52.  Screening for Problem Drinking

RECOMMENDATION

Screening to detect problem drinking is recommended for all adult and adolescent patients.

Screening should involve a careful history of alcohol use and/or the use of standardized screening

questionnaires (see Clinical Intervention). Routine measurement of biochemical markers is not

recommended in asymptomatic persons. Pregnant women should be advised to limit or cease

drinking during pregnancy. Although there is insufficient evidence to prove or disprove harms

from light drinking in pregnancy, recommendations that women abstain from alcohol during

pregnancy may be made on other grounds (see Clinical Intervention). All persons who use alcohol

should be counseled about the dangers of operating a motor vehicle or performing other potentially

dangerous activities after drinking alcohol.

Burden of Suffering

Over half a million Americans are under treatment for alcoholism, but there is growing

recognition that alcoholism (i.e., alcohol dependence) represents only one end of the spectrum of

"problem drinking."1 Many problem drinkers have medical or social problems attributable to

alcohol (i.e., alcohol abuse or "harmful drinking") without typical signs of dependence,2,3 and

other asymptomatic drinkers are at risk for future problems due to chronic heavy alcohol

consumption or frequent binges (i.e., "hazardous drinking"). Heavy drinking (more than 5 drinks

per day, 5 times per week) is reported by 10% of adult men and 2% of women.4 In large

community surveys using detailed interviews,5-8 the prevalence of alcohol abuse and dependence

in the previous year among men was 17-24% among 18-29-year-olds, 11-14% among 30-

44-year-olds, 6-8% among 45-64-year-olds, and 1-3% for men over 65; among women in the

corresponding age groups, prevalence of abuse or dependence was 4-10%, 2-4%, 1-2%, and less

than 1%, respectively. Problem drinking is even more common among patients seen in the

primary care setting (8-20%).9

Medical problems due to alcohol dependence include alcohol withdrawal syndrome, psychosis,

hepatitis, cirrhosis, pancreatitis, thiamine deficiency, neuropathy, dementia, and

cardiomyopathy.10 Nondependent heavy drinkers, however, account for the majority of

alcohol-related morbidity and mortality in the general population.1 There is a dose-response

relationship between daily alcohol consumption and elevations in blood pressure and risk of

cirrhosis, hemorrhagic stroke, and cancers of the oropharynx, larynx, esophagus, and liver.11-

13 A number of studies have reported a modest increase in breast cancer among women drinking 2

drinks per day or more, but a causal connection has not yet been proven.14 Three large cohort

studies, involving over 500,000 men and women, observed increasing all-cause mortality

beginning at 4 drinks per day in men11,12 and above 2 drinks per day in women.15 Women

achieve higher blood alcohol levels than do men, due to smaller size and slower metabolism.11,15

Compared to nondrinkers and light drinkers, overall mortality was 30-38% higher among men,

and more than doubled among women, who drank 6 or more drinks per day.11,12 Of the more than

100,000 deaths attributed to alcohol annually, nearly half are due to unintentional and intentional

injuries,16 including 44% of all traffic fatalities in 199317 and a substantial proportion of

deaths from fires, drownings, homicides, and suicides (see Chapters 50, 51, 57, 58, and 59).

The social consequences of problem drinking are often as damaging as the direct medical

consequences. Nearly 20% of drinkers report problems with friends, family, work, or police due

to drinking.10 Persons who abuse alcohol have a higher risk of divorce, depression, suicide,

domestic violence, unemployment, and poverty (see Chapters 49-51).10 Intoxication may lead to

unsafe sexual behavior that increases the risk of sexually transmitted diseases, including human

immunodeficiency virus (HIV). Finally, an estimated 27 million American children are at risk for

abnormal psychosocial development due to the abuse of alcohol by their parents.25

Moderate alcohol consumption has favorable effects on the risk of coronary heart disease

(CHD).18-23 CHD incidence and mortality rates are 20-40% lower in men and women who drink

1-2 drinks/day than in nondrinkers.15,21,22 A meta-analysis of epidemiologic studies suggests

little additional benefit of drinking more than 0.5 drinks per day.20 The exact mechanism for the

protective effect of alcohol is not known but may involve increases in high-density lipoprotein23

and/or fibrinolytic mediators.24

Alcohol Use during Pregnancy.  The proportion of pregnant women who report drinking has

declined steadily in the U.S.26 Recent surveys indicate 12-14% of pregnant women continue to

consume some alcohol,27,28 with most reporting only occasional, light drinking (median: 4

drinks per month).26 Binge drinking or daily risk drinking (usually defined as 2 drinks per day

or greater) is reported by 1-2% of pregnant women,27-29 but higher rates (4-6%) have been

reported in some screening studies.30,31 Excessive use of alcohol during pregnancy can produce

the fetal alcohol syndrome (FAS), a constellation of growth retardation, facial deformities, and

central nervous system dysfunction (microcephaly, mental retardation, or behavioral

abnormalities).32 Other infants display growth retardation or neurologic involvement in the

absence of full FAS (i.e., fetal alcohol effects [FAE]).10 FAS has been estimated to affect

approximately 1 in 3,000 births in the U.S. (1,200 children annually), making it a leading

treatable cause of birth defects and mental retardation.33,34

The level of alcohol consumption that poses a risk during pregnancy remains controversial.10,35

