.

15. Vogel-Sprott, M.; Rawana, E.; & Webster, R. Mental rehearsal of a task under ethanol facilitates tolerance. Pharmacology Biochemistry & Behavior 21(3):329-331, 1984.

16. Sdao-Jarvie, K., & Vogel-Sprott, M. Response expectancies affect the acquisition and display of behavioral tolerance to alcohol. Alcohol 8(6):491-498, 1991.

17. Siegel, S., & Sdao-Jarvie, K. Attenuation of ethanol tolerance by a novel stimulus. Psychopharmacology 88(2):258-261, 1986.

18. Tsibulsky, V.L., & Amit, Z. Role of environmental cues as Pavlovian-conditioned stimuli in enhancement of tolerance to ethanol effects: 1. Lethal effects in mice and rats. Pharmacology Biochemistry & Behavior 45(2):473-479, 1993.

19. Tabakoff, B., & Culp, S.G. Studies on tolerance development in inbred and heterogeneous stock National Institutes of Health rats. Alcoholism: Clinical and Experimental Research 8(5):495-499, 1984.

20. Melchior, C.L., & Tabakoff, B. Modification of environmentally cued tolerance to ethanol in mice. Journal of Pharmacology and Experimental Therapeutics 219(1):175-180, 1981. (21) Lieber, C.S. Metabolism of ethanol and associated hepatotoxicity. Drug and Alcohol Review 10(3):175-202, 1991.

22. Lieber, C.S. The microsomal ethanol oxidizing system: Its role in ethanol and xenobiotic metabolism. Biochemical Society Transactions 16(3):232-239, 1988.

23. Misra, P.S.; Lefèvre, A.; Ishii, H.; Rubin, E.; & Lieber, C. S. Increase of ethanol, meprobamate and pentobarbital metabolism after chronic ethanol administration in man and in rats. American Journal of Medicine 51(3):346-351, 1971.

24. Lieber, C.S. Interaction of ethanol with other drugs. In: Lieber, C.S., ed. Medical and Nutritional Complications of Alcoholism: Mechanisms and Management. New York: Plenum Press, 1992. pp. 165- 183.

25. Sato, C.; Matsuda, Y.; and Lieber, C.S. Increased hepatotoxicity of acetaminophen after chronic ethanol consumption in the rat. Gastroenterology 80(1):140-148, 1981.

26. Waller, M.B.; McBride, W.J.; Lumeng, L.; & Li, T.-K. Initial sensitivity and acute tolerance to ethanol in the P and NP lines of rats. Pharmacology Biochemistry & Behavior 19(4):683-686, 1983.

27. Lê, A.D., & Kiianmaa, K. Characteristics of ethanol tolerance in alcohol drinking (AA) and alcohol avoiding (ANA) rats. Psychopharmacology 94(4):479-483, 1988.

28. Schuckit, M.A. Ethanol-induced changes in body sway in men at high alcoholism risk. Archives of General Psychiatry 42(4):375-379, 1985.

29. Schuckit, M.A., & Gold, E.O. A simultaneous evaluation of multiple markers of ethanol/placebo chal- lenges in sons of alcoholics and controls. Archives of General Psychiatry 45(3):211-216, 1988.

30. Newlin, D.B., & Thomson, J.B. Alcohol challenge with sons of alcoholics: A critical review and analysis. Psychological Bulletin 108(3):383-402, 1990.

Source: National Institute on Alcohol Abuse (July 1999)                                                         National Institutes of Health

v Alcohol and Cognition

Research shows that alcohol adversely affects the brain. When health professionals encounter patients who are having cognitive difficulties, such as impaired memory or reasoning ability, alcohol use may be the cause of the problem. When treating patients who have abused alcohol, it may be of value to attempt to identify the level of any impairment and to modify the treatment accordingly.

Some researchers have investigated whether or not there is measurable alcohol-related cognitive impairment among nonalcoholic social drinkers. Their findings suggest a dose-response relationship between alcohol consumption and diminished scores on certain neuropsychological tests (e.g., Parker & Noble 1977; Parker et al. 1983). Statistically significant decreases in test performance have been found for people whose self-reported alcohol consumption was in the range of what was considered social drinking. This is not to say these people were clinically impaired, only that they exhibited certain performance deficits that correlated with alcohol consumption. It is important to note that similar correlations from other studies have not been found to be consistently significant. For example, the results of one general population study (Bergman et al. 1983) showed no correlation between self-reported alcohol consumption and neuropsychological test scores; other findings (Emmerson et al. 1988) failed to show a simple dose-response relationship. In a recent review of such studies, Parsons (1986) concluded that data on the relationship of cognitive impairment to amount of alcohol consumed by social drinkers are inconclusive.

Alcoholics in treatment present a different picture. Although most alcoholics entering treatment do not have decreased overall intelligence scores, approximately 45 to 70 percent of these patients have specific deficits in problem solving, abstract thinking, concept shifting, psychomotor performance, and difficult memory tasks (Parsons & Leber 1981; Eckardt & Martin 1986; Tabakoff & Petersen 1988). Such deficits usually are not apparent without neuropsychological testing. In addition, structural changes in the brains of alcoholics have been reported (Ron 1979; Wilkinson 1987), as well as reduced cerebral blood flow (Ishikawa et al. 1986) and altered electrical activity (Porjesz & Begleiter 1981), but there is not yet any clear evidence implicating these changes as the cause of observed cognitive deficits.

For the most severe alcoholics, serious organic cerebral impairment is a common complication, occurring in about 10 percent of patients (Horvath 1975). The diverse signs of severe brain dysfunction that persist after cessation of alcohol consumption have been conceptualized in terms of two organic mental disorders: alcohol amnestic disorder (memory disorder) and dementia associated with alcoholism (Lishman 1981; American Psychiatric Association 1987). Recently however, it has been recognized that these two disorders are not mutually exclusive and that some features of each often coexist in the same patient (Martin & Eckardt 1985). Alcohol amnestic disorder, commonly called Korsakoff's psychosis or Wernicke-Korsakoff syndrome, is characterized by short-term memory, impairments and behavioral changes that occur without clouding of consciousness or general loss of intellectual abilities. Dementia associated with alcoholism consists of global loss of intellectual abilities with an impairment in memory function, together with disturbance(s) of abstract thinking, judgment, other higher cortical functions, or personality change without a clouding of consciousness. It has been suggested that subcortical lesions due to nutritional (thiamine) deficiency are characteristic of Korsakoff's, whereas alcoholic dementia is associated more with cortical changes (Victor & Laureno 1978). There is some evidence that a genetic abnormality may predispose some people to Korsakoff's in the presence of excessive alcohol use and malnutrition (Blass & Gibson 1977; Mukherjee et aI. 1987).

Tarter and Edwards (1986) summarize evidence suggesting that neuropsychological impairment in alcoholics may occur for a number of reasons. The toxic effects of alcohol on the brain may cause impairment directly. In addition, some alcoholics may exhibit impairment as an indirect result of alcohol abuse, e.g., they may have experienced a craniocerebral trauma, they may be eating poorly and suffering nutritional deficits (such as thiamine or niacin deficiencies), or they may have cognitive impairments associated with liver disease.

Some alcoholics may have been cognitively impaired before they began drinking. There is some evidence that persons in groups considered to be at risk for alcoholism (e.g., children of alcoholics) are less adept at certain learning tests and visual-spatial integration than are persons in groups not deemed at risk for alcoholism; this area of research is still under active investigation.

Some researchers have observed that cognitive deficits in some alcoholics resemble those seen in normal elderly persons, leading to speculation that alcohol's effect on cognition may be explained as premature aging (Tarter 8 Edwards 1986). However, it is more likely that such deficits are independent of any deficits associated with normal aging (Grant et al. 1984; Cutting 1988).

Laying aside issues of etiology, evidence indicates that some cognitive impairment in alcoholics is reversible. Researchers (Albert et al. 1982; Grant et al. 1984; Goldman 1986, 1987) report apparent "spontaneous" recovery of cognitive function (recovery seen after the passage of time with no active intervention) among abstinent alcoholics, a result that may be due solely to the absence of alcohol but that also may be due in part to other changes, such as better nutrition and opportunities for social interaction provided in an alcohol treatment setting. There is some evidence that cognitive training and practice experience (remedial mental exercises) can facilitate recovery from impairment (Godfrey et al. 1985; Goldman 1986,1987).

Because even with prolonged abstinence many alcoholic patients with chronic organic mental disorders may exhibit only modest clinical improvement in brain functioning, there is a need for pharmacological interventions to complement behavioral methods. Recent findings that pharmacological intervention may be useful in restoring some cognitive ability (McEntee & Mair 1980) are encouraging.

Although degree of cognitive impairment may not be a clinically significant predictor of post-treatment alcohol consumption (Donovan et al. 1987; Eckardt et al. 1988), identifying cognitive impairment may have implications for successfully treating some patients. Particularly in the first weeks of abstinence during treatment, cognitive impairments may make it difficult for some alcoholics to benefit from the educational and skill development sessions that are important components of many treatment programs (McCrady & Smith 1986; McCrady 1987). For example, Becker and Jaffe (1984) reported that alcoholics who were tested soon after beginning abstinence were unable to recall treatment-related information presented in a film that was part of the regular treatment program. An implication of such findings is that information presented to alcoholics during the period of impairment in the early weeks of abstinence should be repeated at later stages in the treatment program. Alternatively, presentation of treatment-related information should be delayed until tests indicate some improvement in cognitive function.

Conclusion

Awareness of alcohol's effects on cognition can help general health care providers identify alcoholics and refer them to appropriate treatment. Awareness also can assist the efforts of alcoholism treatment personnel to maximize the potential benefit of treatment for their patients.

In general health care situations, practitioners should use standard alcoholism assessment instruments to determine the extent of alcohol use by patients who show signs of cognitive dysfunction. Patients in whom alcohol use is identified as either a primary or a contributing cause of cognitive dysfunction must be referred to alcoholism treatment. Evidence suggests that some cognitive impairment in alcoholics is reversible. Moreover, cognitive deterioration will worsen with continued drinking.

In addition, alcoholism treatment personnel should know that alcohol-induced cognitive impairment may make it difficult during the first weeks of absence for some of their patients to benefit from exposure to the full range of treatment services. Although it may not be possible or necessary for treatment programs to administer extensive neuropsychiatric tests to all patients, a simple test of the patient's ability to benefit from the didactic elements of alcoholism treatment can be made. One test might be to determine what a patient remembers from an initial counseling session.

If there is evidence of cognitive deficiency, patients must be allowed time to recover adequate cognitive function so that, at a minimum, information provided during treatment can be retained. However, other important elements of rehabilitation, such as improving patient nutritional status and exposure to physical exercise and resocialization activities, can be undertaken immediately. As cognitive function improves, patients can begin to participate in such treatment components as individual and group therapy, educational programs, and introduction to Alcoholics Anonymous, with a better chance for understanding—and perhaps for acting on—the information provided.

References

1. Albert, M.: Butters, N.; Rogers, S.; Pressman, J.; and Geller, A. A preliminary report: Nutritional levels and cognitive performance in chronic alcohol abusers. Drug and Alcohol Dependence 9(2):131-142, 1982.

2. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Third Edi tion, Revised. Washington, D.C.: American Psychiatric Association, 1987.

3. Becker, J.T. & Jaffe, J.H. Impaired memory for treatment-relevant information in inpatient men alcoholics. Journal of Studies on Alcohol 45(4):339-343, 1984.

4. Bergman, H.; Axelsson, G.; Idestrom, C.M.; Borg, S.; Hindmarsh, T.; Makower, J.; and Mutzell, S. Alcohol consumption, neuropsychological status and computer-tomographic findings on a random sample of men and women from the general population. Pharmacology Biochemistry & Behavior 18(Suppl. 1):501-505, 1983.

5. Blass, J.P. & Gibson, G.E. Abnormality of a thiamine-requiring enzyme in patients with Wernicke- Korsakoff syndrome. The New England Journal of Medicine 297(25):1367-1370, 1977.

6. Cutting, J.C. Alcohol cognitive impairment and aging: Still an uncertain relationship. British Journal of Addiction 83(9):995-997, 1988.

7. Donovan, D.M.; Walker, R.D.; and Kivlahan, D.R. Recovery and remediation of neuropsychological functions: Implications for alcoholism rehabilitation process and outcome. In: Parsons, O.A.; Butters, N., and Nathan, P.E., eds. Neuropsychology of Alcoholism: Implication for Diagnosis and Treatment. New York: The Guilford Press, 1987. pp. 339-360.

8. Eckardt, M.J. & Martin, P.R. Clinical assessment of cognition in alcoholism. Alcoholism: Clinical and Experimental Research 10(2):123-127, 1986.

9. Eckardt, M.J.; Rawlings, R.R.; Grau bard, B.I.; Faden, V.; Martin, P.R.; and Gottschalk, L.A. Neuropsy- chological performance and treatment outcome in male alcoholics. Alcoholism: Clinical and Experimen tal Research 12(1):88-93, 1988.

10. Emmerson, R.Y.; Dustman, D.A.; and Shearer, D.E. Neuropsychological performance of young nondrink ers, social drinkers, and long- and short-term sober alcoholics. Alcoholism: Clinical and Experimental Research 12(5):625-629, 1985.

11. Godfrey, H.P.D.; Spittle, B.J.; and Knight, R.G. Cognitive rehabilitation of amnesic alcoholics: A twelve month follow-up study. New Zealand Medical Journal 98(784):650-651, 1985.

12. Goldman, M.S. The role of time and practice in recovery of function of alcoholics. In: Parsons, O.A.; Butters, N.; and Nathan, P.E., eds. Neuropsychology of alcoholism: Implications for Diagnosis and Treatment. New York: The Guilford Press, 1987. pp.291-321.

13. Goldman, M.S. Neuropsychological recovery in alcoholics: Endogenous and exogenous processes. Alcoholism: Clinical and Experimental Research 10(2):136-144, 1986.

14. Grant, I.; Adams, K.E.; and Reed, R. Aging, Abstinence, and medical risk factors in the prediction of neuropsychological deficit among long-term alcoholics. Archives of General Psychiatry 41:710-718, 1984.

15. Horwath, T.B. Clinical spectrum and epidemiologic features of alcoholic dementia. In: Rankin, J.G., ed. Alcohol, Drugs, and Brain Damage. Toronto: Addition Research Center, 1975. pp.1-16.

16. Ishikawa, Y.; Meyer, J.S.; Tanahashi, N.; Hata, T.; Velez, M.; Fann, W.E.; Kandula P.; Motel, K.F.; and Rogers, R.L. Abstinence improves cerebral perfusion and brain volume in alcoholic neurotoxicity with out Wernicke-Korsakoff syndrome. Journal of Cerebral Blood Flow and Metabolism 6(1):86-94, 1986

17. Listman, W.A. Cerebral disorder in alcoholism: Syndromes of impairment. Brain 104(1):1-20, 1981.

18. Martin, P.R. & Eckardt, M.J. Pharmacological interventions in chronic organic brain syndromes associ ated with alcoholism. In: Naranjo, C.A. & Sellers, E.M., eds. Research Advances in New Psychopharmacological Treatments of Alcoholism. Amsterdam: Elsevier, 1985. pp.257-272.

19. McGrady, B.S. & Smith, D.E. Implications of cognitive impairment for the treatment of alcoholism. Alcoholism: Clinical and Experimental Research 19(2):145-149, 1986.

20. McGrady, B.S. Implications of neuropsychological research findings for the treatment and rehabilitation of alcoholics. In: Parsons, O.A.; Butters, N.; and Nathan, P.E., eds. Neuropsychology of Alcoholism: Implications for Diagnosis and Treatment. New York: The Guilford Press, 1987. pp.381-391.

21. McEntee, W.J. & Mair, R.G. Memory enhancement in Korsakoff;s Psychosis by clonidine: Further evidence for a noradrenergic deficit. Annals of Neurology 7(5):466-470, 1980.