FAS has only been described in infants born to alcoholic mothers, but the variable incidence of FAS

among alcoholic women (from 3-40%)33 suggests that other factors (e.g., genetic, nutritional,

metabolic, or temporal) may influence the expression of FAS.10 The reported incidence of FAS is

higher in Native Americans and blacks than in whites.33,36 Most studies report an increased risk

of FAE among mothers who consume 14 drinks per week or more,35,37-39 but the effects of

lower levels of drinking have been inconsistent.35,40,41 Modest developmental effects have been

attributed to light drinking (7 drinks per week) in some studies, but underreporting by heavy

drinkers and confounding effects of other important factors (nutrition, environment, etc.) make it

difficult to prove or disprove a direct effect of light drinking.10,35,42 Timing of exposure and

pattern of drinking may be important, with greater effects proposed for exposure early in

pregnancy and for frequent binge drinking.10

Alcohol Use by Adolescents and Young Adults.  Use of alcohol by adolescents and young adults has

declined over the past decade, but remains a serious problem.43 Among 12-17-year-olds

surveyed in 1993, 18% had used alcohol in the last month, and 35% in the last year.4 In a

separate 1993 survey, 45% and 33%, respectively, of male and female 12th graders reported

"binge" drinking (5 or more drinks on one occasion) within the previous month.44 The leading

causes of death in adolescents and young adults_motor vehicle and other unintentional injuries,

homicides, and suicides_are each associated with alcohol or other drug intoxication in about half of

the cases. Driving under the influence of alcohol is more than twice as common in adolescents than

in adults.45 Binge drinking is especially prevalent among college students: half of all men and

roughly one third of all women report heavy drinking within the previous 2 weeks.43,46 Most

frequent binge drinkers report numerous alcohol-related problems, including problems with

school work, unplanned or unsafe sex, and trouble with police.46

Accuracy of Screening Tests

Accurately assessing patients for drinking problems during the routine clinical encounter is

difficult. The diagnostic standard for alcohol dependence or abuse (Diagnostic and Statistical

Manual of Mental Disorders [DSM] IV)2 requires a detailed interview and is not feasible for

routine screening. Physical findings (hepatomegaly, skin changes, etc.) are only late

manifestations of prolonged, heavy alcohol abuse.47 Asking the patient about the quantity and

frequency of alcohol use is an essential component of assessing drinking problems, but it is not

sufficiently sensitive or specific by itself for screening. In one study, drinking 12 or more drinks

a week was specific (92%) but insensitive (50%) for patients meeting DSM criteria for an active

drinking disorder.48 The reliability of patient report is highly variable and dependent on the

patient, the clinician, and individual circumstances. Heavy drinkers may underestimate the

amount they drink because of denial, forgetfulness, or fear of the consequences of being diagnosed

with a drinking problem.

A variety of screening questionnaires have been developed which focus on consequences of drinking

and perceptions of drinking behavior. The 25-question Michigan Alcoholism Screening Test

(MAST)49 is relatively sensitive and specific for DSM-diagnosed alcohol abuse or dependence

(84-100% and 87-95%, respectively)49,50 but it is too lengthy for routine screening.

Abbreviated 10- and 13-item versions are easier to use but are less sensitive and specific in

primary care populations (66-78% and 80%, respectively).51,52 The four-question CAGE

instrumenta is the most popular screening test for use in primary care53 and has good sensitivity

and specificity for alcohol abuse or dependence (74-89% and 79-95%, respectively) in both

inpatients54,55 and outpatients.56-58 The CAGE is less sensitive for early problem drinking or

heavy drinking, however (49-73%).58,59 Both the CAGE and MAST questionnaires share

important limitations as screening instruments in the primary care setting: an emphasis on

symptoms of dependence rather than early drinking problems, lack of information on level and

pattern of alcohol use, and failure to distinguish current from lifetime problems.52

Some of these weaknesses are addressed by the Alcohol Use Disorders Identification Test (AUDIT),

a 10-item screening instrument developed by the World Health Organization (WHO) in

conjunction with an international intervention trial. The AUDIT incorporates questions about

drinking quantity, frequency, and binge behavior along with questions about consequences of

drinking.60 For the study population in which it was derived, a score of 8 of 40 on the AUDIT had

high sensitivity and specificity for "harmful and hazardous drinking" (92% and 94%,

respectively) as assessed by more extensive interview.60 Validation studies have reported more

variable performance of the AUDIT. Sensitivity and specificity for current abuse/dependence were

high (96% and 96%, respectively) in an inner-city clinic;61 among rural outpatients, AUDIT

was less sensitive and specific (61% and 90%) for current drinking problems  but superior to

the Short MAST-13.51 Because it focuses on drinking in the previous year, however, AUDIT is

less sensitive for past drinking problems.62 Further validation studies in other populations are

under way.

Brief screening tests may be less sensitive or less specific in young persons: sensitivity of the

CAGE for problems due to alcohol among college freshmen was 42% in men and 25% in women.63

Only 38% of college students with an AUDIT score of 8 or greater met DSM criteria for abuse or

dependence;64 many of these "false-positive" results were due to drinking patterns (frequent

binge drinking) that would be considered hazardous. Alternative screens have been developed for

adolescents, such as the Perceived-Benefit-of-Drinking scale65 and the Problem Oriented

Screening Instrument for Teenagers (POSIT),66 but they have not yet been adequately validated in

the primary care setting.

Instruments that focus on alcohol dependency (e.g., CAGE or MAST) are not sensitive for levels of

drinking considered dangerous in pregnancy.67 Women may underreport alcohol consumption

while pregnant,68 and direct questions about drinking may provoke denial.69 Brief instruments

that incorporate questions about tolerance to alcohol ("How many drinks does it take to make you

feel high?" or "How many drinks can you hold?") were more sensitive than the CAGE (69-79%

vs. 49%) for risk-drinking in pregnancy (2 drinks per day or greater).30,70 Women who

require 3 or more drinks to feel high, or who can drink more than 5 drinks at a time, are likely to

be at risk.71

Laboratory tests are generally insensitive and nonspecific for problem drinking. Elevations in

hepatocellular enzymes, such as aspartate aminotransferase (AST), or the erythrocyte mean

corpuscular volume (MCV) are found in less than 10% and 30% of problem drinkers,

respectively.72 Serum g-glutamyl transferase (GGT) is more sensitive (33-60%) in various

studies,54,55,72 but elevations in GGT may be due to other causes (medications, trauma,

diabetes, and heart, kidney, or biliary tract disease). Even when the prevalence of problem

drinking is high (30%), the predictive value of an elevated GGT has been estimated at only

56%.72

Effectiveness of Early Detection

Numerous studies demonstrate that clinicians are frequently unaware of problem drinking by

their patients.10 Early detection and intervention may alleviate ongoing medical and social

problems due to drinking and reduce the future risks from excessive alcohol use.

Nondependent Drinkers.  A number of randomized trials have now demonstrated the efficacy of

brief outpatient counseling (5-15 minutes) for nondependent problem drinkers. In four

Scandinavian studies, which enrolled patients with elevated GGT and heavy alcohol consumption,

brief counseling to reduce drinking and regular follow-up produced significant improvements

(decreased GGT and/or decreased alcohol consumption) in treated versus control subjects;73-76

counseling reduced reported sick days in one study.74 In the longest of these studies, patients

receiving counseling had fewer hospitalizations and 50% lower mortality after 5 years.73 Some

of this benefit, however, may have been due to the close medical follow-up (every 1-3 months) in

the intervention group rather than the initial counseling.

Additional trials have demonstrated that brief interventions can reduce alcohol consumption in

problem drinkers identified by screening questionnaires or self-reported heavy drinking.77-79

Most recently, an international WHO study examined the effects of 5 or 20 minutes of counseling

about drinking in 1,500 "at-risk" male and female drinkers: >35 drinks per week for men; >21

drinks per week for women; or intoxicated twice per month; or self-perceived drinking

problem.80 After 9 months, self-reported alcohol consumption among men was reduced 32-38%

in the intervention groups and 10% in controls. Among women, alcohol consumption declined

significantly (>30%) among both treated and control groups. A meta-analysis of six

brief-intervention trials estimated that interventions reduced average alcohol consumption by

24%.81 Although self-reported consumption may be subject to bias, reported changes in drinking

correlated with objective measures (GGT, blood pressure) in most studies. Two additional studies

demonstrated significant reductions in blood pressure as a result of advice to stop drinking or

substitution of nonalcoholic beer.82,83

Pregnancy.  There are no definitive controlled trials of treatments for excessive drinking in

pregnancy.84 In several uncontrolled studies, a majority of heavy-drinking pregnant women who

received counseling reduced alcohol consumption,32,85,86 and reductions in drinking were

associated with lower rates of FAS.32,86 Many women spontaneously reduce their drinking while

pregnant, however, and women who continue to drink differ in many respects from women who cut

down (e.g., heavier drinking, poorer prenatal care and nutrition). As a result, it is difficult to

determine precisely the benefit of screening and counseling during pregnancy. In two trials that

employed a control group, the proportions of women abstaining or reducing consumption were

similar in intervention and control groups.87,88

Adolescents.  A 1990 Institute of Medicine (IOM) report concluded that specific recommendations

for the treatment of alcohol problems in young persons were impossible, due to disagreement over

what constitutes a drinking problem in adolescents, the wide variety of interventions employed,

and the absence of any rigorous evaluation of different treatments.1 Alcohol interventions in

adolescents have focused on primary prevention of alcohol use.10 Recent reviews of school-based

programs found that most effects were inconsistent, small, and short-lived; programs that sought

to develop social skills to resist drug use seem to be more effective than programs that emphasize

factual knowledge.89,90

Alcohol-Dependent Patients.  Patients with alcohol dependence usually receive more intensive

treatment. A 1989 report of the IOM91 reviewed a variety of alcohol treatment modalities and

concluded that various treatments were effective, but there was no single superior treatment for

all patients, and few treatments were effective for the majority of patients. They found no evidence

that residential versus nonresidential programs, or long- versus short-duration programs, were

more effective for the average patient, and no studies existed that adequately evaluated the

independent effect of Alcoholics Anonymous (AA). In a subsequent trial among employees referred

for alcohol problems, patients who received inpatient treatment and mandatory AA follow-up were