22. Mukherjee, A.B.; Svoronos, S.; Ghazanfari, A.; et al. Transketolase abnormality in cultured fibroblasts from familial chronic alcoholic men and their male offspring. Journal of Clinical Investigation 79:1039- 1043, 1987.

23. Parker, E.S. & Noble, E.P. Alcohol consumption and cognitive functioning in social drinkers. Journal of Studies on Alcohol 38(7):1224-1232, 1977.

24. Parker, D.A.; Parker, E.S.; Brody, J.A.; and Schoenberg, R. Alcohol use and cognitive loss among employed men and women. American Journal of Public Health 73(5):521-526, 1983.

25. Parsons, O.A. & Leber, W.R. The relationship between cognitive dysfunction and brain damage in alcoholics: Causal, interactive, or epiphenomenal? Alcoholism: Clinical and Experimental Research 5:326-343, 1981.

24. Parsons, O.A. Cognitive functioning in sober social drinkers: A review and critique. Journal of Studies on Alcohol 47(2):101-114, 1986.

25. Porjesz, B. Begleiter, H. Human evoked brain potentials and alcohol. Alcoholism: Clinical and Experimen- tal Research 5(2):304-317, 1981.

26. Ron, M.A. Organic psychosyndromes in chronic alcoholics. British Journal of Addiction 74:353-358, 1979.

27. Tabakoff,TABAKOFF, B. & Petersen, R.C. Brain damage and alcoholism. The Counselor 6(5):13-16, 1988.

28. Tarter, R.E. & Edwards, K.L. Multifactorial etiology of neuropsychological impairment in alcoholics. Alcoholism: Clinical and Experimental Research 10(2):128-135, 1986. 

29. Victor, M. & Laureno, R. Neurologic complications of alcohol abuse: Epidemiologic aspects. Advances in Neurology 19:603-617, 1978.

30. Wilkinson, D.A. CT scan and neuropsychological assessments of alcoholism. In: Parson, O.A.; Butters, N.; and Nathan, P.E., eds. Neuropsychology of Alcoholism: Implications for Diagnosis and Treatment. New York: The Guilford Press, 1987. pp.76-102.

Source: National Institute on Alcohol Abuse (July 1999)                                                                 National Institutes of Health 

v Alcohol and Stress

The term "stress" often is used to describe the subjective feeling of pressure or tension. However, when scientists refer to stress, they mean the many objective physiological processes that are initiated in response to a stressor. As this chapter explains, the stress response is a complex process; the association between drinking and stress is more complicated still. Because both drinking behavior and an individual's response to stress are determined by multiple genetic and environmental factors (1-3), studying the link between alcohol consumption and stress may further our understanding of drinking behavior.

The Stress Response

The maintenance of the body's relatively steady internal state, or homeostasis, is essential for survival. The body's delicate balance of biochemical and physiological function is constantly challenged by a wide variety of stressors, including illness, injury, and exposure to extreme temperatures; by psychological factors, such as depression and fear; and by sexual activity and some forms of novelty-seeking. In response to stress, or even perceived stress, the body mobilizes an extensive array of physiological and behavioral changes in a process of continual adaptation, with the goal of maintaining homeostasis and coping with the stress ⁽⁴⁾.

The stress response is a highly complex, integrated network involving the central nervous system, the adrenal system, and the cardiovascular system. When homeostasis is threatened, the hypothalamus gland, at the base of the brain, initiates the stress response by secreting corticotropin releasing factor (CRF). CRF coordinates the stress response by triggering an integrated series of physiological and behavioral reactions. CRF is transported in blood within the brain and in seconds triggers the pituitary gland to release adrenocorticotropin hormone (ACTH), also referred to as corticotropin. ACTH then triggers secretion of glucocorticoid hormones (i.e., "steroids") by the adrenal glands, located at the top of the kidneys. Glucocorticoid hormones play a key role in the stress response and its termination ⁽⁴⁾.

Activation of the stress response affects smooth muscle, fat, the gastrointestinal tract, the kidneys, and many other organs and the body functions that they control ⁽⁴⁾. The stress response affects the body's regulation of temperature; appetite and satiety; arousal, vigilance, and attention; mood; and more ⁽⁴⁾. Physical adaptation to stress allows the body to redirect oxygen and nutrients to the stressed body site, where they are needed most ⁽⁴⁾.

Both the perception of what is stressful and the physiological response to stress vary considerably among individuals. These differences are based on genetic factors and environmental influences that can be traced back to infancy ⁽⁵⁾.

Stress is usually thought of as harmful; but when the stress response is acute and transient, homeostasis is maintained and no adverse effects result. Under chronic stress, however, when the body either fails to compensate or when it overcompensates, damage can occur ⁽⁴⁾. Such damage may include suppression of growth, immune system dysfunction, and cell damage resulting in impaired learning and memory (4,6).

Does Stress Influence Drinking?

Human research to clarify the connection between alcohol and stress usually has been conducted using either population surveys based on subject self-reports or experimental studies. In many but not all of these studies, individuals report that they drink in response to stress and do so for a variety of reasons. Studies indicate that people drink as a means of coping with economic stress, job stress, and marital problems, often in the absence of social support, and that the more severe and chronic the stressor, the greater the alcohol consumption ⁽⁷⁾. However, whether an individual will drink in response to stress appears to depend on many factors, including possible genetic determinants of drinking in response to stress, an individual's usual drinking behavior, one's expectations regarding the effect of alcohol on stress, the intensity and type of stressor, the individual's sense of control over the stressor, the range of one's responses to cope with the perceived stress, and the availability of social support to buffer the effects of stress (1,2,7,8). Some researchers have found that high levels of stress may influence drinking when alternative resources are lacking, when alcohol is accessible, and when the individual believes that alcohol will help to reduce the stress (1,8).

Numerous studies have found that stress increases alcohol consumption in animals ⁽⁹⁾ and that individual animals may differ in the amount of alcohol they consume in response to stress ⁽¹⁰⁾. Such differences may be related in part to an animal's experiencing chronic stress early in life: Prolonged stress in infancy may permanently alter the hormonal stress response and subsequent reactions to new stressors, including alcohol consumption ^(10,11). For example, monkeys who were reared by peers, a circumstance regarded as a stressor compared to mother-rearing, consumed twice as much alcohol as monkeys who were mother-reared ⁽¹⁰⁾. According to Viau and colleagues ⁽¹¹⁾, adult rats handled for the first 3 weeks of life demonstrate markedly reduced hormonal responses to a variety of stressors compared with rats not handled during this time ⁽¹¹⁾. In humans, Cloninger reported an association between certain types of alcoholism and adverse early childhood experiences ⁽¹²⁾.

Animal studies reporting a positive correlation between stress and alcohol consumption suggest that drinking may take place in response to chronic stress perceived as unavoidable (2,13). For instance, rats chronically exposed to unavoidable shock learn to be helpless or passive when faced with any new stressor including shock that is avoidable and to demonstrate increased alcohol preference compared with rats that received only avoidable shock ⁽²⁾. The rats exposed to unavoidable shock exhibit the hormonal changes indicative of the stress response, including increased levels of corticosteroid hormones ⁽²⁾.

Whether humans drink in response to uncontrollable stress is less clear, according to Pohorecky ⁽⁷⁾. In a review investigating the connection between alcohol consumption and stress, Pohorecky notes several studies in which researchers sampled individuals from areas affected by natural disaster. One study found that alcohol consumption increased by 30 percent in the 2 years following a flood at Buffalo Creek, West Virginia. Similarly, there was evidence of increased drinking in the towns surrounding Mount St. Helens following eruption of the volcano ⁽⁷⁾. Following the nuclear plant accident at Three Mile Island, however, alcohol consumption was infrequently used by those sampled as a means of coping with the resulting stress ⁽¹⁴⁾.

In both humans and animals, drinking appears to follow stress (2,3,7,13). Some human research, however, shows that drinking may take place in anticipation of or during times of stress ⁽¹⁵⁾.

Does Drinking Reduce or Induce Stress?