more likely to be abstinent at 2-year follow-up (37% vs. 16%) than patients assigned to

mandatory AA only.92

Two short-term (12 weeks) randomized trials demonstrated a significant benefit of naltrexone,

an opioid antagonist, as an adjunct to treatment of alcohol dependence. In one study, patients

receiving naltrexone and supportive psychotherapy had significantly higher abstinence rates than

did subjects receiving placebo (61% vs. 19%).93 In the second, men receiving naltrexone

reported less alcohol craving and fewer drinking days than placebo-treated men.94 In both trials,

naltrexone significantly reduced the likelihood of relapse (heavy drinking or steady drinking)

among subjects who did not achieve complete abstinence. The benefits of alcohol-sensitizing

agents, however, remain uncertain.10 Disulfiram (i.e., Antabuse) did not improve long-term

abstinence rates in a controlled trial, but it did reduce drinking days among patients receiving the

highest dose.95

In a 10-year follow-up of 158 patients completing inpatient treatment, 61% reported complete

or stable remission of alcoholism.96 Completing an extended inpatient program was associated

with significantly lower mortality among alcoholic patients in a second study.97 Many such

studies of alcohol treatment, however, suffer from important methodologic limitations: inadequate

control groups, insufficient or selective follow-up, and selection bias due to the characteristics of

patients who successfully complete voluntary treatment programs.91,98,99 Since spontaneous

remission occurs in as many as 30% of alcoholics,100,101 reduced consumption may be

inappropriately attributed to treatment. Successful treatment is likely to represent a complex

interaction of patient motivation, treatment characteristics, and the posttreatment environment

(family support, stress, etc.).1,10 The IOM review concluded that treatment of other life

problems (e.g., with antidepressant medication, family or marital therapy, or stress

management) and empathetic therapists were likely to improve treatment outcomes.91

Recommendations of Other Groups

There is a consensus among professional groups such as the American Medical Association

(AMA)102 and the American Academy of Family Physicians (AAFP)103 that clinicians should be

alert to the signs and symptoms of alcohol abuse and should routinely discuss patterns of alcohol

use with all patients. AAFP recommendations are under review. The Canadian Task Force on the

Periodic Health Examination (CTF)104 and a 1990 IOM panel1 recommended screening adults for

problem drinking, using patient inquiry or standardized instruments, and offering brief

counseling to nondependent problem drinkers.

The American Academy of Pediatrics (AAP),105 AMA Guidelines for Adolescent Preventive

Services (GAPS),106 the Bright Futures guidelines,107 and the AAFP103 all recommend careful

discussion with all adolescents regarding alcohol use and regular advice to abstain from alcohol.

The AAP also advises physicians to counsel parents regarding their own use of alcohol in the home.

Recommendations of the U.S. Surgeon General,108 the American College of Obstetricians and

Gynecologists,109 and the AAP109,110 advise counseling all women who are pregnant or planning

pregnancy that drinking can be harmful to the fetus and that abstinence is the safest policy. The

CTF recommends that all women be screened for problem drinking and advised to reduce alcohol

use during pregnancy.104

Several organizations have made recommendations about "safe" levels of alcohol consumption for

nonpregnant adults. The National Institute on Alcohol Abuse and Alcoholism,111 the U.S. Surgeon

General,112 and dietary guidelines produced jointly by the U.S. Departments of Health and Human

Services and Agriculture113,114 recommend no more than 2 drinks per day for men and 1 drink

per day for nonpregnant women. Slightly higher limits were proposed by national health

authorities in the U.K.115

Discussion

Alcohol problems are common in the primary care setting, but they often go undetected by

clinicians. Although imperfect, asking patients direct questions about the quantity, frequency, and

pattern of their drinking is an important way to identify those who are most likely to experience

problems due to alcohol. Questions about tolerance to the effects of alcohol may circumvent denial

among pregnant women and heavy drinkers. The CAGE and other brief screening instruments are

useful supplements to the standard patient history, but they may be less sensitive for early

problems and hazardous drinking. The AUDIT may detect a broader range of current drinking

problems, but its performance in the primary care setting needs further evaluation. Although

laboratory tests such as GGT are not sufficiently sensitive or specific for routine screening, they

may be useful in selected high-risk patients to confirm clinical suspicion or to motivate changes

in drinking. Neither questionnaires nor laboratory tests should be considered diagnostic of

problem drinking without more detailed evaluation (see Clinical Intervention).

Detecting early problem drinkers is important, because they account for a large proportion of all

alcohol problems and they are more likely to respond to simple interventions than patients with

alcohol dependency. There is now good evidence that brief counseling can reduce alcohol

consumption in problem drinkers, and several trials have also reported improved clinical

outcomes. Since the risks from alcohol rise steadily at higher levels of consumption, reducing

drinking should also benefit heavy drinkers (i.e., hazardous drinkers) who do not yet manifest

problems due to drinking. Early attention to problem drinking is especially important in young

adults: hazardous drinking is common, adverse effects of alcohol increase with duration of use, and

few persons initiate drinking after age 30.116 Early detection is also important for

alcohol-dependent patients, but effective treatment requires more intensive and sustained efforts

to promote abstinence.

Uncertainties remain about optimal screening methods and interventions during pregnancy, but

screening is justified by the strong evidence of the adverse effects of alcohol on the fetus. Although

the risks of occasional, light drinking during pregnancy have not been established, abstinence can

be recommended as a prudent approach for pregnant women. At the same time, women concerned

about the effects of previous moderate drinking early in pregnancy can be reassured that

important harms have not been demonstrated from such limited exposures. Because exposure early

in pregnancy may be most important, screening and advice should be directed toward women

contemplating pregnancy and those at risk for unintended pregnancy, not just women who are

already pregnant.

There is insufficient evidence to make precise recommendations about desirable levels of drinking,

but the strong association between heavy alcohol use and risk of future complications justifies

advising all drinkers to drink moderately and avoid frequent intoxication, even in the absence of

current problems (see below).

CLINICAL INTERVENTION

Screening to detect problem drinking and hazardous drinking is recommended for all adult and

adolescent patients ("B" recommendation). Screening should involve a careful history of alcohol

use and/or the use of standardized screening questionnaires. Patients should be asked to describe

the quantity, frequency, and other characteristics of their use of wine, beer, and liquor, including

frequency of intoxication and tolerance to the effects of alcohol. One drink is defined as 12 ounces

of beer, a 5-ounce glass of wine, or 1.5 fluid ounces (one jigger) of distilled spirits. Brief

questionnaires such as the CAGE or AUDIT may help clinicians assess the likelihood of problem

drinking or hazardous drinking (see Table 52.1). Responses suggestive of problem drinking

should be confirmed with more extensive discussions with the patient (and family members where

indicated) about patterns of use, problems related to drinking, and symptoms of alcohol

dependence.2 Routine measurement of biochemical markers, such as serum GGT, is not

recommended for screening purposes. Discussions with adolescents should be approached with

discretion to establish a trusting relationship and to respect the patient's concerns about the

confidentiality of disclosed information.

All pregnant women should be screened for evidence of problem drinking or risk drinking (2

drinks per day or binge drinking) ("B" recommendation). Including questions about tolerance to

alcohol may improve detection of at-risk women. All pregnant women and women contemplating

pregnancy should be informed of the harmful effects of alcohol on the fetus and advised to limit or

cease drinking. Although there is insufficient evidence to prove or disprove harms from

occasional, light drinking during pregnancy, abstinence from alcohol can be recommended on other

grounds: possible risk from even low-level exposure to alcohol, lack of harm from abstaining, and

prevailing expert opinion ("C" recommendation). Women who smoke should be advised that the

risk of low birth weight is greatest for mothers who both smoke and drink.

Patients with evidence of alcohol dependence should be referred, where possible, to appropriate

clinical specialists or community programs specializing in the treatment of alcohol dependence.

Patients with evidence of alcohol abuse or hazardous drinking should be offered brief advice and

counseling. Counseling should involve feedback of the evidence of a drinking problem, discussion of

the role of alcohol in current medical or psychosocial problems, direct advice to reduce

consumption, and plans for regular follow-up. Problems related to alcohol (e.g., physical

symptoms, behavioral or mood problems, or difficulties at work and home) should be monitored to

determine whether further interventions are needed. There is no single definition of "hazardous"

drinking in asymptomatic persons, but successful intervention trials have generally defined 5

drinks per day in men, 3 drinks per day in women, or frequent intoxication to identify persons at

risk. Several U.S. organizations have suggested lower limits for "safe" drinking: 2 drinks per day

in men and 1 drink per day in women.18 All persons who drink should be informed of the dangers

of driving or other potentially dangerous activities after drinking (see Chapter 57). The use of

alcohol should be discouraged in persons younger than the legal age for drinking ("B"

recommendation), although the effectiveness of alcohol abstinence messages in the primary care

setting is uncertain.

The draft update of this chapter was prepared for the U.S. Preventive Services Task Force by David

Atkins, MD, MPH, with contributions from materials prepared for the Canadian Task Force on the

Periodic Health Examination by Deborah L. Craig, MPH, and Jean L. Haggerty, MSc.

REFERENCES

	1. Institute of Medicine. Broadening the base of treatment for alcohol problems: report of a

study by a committee of the Institute of Medicine, Division of Mental Health and Behavioral

Medicine. Washington, DC: National Academy Press, 1990.

	2. American Psychiatric Association. Diagnostic and statistical manual of mental disorders.

4th ed. Washington, DC: American Psychiatric Association, 1994.

	3. World Health Organization. International classification of diseases, 10th revision.

Geneva: World Health Organization, 1992.

	4. Substance Abuse and Mental Health Administration. National Household Survey on Drug

Abuse: population estimates 1993. Rockville, MD: U.S. Department of Health and Human Services,

Substance Abuse and Mental Health Administration, 1994. (Publication no. (SMA) 94-3017.)

	5. Grant BF, Harford TC, Chou P, et al. Epidemiologic Bulletin no. 27: Prevalence of

DSM-III-R alcohol abuse and dependence: United States, 1988. Alcohol Health Res World

1991;15:91-96.

	6. Helzer JE, Burnam A, McEvoy LT. Alcohol abuse and dependence. In: Robins LN, Regier

DA, eds. Psychiatric disorders in America: the Epidemiologic Catchment Area Study. New York:

Free Press, 1991:81-115.