Some studies have reported that acute exposure to low doses of alcohol may reduce the response to a stressor in animals and humans. For example, low doses of alcohol reduced the stress response in rats subjected to strenuous activity in a running wheel ⁽³⁾. In humans, a low dose of alcohol improved performance of a complex mental problem-solving task under stressful conditions ⁽³⁾. However , in some individuals, at certain doses, alcohol may induce rather than reduce the body's stress response ⁽¹⁶⁾.

Much research demonstrates that alcohol actually induces the stress response by stimulating hormone release by the hypothalamus, pituitary, and adrenal glands (4,6,17,18). This finding has been demonstrated in animal studies. In one study with rats, the administration of alcohol initiated the physiological stress response, measured by increased levels of corticosterone ⁽¹⁹⁾. In addition to stimulating the hormonal stress response, chronic exposure to alcohol also results in an increase in adrenaline ⁽²⁰⁾.

Stress, Alcoholism, and Relapse

Stress may be linked to social drinking, and the physiological response to stress is different in actively drinking alcoholics compared with nonalcoholics ⁽¹⁷⁾. Researchers have found that animals preferring alcohol over water have a different physiological response to stress than animals that do not prefer alcohol ⁽²¹⁾. Nonetheless, a clear association between stress, drinking behavior, and the development of alcoholism in humans has yet to be established.

There may, however, in the already established alcoholic, be a clearer connection between stress and relapse: Among abstinent alcoholics, personally threatening, severe, and chronic life stressors may lead to alcohol relapse ^(15,22). Brown and colleagues ⁽¹⁵⁾ studied a group of men who completed inpatient alcoholism treatment and later experienced severe and prolonged psychosocial stress prior to and independent of any alcohol use. The researchers found that subjects who relapsed experienced twice as much severe and prolonged stress before their return to drinking as those who remained abstinent. In this study, severe psychosocial stress was related to relapse in alcoholic males who expected alcohol to reduce their stress. Those most vulnerable to stress-related relapse scored low on measures of coping skills, self-efficacy, and social support. Stress-related relapse was greatest among those who had less confidence in their ability to resist drinking and among those who relied on drinkers for social support. Although many factors can influence a return to drinking, Brown and colleagues note that stress may exert its greatest influence on the initial consumption of alcohol after a period of abstinence ⁽¹⁵⁾.

Conclusion

Stress is commonly believed to be a factor in the development of alcoholism (alcohol dependence). However, current science is more informative about the relationship between drinking and stress than about the relationship between stress and alcohol dependence.

Drinking alcohol produces physiological stress, that is, some of the body's responses to alcohol are similar to its responses to other stressors. Yet, individuals also drink to relieve stress. Why people should engage in an activity that produces effects similar to those they are trying to relieve is a paradox that we do not yet understand. One hypothesis is that stress responses are not exclusively unpleasant; the arousal associated with stress itself may be rewarding. This might explain, for example, compulsive gambling or repeated participation in "thrill-seeking" activities. Current studies may illuminate genetic variations in the physiological response to stress that are important in drinking or other activities with the potential to become addictive.

Training clinical staff to accurately appraise patients' drink-provoking stressors may help staff to identify individuals at risk for relapse. One route to relapse prevention is the teaching of coping skills where patients learn how to deal with these stressors without drinking. How this treatment approach compares with others remains of special interest.

References

1. Hunt, W.A., & Witt, E.D. Behavioral effects of alcohol ingestion: Implications for drug testing. Toxic Substances Journal 13:41-49, 1994.

2. Zobeck, T.S.; Stinson, F.S.; Grant, B.F.; & Bertolucci, D. Surveillance Report #26: Trends in Alcohol- Related Fatal Traffic Crashes, United States: 1979-91. Rockville, MD: National Institute on Alcohol Abuse and Alcoholism, Division of Biometry and Epidemiology, Nov. 1993.

3. Modell, J.G., & Mountz, J.M. Drinking and flying—The problem of alcohol use by pilots. New En gland Journal of Medicine 323(7):455-461, 1990.

4. Howland, J.; Smith, G.S.; Mangione, T.; Hingson, R.; DeJong, W.; & Bell, N. Missing the boat on drinking and boating. Journal of the American Medical Association 270(1):91-92, 1993.

5. Kolstad, J. Alcohol, drugs and transportation. Alcohol, Drugs and Driving 8(3-4):177-184, 1992.

6. Moody, D.E.; Crouch, D.J.; Smith, R.P.; Cresalia, C.W.; Francom, P.; Wilkins, D.G.; & Rollins, D.E. Drug and alcohol involvement in railroad accidents. Journal of Forensic Sciences 36(5):1474-1484, 1991.

7. Fisher, H.R.; Simpson, R.I.; & Kapur, B.M. Calculation of blood alcohol concentration (BAC) by sex, weight, number of drinks and time. Canadian Journal of Public Health 78(5):300-304, 1987.

8. Busloff, S.E. Can your eyes be used against you? The use of the horizontal gaze nystagmus test in the courtroom. Journal of Criminal Law and Criminology 84(1):203-238, 1993.

9. Katoh, Z. Slowing effects of alcohol on voluntary eye movements. Aviation, Space, and Environmen tal Medicine 59:606-610, 1988.

10. Baloh, R.W.; Sharma, S.; Moskowitz, H.; & Griffith, R. Effect of alcohol and marijuana on eye move ments. Aviation, Space, and Environmental Medicine 50(1):18-23, 1979.

11. Linnoila, M.; Erwin, C.W.; Ramm, D.; & Cleveland, W.P. Effects of age and alcohol on psychomotor performance of men. Journal of Studies on Alcohol 41(5):488-495, 1980.

12. Moskowitz, H., & Burns, M. Effects of alcohol on driving performance. Alcohol Health & Research World 14(1):12-14, 1990.

13. Mundt, J.C., & Ross, L.E. Methodological issues for evaluation of alcohol and other drug effects: Ex- amples from flight-simulator performance. Behavior Research Methods, Instruments, & Computers 25(3):360-365, 1993.

14. Morrow, D.; Leirer, V.; & Yesavage, J. The influence of alcohol and aging on radio communication during flight. Aviation, Space, and Environmental Medicine 61(1):12-20, 1990.

15. Howat, P.; Sleet, D.; & Smith, I. Alcohol and driving: Is the 0.05% blood alcohol concentration limit justified? Drug and Alcohol Review 10(2):151-166, 1991.

16. Billings, C.E.; Demosthenes, T.; White, T.R.; & O'Hara, D.B. Effects of alcohol on pilot performance in simulated flight. Aviation, Space, and Environmental Medicine 62(3):233-235, 1991.

17. Moskowitz, H.; Burns, M.M.; & Williams, A.F. Skills performance at low blood alcohol levels. Journal of Studies on Alcohol 46(6):482-485, 1985.

18. Dubowski, K.M. The Technology of Breath-Alcohol Analysis. DHHS Pub. No. (ADM)92-1728. Washington, DC: Supt. of Docs., U.S. Govt. Print. Off., 1992. (19) Chesher, G., & Greeley, J. Tolerance to the effects of alcohol. Alcohol, Drugs and Driving 8(2):93-106, 1992.

20. Morrow, D.; Yesavage, J.; Leirer, V.; Dolbert, N.; Taylor, J.; & Tinklenberg, J. The time-course of alcohol impairment of general aviation pilot performance in a Frasca 141 simulator. Aviation, Space, and Environmental Medicine 64(8):697-705, 1993.

21. Zador, P.L. Alcohol-related relative risk of fatal driver injuries in relation to driver age and sex. Journal of Studies on Alcohol 52(4):302-310, 1991.

22. Hingson, R. Prevention of alcohol-impaired driving. Alcohol Health & Research World 17(1):28-34, 1993.

23. Al-Lanqawi, Y.; Moreland, T.A.; McEwen, J.; Halliday, F.; Durnin, C.J.; & Stevenson, I.H. Ethanol kinetics: Extent of error in back extrapolation procedures. British Journal of Clinical Pharmacology 34(4):316-321, 1992.

24. Van Berkom, L.C. Chemical test evidence in DWI cases: Some issues and challenges. Alcohol, Drugs and Driving 7(3-4):229-234, 1991.