	7. Grant BF, Harford TC, Dawson D, et al. Prevalence of DSM-IV alcohol abuse and

dependence: United States, 1992. Alcohol Health Res World 1994;18:243-248.

	8. Kessler RC, McGonagle KA, Zhao S, et al. Lifetime and 12-month prevalence of

DSM-III-R psychiatric disorders in the United States: results from the National Comorbidity

Survey. Arch Gen Psychiatry 1994;51:8-19.

	9. Bradley KA. The primary care provider's role in the prevention and management of

alcohol problems. Alcohol Health Res World 1994;18:97-104.

	10. National Institute on Alcohol Abuse and Alcoholism. Alcohol and health: eighth special

report to the U.S. Congress from the Secretary of Health and Human Services. Rockville, MD: U.S.

Department of Health and Human Services, National Institutes of Health, 1993. (NIH Publication

no. 94-3699.)

	11. Klatsky AL, Armstrong AA, Friedman GD. Alcohol and mortality. Ann Intern Med

1992;117:646-654.

	12. Boffetta P, Garfinkel L. Alcohol drinking and mortality among men enrolled in an

American Cancer Society prospective study. Epidemiology 1990;1:342-348.

	13. Anderson P, Cremona A, Paton A, et al. The risk of alcohol. Addiction 1993;88:1493-

1508.

	14. Rosenberg L, Metzger LS, Palmer JR. Alcohol consumption and risk of breast cancer: a

review of the epidemiologic evidence. Epidemiol Rev 1993;15:133-168.

	15. Fuchs CS, Stampfer MJ, Colditz GA, et al. Alcohol consumption and mortality among

women. N Engl J Med 1995;332:1245-1250.

	16. Centers for Disease Control. Alcohol-related mortality and years of potential life

lost_United States, 1987. MMWR 1990;39:173-178.

	17. National Highway Traffic Safety Administration. Traffic safety facts 1993: alcohol.

Washington, DC: U.S. Department of Transportation, National Highway Traffic Safety

Administration, National Center for Statistics and Analysis, 1994.

	18. Bradley KA, Donovan DM, Larson EB. How much is too much? Advising patients about

safe levels of alcohol consumption. Arch Intern Med 1993;153:2734-2740.

	19. Stampfer MJ, Rimm EB, Walsh DC. Commentary: alcohol, the heart, and public policy.

Am J Public Health 1993;83:801-804.

	20. Maclure M. Demonstration of deductive meta-analysis: ethanol intake and risk of

myocardial infarction. Epidemiol Rev 1993;15:328-351.

	21. Klatsky AL, Armstrong AA, Friedman GD. Risk of cardiovascular mortality in alcohol

drinkers, ex-drinkers and non-drinkers. Am J Cardiol 1990;66:1237-1242.

	22. Stampfer MJ, Colditz GA, Willett WC, et al. A prospective study of moderate alcohol

consumption and the risk of coronary disease and stroke in women. N Engl J Med 1988;319:267-

273.

	23. Gaziano JM, Buring JE, Breslow JL, et al. Moderate alcohol intake, increased levels of

high-density lipoprotein and its subfractions, and decreased risk of myocardial infarction. N Engl

J Med 1993;329:1829-1835.

	24. Ridker PM, Vaughan DE, Stampfer MJ, et al. Association of moderate alcohol

consumption and plasma concentration of endogenous tissue-type plasminogen activator. JAMA

1994;272:929-933.

	25. Sher KJ, ed. Children of alcoholics: a critical appraisal of theory and research. Chicago:

University of Chicago Press, 1991.

	26. Serdula M, Williamson DF, Kendrick J, et al. Trends in alcohol consumption by

pregnant women: 1985 through 1988. JAMA 1991;265:876-879.

	27. Goodwin MM, Bruce C, Zahniser SC, et al. Behavioral risk factors before and during

pregnancy. In: Wilcox LS, Marks JS, eds. From data to action: CDC's public health surveillance for

women, infants, and children. Washington, DC: Department of Health and Human Services,

1994:93-104.

	28. Centers for Disease Control and Prevention. Frequent alcohol consumption among

women of childbearing age_Behavioral Risk Factor Surveillance System, 1991. MMWR

1994;43:328-329, 335.

	29. Centers for Disease Control and Prevention. Sociodemographic and behavioral

characteristics associated with alcohol consumption during pregnancy_United States, 1988.

MMWR 1995;44:261-264.

	30. Sokol RJ, Martier SS, Ager JW. The T-ACE questions: practical prenatal detection of

risk-drinking. Am J Obstet Gynecol 1989;160:863-870.

	31. Russell M, Martier SS, Sokol RJ, et al. Screening for pregnancy risk-drinking.

Alcohol Clin Exp Res 1994;18: 1156-1161.

	32. Rosett HL, Weiner L, Edelin KC. Treatment experience with pregnant problem

drinkers. JAMA 1983;249:2029-2033.

	33. Abel EA, Sokol RJ. A revised conservative estimate of the incidence of FAS and its

economic impact. Alcohol Clin Exp Res 1991;15:514-524.

	34. Centers for Disease Control and Prevention. Fetal alcohol syndrome_United States,

1979-1992. MMWR 1993;42:339-341.

	35. Russell M. Clinical implications of recent research on the fetal alcohol syndrome. Bull

NY Acad Sci 1991;67: 207-222.

	36. Burd L, Moffatt ME. Epidemiology of fetal alcohol syndrome in American Indians,

Alaskan Natives, and Canadian Aboriginal peoples: a review of the literature. Public Health Rep

1994;109:688-693.

	37. Virji SK. The relationship between alcohol consumption during pregnancy and infant

birthweight: an epidemiologic study. Acta Obstet Gynecol Scand 1991;303-308.

	38. Forrest F, Florey CDV, Taylor D, et al. Reported social alcohol consumption during

pregnancy and infants' development at 18 months. BMJ 1991;303:22-26.

	39. Verkerk PH, Noord-Zaadstra BMV, Florey CDV, et al. The effect of moderate maternal

alcohol consumption on birth weight and gestational age in a low risk population. Early Hum Dev

1993;32:121-129.

	40. Jacobson JL, Jacobson SW, Sokol RJ, et al. Teratogenic effects of alcohol on infant

development. Alcohol Clin Exp Res 1993;17:174-183.

	41. Streissguth AP, Barr HM, Sampson PD. Moderate prenatal alcohol exposure: effects on

child IQ and learning problems at age 7.5 years. Alcohol Clin Exp Res 1990;14:662-669.

	42. Knupfer G. Abstaining for fetal health: the fiction that even light drinking is dangerous.

Br J Addict 1991;86: 1063-1073.

	43. National Institute on Drug Abuse. National survey results on drug use from the

Monitoring the Future Study, 1975-1992. Vols 1 and 2. Rockville, MD: Department of Health and

Human Services, National Institute on Drug Abuse, 1993. (NIH Publications nos. 93-3596 and

3597.)

	44. Centers for Disease Control and Prevention. Youth Risk Behavior Surveillance_United

States, 1993. MMWR 1995;44(SS-1):1-56.

	45. Centers for Disease Control. Drinking and driving and binge drinking in selected states,

1982 and 1985: the Behavioral Risk Factor Surveys. MMWR 1987;35:788-791.

	46. Wechsler H, Davenport A, Dowdall G, et al. Health and behavioral consequences of binge

drinking in college: a national survey of students at 140 campuses. JAMA 1994;272:1672-1677.

	47. Glaze LW, Coggan PG. Efficacy of an alcoholism self-report questionnaire in a

residency clinic. J Fam Pract 1987; 25:60-64.

	48. Buchsbaum DG, Welsh J, Buchanan RG, et al. Screening for drinking problems by

patient self-report: even "safe" levels may indicate a problem. Arch Intern Med 1995;155:104-

108.

	49. Selzer ML. The Michigan Alcoholism Screening Test: the quest for a new diagnostic

instrument. Am J Psychiatry 1971;127:1653-1658.

	50. Pokorny AD, Miller BA, Kaplan HB. The Brief MAST: a shortened version of the

Michigan Alcoholism Screening Test. Am J Psychiatry 1972;129:342-345.

	51. Barry K, Fleming M. The Alcohol Use Disorders Identification Test (AUDIT) and the

SMAST-13: predictive validity in a rural primary care sample. Alcohol Alcohol 1993;28:33-42.

	52. Chan AWK, Pristach EA, Welte JW, et al. Use of the TWEAK test in screening for

alcoholism/heavy drinking in three populations. Alcohol Clin Exp Res 1993;17:1188-1192.

	53. Ewing JA. Detecting alcoholism: the CAGE questionnaire. JAMA 1984;252:1905-

1907.

	54. Bernadt MW, Mumford J, Taylor C, et al. Comparison of questionnaire and laboratory

tests in the detection of excessive drinking and alcoholism. Lancet 1982;1:325-328.

	55. Bush B, Shaw S, Cleary P, et al. Screening for alcohol abuse using the CAGE

questionnaire. Am J Med 1987;82:231-235.

	56. King M. At risk drinking among general practice attenders: validation of the CAGE

questionnaire. Psychol Med 1986;16:213-217.

	57. Buchsbaum DG, Buchanan RG, Centor RM, et al. Screening for alcohol abuse using CAGE

scores and likelihood ratios. Ann Intern Med 1991;115:774-777.

	58. Chan AWK, Pristach EA, Welte JW. Detection by the CAGE of alcoholism or heavy

drinking in primary care outpatients and the general population. J Subst Abuse 1994;6:123-

135.

	59. Hays JT, Spickard WA. Alcoholism: early diagnosis and intervention. J Gen Intern Med

1987;2:420-427.

	60. Saunders JB, Aasland OG, Babor TF, et al. Development of the Alcohol Use Disorders

Identification Test (AUDIT): WHO collaborative project on early detection of persons with harmful

alcohol consumption_II. Addiction 1993;88:791-804.

	61. Isaacson JH, Butler R, Zacharek M, et al. Screening with the Alcohol Use Disorders

Identification Test (AUDIT) in an inner-city population. J Gen Intern Med 1994;9:550-553.

	62. Schmidt A, Barry K, Fleming MF. Detection of problem drinkers: the Alcohol Use

Disorders Identification Test (AUDIT). Southern Med J 1995;88:52-59.