25. Canfield, D.V.; Kupiec, T.; & Huffine, E. Postmortem alcohol production in fatal aircraft accidents. Journal of Forensic Sciences 38(4):914-917, 1993.

26. Chao, T.C., & Lo, D.S.T. Relationship between postmortem blood and vitreous humor ethanol levels. American Journal of Forensic Medicine and Pathology 14(4):303-308, 1993.

Source: National Institute on Alcohol Abuse (July 1999)                                                                 National Institutes of Health 

v Alcohol and Sleep

The average adult sleeps 7.5 to 8 hours every night. Although the function of sleep is unknown, abundant evidence demonstrates that lack of sleep can have serious consequences, including increased risk of depressive disorders, impaired breathing, and heart disease. In addition, excessive daytime sleepiness resulting from sleep disturbance is associated with memory deficits, impaired social and occupational function, and car crashes (1,2). Alcohol consumption can induce sleep disorders by disrupting the sequence and duration of sleep states and by altering total sleep time as well as the time required to fall asleep (i.e., sleep latency). This chapter explores the effects of alcohol consumption on sleep patterns, the potential health consequences of alcohol consumption combined with disturbed sleep, and the risk for relapse in those with alcoholism who fail to recover normal sleep patterns.

Sleep Structure, Onset, and Arousal

Before discussing alcohol's effects on sleep, it is helpful to summarize some basic features of normal sleep. A person goes through two alternating states of sleep, characterized in part by different types of brain electrical activity (i.e., brain waves). These states are called slow wave sleep (SWS), because in this type of sleep the brain waves are very slow, and rapid eye movement (REM) sleep, in which the eyes undergo rapid movements although the person remains asleep.

Most sleep is the deep, restful SWS. REM sleep occurs periodically, occupying about 25 percent of sleep time in the young adult. Episodes of REM normally recur about every 90 minutes and last 5 to 30 minutes. REM sleep is less restful than SWS and is usually associated with dreaming. Although its function is unknown, REM appears to be essential to health. In rats, deprivation of REM sleep can lead to death within a few weeks ⁽³⁾. In addition, a transitional stage of light sleep occurs at intervals throughout the sleep period ⁽⁴⁾.

Sleep was formerly attributed to decreased activity of brain systems that maintain wakefulness. More recent data indicate that sleep, like consciousness, is an active process. Sleep is controlled largely by nerve centers in the lower brain stem, where the base of the brain joins the spinal cord. Some of these nerve cells produce serotonin, a chemical messenger associated with sleep onset ⁽⁵⁾ and with the regulation of SWS. Certain other nerve cells produce norepinephrine, which helps regulate REM sleep and facilitates arousal ⁽⁶⁾. The exact roles and interactions of these and other chemical messengers in orchestrating sleep patterns are not known ⁽⁶⁾. Significantly, however, alcohol consumption affects the function of these and other chemical messengers that appear to influence sleep.

Alcohol and Sleep in Those Without Alcoholism

Alcohol consumed at bedtime, after an initial stimulating effect, may decrease the time required to fall asleep. Because of alcohol's sedating effect, many people with insomnia consume alcohol to promote sleep. However, alcohol consumed within an hour of bedtime appears to disrupt the second half of the sleep period ⁽⁷⁾. The subject may sleep fitfully during the second half of sleep, awakening from dreams and returning to sleep with difficulty. With continued consumption just before bedtime, alcohol's sleep-inducing effect may decrease, while its disruptive effects continue or increase ⁽⁸⁾. This sleep disruption may lead to daytime fatigue and sleepiness. The elderly are at particular risk, because they achieve higher levels of alcohol in the blood and brain than do younger persons after consuming an equivalent dose. Bedtime alcohol consumption among older persons may lead to unsteadiness if walking is attempted during the night, with increased risk of falls and injuries ⁽³⁾.

Alcoholic beverages are often consumed in the late afternoon (e.g., at "happy hour" or with dinner) without further consumption before bedtime. Studies show that a moderate dose1 of alcohol consumed as much as 6 hours before bedtime can increase wakefulness during the second half of sleep. By the time this effect occurs, the dose of alcohol consumed earlier has already been eliminated from the body, suggesting a relatively long-lasting change in the body's mechanisms of sleep regulation ^(7,8).

The adverse effects of sleep deprivation are increased following alcohol consumption. Subjects administered low doses of alcohol following a night of reduced sleep perform poorly in a driving simulator, even with no alcohol left in the body ^(9,10). Reduced alertness may potentially increase alcohol's sedating effect in situations such as rotating sleep-wake schedules (e.g., shift work) and rapid travel across multiple time zones (i.e., jet lag) ⁽⁹⁾. A person may not recognize the extent of sleep disturbance that occurs under these circumstances, increasing the danger that sleepiness and alcohol consumption will co-occur.

Alcohol and Breathing Disorders

Approximately 2 to 4 percent of Americans suffer from obstructive sleep apnea (OSA), a disorder in which the upper air passage (i.e., the pharynx, located at the back of the mouth) narrows or closes during sleep ⁽¹¹⁾. The resulting episode of interrupted breathing (i.e., apnea) wakens the person, who then resumes breathing and returns to sleep. Recurring episodes of apnea followed by arousal can occur hundreds of times each night, significantly reducing sleep time and resulting in daytime sleepiness. Those with alcoholism appear to be at increased risk for sleep apnea, especially if they snore ⁽¹²⁾. In addition, moderate to high doses of alcohol consumed in the evening can lead to narrowing of the air passage ^(13,14), causing episodes of apnea even in persons who do not otherwise exhibit symptoms of OSA. Alcohol's general depressant effects can increase the duration of periods of apnea, worsening any preexisting OSA ⁽¹⁴⁾.

OSA is associated with impaired performance on a driving simulator as well as with an increased rate of motor vehicle crashes in the absence of alcohol consumption (9,10). Among patients with severe OSA, alcohol consumption at a rate of two or more drinks per day is associated with a fivefold increased risk for fatigue-related traffic crashes compared with OSA patients who consume little or no alcohol ⁽¹⁵⁾. In addition, the combination of alcohol, OSA, and snoring increases a person's risk for heart attack, arrhythmia, stroke, and sudden death ⁽¹⁶⁾.

Age-Related Effects and the Impact of Drinking

Little research has been conducted on the specific effects of alcohol on sleep states among different age groups. Scher ⁽¹⁷⁾ investigated the effects of prenatal alcohol exposure on sleep patterns in infants. Measurements of brain electrical activity demonstrated that infants of mothers who consumed at least one drink per day during the first trimester of pregnancy exhibited sleep disruptions and increased arousal compared with infants of nondrinking women. Additional studies revealed that infants exposed to alcohol in mothers' milk fell asleep sooner but slept less overall than those who were not exposed to alcohol ⁽¹⁸⁾. The exact significance of these findings is unclear.

Normal aging is accompanied by a gradual decrease in SWS and an increase in nighttime wakefulness. People over 65 often awaken 20 times or more during the night, leading to sleep that is less restful and restorative ⁽³⁾. Age-related sleep deficiencies may encourage the use of alcohol to promote sleep, while increasing an older person's susceptibility to alcohol-related sleep disturbances ^(3,19). Potential sources of inconsistency among study results include different doses of alcohol employed and failure to screen out subjects with preexisting sleep disorders ⁽³⁾.

Effects of Alcohol on Sleep in Those With Alcoholism

Active Drinking and Withdrawal. Sleep disturbances associated with alcoholism include increased time required to fall asleep, frequent awakenings, and a decrease in subjective sleep quality associated with daytime fatigue ⁽³⁾. Abrupt reduction of heavy drinking can trigger alcohol withdrawal syndrome, accompanied by pronounced insomnia with marked sleep fragmentation. Decreased SWS during withdrawal may reduce the amount of restful sleep. It has been suggested that increased REM may be related to the hallucinations that sometimes occur during withdrawal. In patients with severe withdrawal, sleep may consist almost entirely of brief periods of REM interrupted by numerous awakenings (3,20).

Recovery and Relapse. Despite some improvement after withdrawal subsides, sleep patterns may never return to normal in those with alcoholism, even after years of abstinence (3,21). Abstinent alcoholics tend to sleep poorly, with decreased amounts of SWS and increased nighttime wakefulness that could make sleep less restorative and contribute to daytime fatigue ⁽²²⁾. Resumption of heavy drinking leads to increased SWS and decreased wakefulness. This apparent improvement in sleep continuity may promote relapse by contributing to the mistaken impression that alcohol consumption improves sleep (23-25). Nevertheless, as drinking continues, sleep patterns again become disrupted ⁽³⁾.

Researchers have attempted to predict relapse potential using measures of sleep disruption. Gillin and colleagues ⁽²⁶⁾ measured REM sleep in patients admitted to a 1-month alcoholism treatment program. Higher levels of REM predicted those who relapsed within 3 months after hospital discharge in 80 percent of the patients. A review of additional research ⁽³⁾ concluded that those who eventually relapsed exhibited a higher proportion of REM and a lower proportion of SWS at the beginning of treatment, compared with those who remained abstinent. Although additional research is needed, these findings may facilitate early identification of patients at risk for relapse and allow clinicians to tailor their treatment programs accordingly.

Conclusion

According to recent news reports, Americans are at risk for a variety of sleep-related health problems. Alcohol use affects sleep in a number of ways and can exacerbate these problems. Because alcohol use is widespread, it is important to understand how this use affects sleep to increase risk for illness. For example, it is popularly believed that a drink before bedtime can aid falling asleep. However, it also can disrupt normal sleep patterns, resulting in increased fatigue and physical stress to the body. Alcohol use can aggravate sleeping disorders, such as sleep apnea; those with such disorders should be cautious about alcohol use. Many nursing mothers are still regularly advised by their physicians to have a drink to promote lactation (so-called let-down reflex). Babies who receive alcohol in breast milk are known to have disrupted sleeping patterns. Because researchers do not yet know what effect this disruption has on nursing infants, physicians should reconsider this advice.

Alcoholism treatment also can be complicated by sleep problems during withdrawal and during subsequent behavioral treatment, where sleeping problems experienced by many recovering alcoholics may increase their risk for relapse. Because it is likely that alcohol may act on the same neurotransmitters involved in sleep, increased knowledge of alcohol's effects on the brain will help to promote new therapeutic techniques for alcohol-related sleep disorders and, perhaps, improve the chance for long-term sobriety.

References

1. Roehrs, T., and Roth, T. Alcohol-induced sleepiness and memory function. Alcohol Health Res World 19(2):130-135, 1995.

2. Kupfer, D.J., and Reynolds, C.F. Management of insomnia. N Engl J Med 336(5):341-346, 1997.

3. Aldrich, M.S. Effects of alcohol on sleep. In: Lisansky Gomberg, E.S., et al., eds. Alcohol Problems and Aging. NIAAA Research Monograph No. 33. NIH Pub. No. 98-4163. Bethesda, MD: NIAAA, in press.

4. Guyton, A.C. Human Physiology and Mechanisms of Disease. 5th ed. Philadelphia: W.B. Saunders, 1992.

5. Zajicek, K., et al. Rhesus macaques with high CSF 5-HIAA concentrations exhibit early sleep onset. Neuropsychopharmacology, in press.

6. Shepherd, G.M. Neurobiology. 3d ed. New York: Oxford University Press, 1994.

7. Landolt, H.-P., et al. Late-afternoon ethanol intake affects nocturnal sleep and the sleep EEG in middle- aged men. J Clin Psychopharmacol 16(6):428-436, 1996.

8. Vitiello, M.V. Sleep, alcohol and alcohol abuse. Addict Biol (2):151-158, 1997.

9. Roehrs, T., et al. Sleepiness and ethanol effects on simulated driving. Alcohol Clin Exp Res 18(1):154- 158, 1994.

10. Krull, K.R., et al. Simple reaction time event-related potentials: Effects of alcohol and sleep depriva tion. Alcohol Clin Exp Res 17(4):771-777, 1993.

11. Strollo, P.J., and Rogers, R.M. Obstructive sleep apnea. N Engl J Med 334(2):99-104, 1996.

12. Aldrich, M.S., et al. Sleep-disordered breathing in alcoholics: Association with age. Alcohol Clin Exp Res 17(6):1179-1183, 1993.

13. Mitler, M.M., et al. Bedtime ethanol increases resistance of upper airways and produces sleep apneas in asymptomatic snorers. Alcohol Clin Exp Res 12(6):801-805, 1988.

14. Dawson, A., et al. Effect of bedtime ethanol on total inspiratory resistance and respiratory drive in normal nonsnoring men. Alcohol Clin Exp Res 17(2):256-262, 1993.

15. Aldrich, M.S., and Chervin, R.D. Alcohol use, obstructive sleep apnea, and sleep-related motor vehicle accidents. Sleep Res, in press.

16. Bassetti, C., and Aldrich, M.S. Alcohol consumption and sleep apnea in patients with TIA and ischemic stroke. Sleep Res 25:400, 1996.

17. Scher, M., et al. The effects of prenatal alcohol and marijuana exposure: Disturbances in neonatal sleep cycling and arousal. Pediatr Res 24(1):101-105, 1988.

18. Mennella, J.A., and Gerrish, C.J. Effects of exposure to alcohol in mothers' milk on the infants' sleep and activity levels. Pediatrics, in press.

19. Block, A.J., et al. Effect of alcohol ingestion on breathing and oxygenation during sleep. Am J Med 80(4):595-600, 1986.

20. Allen, R.P., et al. Electroencephalographic (EEG) sleep recovery following prolonged alcohol intoxica tion in alcoholics. J Ner and Ment Dis 153(6):424-433, 1971.

21. Williams, H.L., and Rundell, Jr., O.H. Altered sleep physiology in chronic alcoholics: Reversal with abstinence. Alcohol Clin Exp Res 5(2):318-325, 1981.

22. Gillin, J.C., et al. EEG sleep studies in "pure" primary alcoholism during subacute withdrawal: Relation- ships to normal controls, age, and other clinical variables. Bio Psychiatry 27:477-488, 1990.

23. Lester, B.K., et al. Chronic alcoholism, alcohol and sleep. In: Gross, M.M., ed. Advances in Experimen tal Medicine and Biology: Volume 35. Alcohol Intoxication and Withdrawal: Experimental Studies. New York: Plenum Press, 1973. pp. 261-279.

24. Skoloda, T.E., et al. Sleep quality reported by drinking and non-drinking alcoholics. In: Gottheil, E.L., et al., eds. Addiction Research and Treatments: Converging Trends. New York: Pergamon Press, 1979. pp. 102-112.

25. Zarcone, V., et al. Alcohol, sleep and cerebrospinal fluid changes in alcoholics: Cyclic AMP and biogenicamine metabolites in CSF. In: Gross, M.M., ed. Advances in Experimental Medicine and Biology: Volume 85A. Alcohol Intoxication and Withdrawal—IIIa: Biological Aspects of Ethanol. New York: Plenum Press, 1977. pp. 593-599.

26. Gillin, J.C., et al. Increased pressure for rapid eye movement sleep at time of hospital admission predicts relapse in nondepressed patients with primary alcoholism at 3-month follow-up. Arch Gen Psychiatry 51:189-197, 1994.

Source: National Institute on Alcohol Abuse (July 1999)                                                                 National Institutes of Health

v Alcohol and Aging

Persons age 65 and older constitute the fastest growing segment of the American population. Although the extent of alcoholism among the elderly is debated, the diagnosis and treatment of alcohol problems are likely to become increasingly important as the elderly population grows. This chapter reviews recent research on the extent of alcohol consumption and associated problems among the elderly.

Drinking Prevalence and Patterns Among the Elderly

Surveys of different age groups in the community suggest that the elderly, generally defined as persons older than 65, consume less alcohol and have fewer alcohol-related problems than younger persons. However, some surveys that track individuals over time suggest that a person's drinking pattern remains relatively stable with age, perhaps reflecting societal norms that prevailed when the person began drinking (1). For example, persons born after World War II may show a higher prevalence of alcohol problems than persons born in the 1920's, when alcohol use was stigmatized (2). In addition, some people increase their alcohol consumption later in life, often leading to late-onset alcoholism (1).

In contrast to most studies of the general population, surveys conducted in health care settings have found increasing prevalence of alcoholism among the older population (3). Surveys indicate that 6 to 11 percent of elderly patients admitted to hospitals exhibit symptoms of alcoholism, as do 20 percent of elderly patients in psychiatric wards and 14 percent of elderly patients in emergency rooms (4). In acute-care hospitals, rates of alcohol-related admissions for the elderly are similar to those for heart attacks (i.e., myocardial infarction) (5). Yet hospital staff are significantly less likely to recognize alcoholism in an older patient than in a younger patient (6).

The prevalence of problem drinking in nursing homes is as high as 49 percent in some studies, depending in part on survey methods (7). The high prevalence of problem drinking in this setting may reflect a trend toward using nursing homes for short-term alcoholism rehabilitation stays (8). Late-onset alcohol problems also occur in some retirement communities, where drinking at social gatherings is often the norm (9).

Comparison among studies is complicated by the diversity of the subject population: The "elderly" span more than four decades in age and range from the actively employed to the disabled and institutionalized. Consequently, different studies employ different definitions of the term (8). In addition, surveys of alcohol consumption among the elderly are subject to potential sources of error for some of the following reasons:

    •     Questionnaires customarily used to screen for alcoholism may be inappropriate for the elderly, who may not exhibit the social, legal, and occupational consequences of alcohol misuse generally used to diagnose problem drinkers (10,11).

    •     Alcohol-related consequences of heavy drinking can be mistaken for medical or psychiatric conditions common among the elderly. Such consequences may include depression, insomnia, poor nutrition, congestive heart failure, and frequent falls (1).

    •     Because alcohol-related illnesses are a major cause of premature death, excess mortality among heavy drinkers may leave a surviving older population who consume less alcohol (1).

Combined Effects of Alcohol and Aging

Although many medical and other problems are associated with both aging and alcohol misuse, the extent to which these two factors may interact to contribute to disease is unclear. Some examples of potential alcohol-aging interactions include the following:

    •     The incidence of hip fractures in the elderly increases with alcohol consumption (12,13). This increase can be explained by falls while intoxicated combined with a more pronounced decrease in bone density in elderly persons with alcoholism compared with elderly nonalcoholics (4).

    •     Studies of the general population suggest that moderate alcohol consumption (up to two drinks per day for men and one drink per day for women) may confer some protection from heart disease (14,15).1 Although research on this issue is limited, evidence shows that moderate drinking also has a protective effect among those older than 65 (16). Because of age-related body changes in both men and women, NIAAA recommends that persons older than 65 consume no more than one drink per day (17).

    •     Alcohol-involved traffic crashes are an important cause of trauma and death in all age groups. The elderly are the fastest growing segment of the driving population. A person's crash risk per mile increases starting at age 55, exceeding that of a young, beginning driver by age 80. In addition, older drivers tend to be more seriously injured than younger drivers in crashes of equivalent magnitude (18). Age may interact with alcoholism to increase driving risk. For example, an elderly driver with alcoholism is more impaired than an elderly driver without alcoholism after consuming an equivalent dose of alcohol, and has a greater risk of a crash (18).

    •     Long-term alcohol consumption activates enzymes that break down toxic substances, includ ing alcohol. Upon activation, these enzymes may also break down some common prescrip tion medications. The average person older than 65 takes two to seven prescription medica tions daily. Alcohol-medication interactions are especially common among the elderly, in creasing the risk of negative health effects and potentially influencing the effectiveness of the medications (19,20).

    •     Depressive disorders are more common among the elderly than among younger people and tend to co-occur with alcohol misuse (11,21). Data from the National Longitudinal Alcohol

Epidemiologic Survey demonstrate that, among persons older than 65, those with alcoholism are approximately three times more likely to exhibit a major depressive disorder than are those without alcoholism (22). In one survey, 30 percent of 5,600 elderly patients with alcoholism were found to have concurrent psychiatric disorders (23). Among persons older than 65, moderate and heavy drinkers are 16 times more likely than nondrinkers to die of suicide, which is commonly associated with depressive disorders (24).

Does Aging Increase Sensitivity to Alcohol?

Limited research suggests that sensitivity to alcohol's health effects may increase with age. One reason is that the elderly achieve a higher blood alcohol concentration (BAC) than younger people after consuming an equal amount of alcohol. The higher BAC results from an age-related decrease in the amount of body water in which to dilute the alcohol. Therefore, although they can metabolize and eliminate alcohol as efficiently as younger persons, the elderly are at increased risk for intoxication and adverse effects (25).

Aging also interferes with the body's ability to adapt to the presence of alcohol (i.e., tolerance). Through a decreased ability to develop tolerance, elderly subjects persist in exhibiting certain effects of alcohol (e.g., incoordination) at lower doses than younger subjects whose tolerance increases with increased consumption (26). Thus, an elderly person can experience the onset of alcohol problems even though his or her drinking pattern remains unchanged. These conclusions are supported by laboratory experiments with rats that indicate age-related changes in tolerance to alcohol (27).

Aging, Alcohol, and the Brain

Aging and alcoholism produce similar deficits in intellectual (i.e., cognitive) and behavioral functioning. Alcoholism may accelerate normal aging or cause premature aging of the brain. Using magnetic resonance imaging techniques, Pfefferbaum and colleagues (28) found more brain tissue loss in subjects with alcoholism than in those without alcoholism, even after their ages had been taken into account. In addition, older subjects with alcoholism exhibited more brain tissue loss than younger subjects with alcoholism, often despite similar total lifetime alcohol consumption. These results suggest that aging may render a person more susceptible to alcohol's effects (29).

The frontal lobes of the brain are especially vulnerable to long-term heavy drinking (28). Research shows that shrinkage of the frontal lobes increases with alcohol consumption and is associated with intellectual impairment in both older and younger subjects with alcoholism (30). In addition, older persons with alcoholism are less likely to recover from cognitive deficits during abstinence than are younger persons with alcoholism (28).

Age-related changes in volume also occur in the cerebellum, a part of the brain involved in regulating posture and balance (31). Thus, long-term alcohol misuse could accelerate the development of age-related postural instability, increasing the likelihood of falls (32).

Treatment of Alcoholism in the Elderly

Studies indicate that elderly persons with alcohol problems are at least as likely as younger persons to benefit from alcoholism treatment. The outcomes are more favorable among persons with shorter histories of problem drinking (i.e., late onset). Additionally, although evidence is not entirely consistent, some studies suggest that treatment outcomes may be improved by treating older patients in age-segregated settings (33,23).

The use of medications to promote abstinence has not been studied extensively in elderly subjects. However, one study has suggested that naltrexone (ReVia®) may help prevent relapse to alcoholism in subjects ages 50 to 70 (34). Results of research in animals suggest that age-related alterations in specific chemical messenger systems in the brain may alter the effectiveness of medications used to treat alcoholism and mental disorders (35).

Conclusion

Because alcohol problems among older persons often are mistaken for other conditions associated with the aging process, alcohol abuse and alcoholism in this population may go undiagnosed and untreated or be treated inappropriately. Health care providers should discuss alcohol use with their older patients as a part of routine care. Advice to older patients should include the medical conditions common to older people, such as high blood pressure and ulcers, that can be worsened by drinking and over-the-counter and prescription drugs that can be dangerous, or fatal, when mixed with alcohol. Where there is no medical condition that would preclude the use of alcohol, older patients should be advised to limit their alcohol intake to one drink per day. Finally, health care providers, including emergency room personnel and admitting physicians who suspect an alcohol problem in their elderly patients, should refer such patients to treatment. It is a mistaken belief that older persons have little to gain from alcoholism treatment; each stage of life has its own rewards for sobriety, and they are all valuable.

References

1. National Institute on Alcohol Abuse and Alcoholism. Alcohol Alert No. 2: Alcohol and Aging. Bethesda, MD: the Institute, 1988.

2. Beresford, T.P. Alcoholic elderly: Prevalence, screening, diagnosis, and prognosis. In: Beresford, T., and Gomberg, E. Alcohol and Aging. New York: Oxford University Press, 1995. pp. 3-18.

3. Adams, W.L. Interactions between alcohol and other drugs. In: Gurnack, A.M., ed. Older Adults' Misuse of Alcohol, Medicines, and Other Drugs: Research and Practice Issues. New York: Springer, 1997. pp. 185-205.

4. Council on Scientific Affairs, American Medical Association. Alcoholism in the elderly. JAMA 275(10):797-801, 1996.

5. Adams, W.L.; Yuan, Z.; Barboriak, J.J.; et al. Alcohol-related hospitalizations of elderly people. JAMA 270(10):1222-1225, 1993.

6. Curtis, J.R.; Geller, G.; Stokes, E.J.; et al. Characteristics, diagnosis, and treatment of alcoholism in elderly patients. J Am Geriatr Soc 37:310-316, 1989.

7. Joseph, C.L. Misuse of alcohol and drugs in the nursing home. In: Gurnack, A.M., ed. Older Adults' Misuse of Alcohol, Medicines, and Other Drugs: Research and Practice Issues. New York: Springer, 1997. pp. 228-254.

8. Adams, W.L., and Cox, N.S. Epidemiology of problem drinking among elderly people. In: Gurnack, A.M., ed. Older Adults' Misuse of Alcohol, Medicines, and Other Drugs: Research and Practice Issues. New York: Springer, 1997. pp. 1-23.

9. Atkinson, R.M.; Tolson, R.L.; and Turner, J.A. Late versus early onset problem drinking in older men. Alcohol Clin Exp Res 14(4):574-579, 1990.

10. Lakhani, N. Alcohol use amongst community-dwelling elderly people: A review of the literature. J Adv Nurs 25(6):1227-1232, 1997.

11. Adams, W.L. Late life outcomes: Health services use and the clinical encounter. In: Gomberg, E.S.L.; Hegedus, A.M.; and Zucker, R.A. Alcohol Problems and Aging. NIAAA Research Monograph No. 33. NIH Pub. No. 98-4163. Bethesda, MD: NIAAA, 1998.

12. Bikle, D.D.; Stesin, A.; Halloran, B.; et al. Alcohol-induced bone disease: Relationship to age and parathyroid hormone levels. Alcohol Clin Exp Res 17(3):690-695, 1993.

13. Schnitzler, C.M.; Menashe, L.; Sutton, C.G.; et al. Serum biochemical and haematological markers of alcohol abuse in patients with femoral neck and intertrochanteric fractures. Alcohol Alcohol 23(2):127- 132, 1988.

14. Klatsky, A.L.; Armstrong, M.A.; and Friedman, G.D. Alcohol and mortality. Ann Intern Med 117(8):646-654, 1992.

15. Thun, M.J.; Peto, R.; Lopez, A.D.; et al. Alcohol consumption and mortality among middle-aged and elderly U.S. adults. New Engl J Med 337(24):1705-1714, 1997.

16. Fried, L.P.; Kronmal, R.A.; Newman, A.B.; et al. Risk factors for 5-year mortality in older adults: The cardiovascular health study. JAMA 279(8):585-592, 1998.

17. Dufour, M.C.; Archer, L.; and Gordis, E. Alcohol and the elderly. Clin Geriatr Med 8(1):127-141, 1992.

18. Waller, P.F. Alcohol, aging, and driving. In: Gomberg, E.S.L.; Hegedus, A.M.; and Zucker, R.A. Alcohol Problems and Aging. NIAAA Research Monograph No. 33. NIH Pub. No. 98-4163. Bethesda, MD: NIAAA, 1998.

19. Korrapati, M.R., and Vestal, R.E. Alcohol and medications in the elderly: Complex interactions. In: Beresford, T., and Gomberg, E., eds. Alcohol and Aging. New York: Oxford University Press, 1995. pp. 42-55.

20. National Institute on Alcohol Abuse and Alcoholism. Alcohol Alert. No. 27: Alcohol-Medication Interactions. Bethesda, MD: the Institute, 1995.

21. Welte, J.W. Stress and elderly drinking. In: Gomberg, E.S.L.; Hegedus, A.M.; and Zucker, R.A. Alcohol Problems and Aging. NIAAA Research Monograph No. 33. NIH Pub. No. 98-4163. Bethesda, MD: NIAAA, 1998.

22. Grant, B.F., and Harford, T.C. Comorbidity between DSM-IV alcohol use disorders and major depres sion: Results of a national survey. Drug Alcohol Depend (39):197-206, 1995.

23. Moos, R.; Brennan, P.; and Schutte, K. Life context factors, treatment, and late-life drinking behavior. In: Gomberg, E.S.L.; Hegedus, A.M.; and Zucker, R.A. Alcohol Problems and Aging. NIAAA Re search Monograph No. 33. NIH Pub. No. 98-4163. Bethesda, MD: NIAAA, 1998.

24. Grabbe, L.; Demi, A.; Camann, M.A.; et al. The health status of elderly persons in the last year of life: A comparison of deaths by suicide, injury, and natural causes. Am J Public Health 87(3):434-437, 1997.

25. Dufour, M., and Fuller, R.K. Alcohol in the elderly. Annu Rev Med 46:123-132, 1995.

26. Kalant, H. Pharmacological interactions of aging and alcohol. In: Gomberg, E.S.L.; Hegedus, A.M.; and Zucker, R.A. Alcohol Problems and Aging. NIAAA Research Monograph No. 33. NIH Pub. No. 98-4163. Bethesda, MD: NIAAA, 1998.

27. Spencer, R.L., and McEwen, B.S. Impaired adaptation of the hypothalamic-pituitary-adrenal axis to chronic ethanol stress in aged rats. Neuroendocrinology 65(5):353-359, 1997.

28. Pfefferbaum, A.; Sullivan, E.V.; Mathalon, D.H.; et al. Frontal lobe volume loss observed with magnetic resonance imaging in older chronic alcoholics. Alcohol Clin Exp Res 21(3):521-529, 1997.

29. Oscar-Berman, M.; Shagrin, B.; Evert, D.L.; et al. Impairments of brain and behavior: The neurological effects of alcohol. Alcohol Health Res World 21(1):65-75, 1997.

30. Harper, C.; Kril, J.; Sheedy, D.; et al. Neuropathological studies: The relationship between alcohol and aging. In: Gomberg, E.S.L.; Hegedus, A.M.; and Zucker, R.A. Alcohol Problems and Aging. NIAAA Research Monograph No. 33. NIH Pub. No. 98-4163. Bethesda, MD: NIAAA, 1998.

31. Sullivan, E.V.; Rosenbloom, M.J.; Deshmukh, A.; et al. Alcohol and the cerebellum. Alcohol Health Res World 19(2):138-141, 1995.

32. Malmivaara, A.; Heliovaara, M.; Knekt, P.; et al. Risk factors for injurious falls leading to hospitalization or death in a cohort of 19,500 adults. Am J Epidemiol 138(6):384-394, 1993.

33. Atkinson, R. Treatment programs for aging alcoholics. In: Beresford, T., and Gomberg, E., eds. Alcohol and Aging. New York: Oxford University Press, 1995. pp. 186-210.

34. Oslin, D.W., and Mellow, A.M. Neurotransmitter-based therapeutic strategies in late-life alcoholism and other addictions. In: Gomberg, E.S.L.; Hegedus, A.M.; and Zucker, R.A. Alcohol Problems and Aging. NIAAA Research Monograph No. 33. NIH Pub. No. 98-4163. Bethesda, MD: NIAAA, 1998.

35. Druse, M.J.; Tajuddin, N.F.; and Ricken, J.D. Effects of chronic ethanol consumption and aging on 5- HT2A receptors and 5-HT reuptake sites. Alcohol Clin Exp Res 21(7):1157-1164, 1997.

Source: National Institute on Alcohol Abuse                                                                               National Institutes of Health