	63. Werner MJ, Walker LS, Greene JW. Screening for problem drinking among college

freshmen. J Adolesc Health 1994;15:303-310.

	64. Fleming MF, Barry KL, MacDonald R. The Alcohol Use Disorders Identification Test

(AUDIT) in a college sample. Int J Addict 1991;26:1173-1185.

	65. Petchers MK, Singer MI. Perceived-benefit-of-drinking Scale: approach to screening

for adolescent alcohol abuse. J Pediatr 1987;110:979-981.

	66. National Institute on Drug Abuse. Problem oriented screening instrument for

teenagers. In: Rahdert E, ed. The adolescent assessment/referral system manual. Rockville, MD:

National Institute on Drug Abuse, 1990:5-9.

	67. Waterson EJ, Murray-Lyon IM. Screening for alcohol-related problems in the

antenatal clinic. Alcohol Alcohol 1989;24:21-30.

	68. Jacobson SW, Jacobson JL, Sokol RJ, et al. Maternal recall of alcohol, cocaine, and

marijuana use during pregnancy. Neurotoxicol Teratol 1991;13:535-540.

	69. Ernhart CB, Morrow-Tlucak M, Sokol RJ, et al. Underreporting of alcohol use in

pregnancy. Alcohol Clin Exp Res 1988;12:506-511.

	70. Russell M, Martier SS, Sokol RJ, et al. Screening for pregnancy risk-drinking.

Alcohol Exp Clin Res 1994;18: 1156-1161.

	71. Russell M. New assessment tools for risk drinking during pregnancy: T-ACE, TWEAK,

and others. Alcohol Health Res World 1994;18:55-61.

	72. Hoeksema HL, de Bock GH. The value of laboratory tests for the screening and

recognition of alcohol abuse in primary care patients. J Fam Pract 1993;37:268-276.

	73. Kristenson H, Trell E, Hood B. Serum glutamyl-transferase in screening and

continuous control of heavy drinking in middle-aged men. Am J Epidemiol 1981;114:862-872.

	 74. Persson J, Magnusson PH. Early intervention in patients with excessive consumption

of alcohol: a controlled study. Alcohol 1989;6:403-408.

 	75. Romelsjo A, Andersson L, Barrner H, et al. A randomized study of secondary prevention

of early stage problem drinkers in primary health care. Br J Addict 1989;84:1319-1327.

 	76. Nilssen O. The Tromso Study: identification of and a controlled intervention on a

population of early-stage risk drinkers. Prev Med 1991;20:518-528.

 	77. Chick J, Lloyd G, Crombie E. Counselling problem drinkers in medical wards: a

controlled study. BMJ 1985;290:965-967.

 	78. Wallace P, Cutler S, Haines A. Randomized controlled trial of general practitioner

intervention in patients with excessive alcohol consumption. BMJ 1988;297:663-668.

 	79. Heather N, Kissoon-Singh J, Fenton GW. Assisted natural recovery from alcohol

problems: effects of a self-help manual with and without supplementary telephone contact. Br J

Addict 1990;85:1177-1185.

 	80. Babor TF, Grant M, eds. Project on identification and management of alcohol-related

problems. Report on Phase II: a randomized clinical trial of brief interventions in primary health

care. Geneva: World Health Organization, 1992.

 	81. Brief interventions and alcohol use. Effective Health Care, bulletin no. 7. Leeds, UK:

Nuffield Institute for Health Care, University of Leeds, 1993.

 	82. Maheswaran R, Beevers M, Beevers DG. Effectiveness of advice to reduce alcohol

consumption in hypertensive patients. Hypertension 1992:19:79-84.

 	83. Cox KL, Puddey IB, Morton AR, et al. The combined effects of aerobic exercise and

alcohol restriction on blood pressure and serum lipids: a two-way factorial study in sedentary

men. J Hypertens 1993;11:191-201.

 	84. Schorling JB. The prevention of prenatal alcohol use: a critical analysis of intervention

studies. J Stud Alcohol 1993;54:261-267.

 	85. Larson G. Prevention of fetal alcohol effects. Acta Obstet Gynecol Scand 1983;62:171-

178.

 	86. Halmesmaki E. Alcohol counselling of 85 pregnant problem drinkers: effect on drinking

and fetal outcome. Br J Obstet Gynaecol 1988;95:243-247.

 	87. Waterson EJ, Murray-Lyon IM. Preventing fetal alcohol effects: a trial of three

methods of giving information in the antenatal clinic. Health Educ Res 1990;5:53-61.

 	88. Meberg A, Halvorsen B, Holter B, et al. Moderate alcohol consumption_need for

intervention programs in pregnancy? Acta Obstet Gynecol Scand 1986;65:861-864.

 	89. Ennett ST, Tobler NS, Ringwalt CL, et al. How effective is drug abuse resistance

education? A meta-analysis of project DARE outcome evaluations. Am J Public Health

1994;84:1394-1401.

 	90. Hansen WB. School-based substance abuse prevention: a review of the state of the art

in curriculum, 1980-1990. Health Educ Res 1992;7:403-430.

 	91. Institute of Medicine. Prevention and treatment of alcohol problems: research

opportunities. Washington, DC: National Academy Press, 1989.

 	92. Walsh DC, Hingson RW, Merrigan DM, et al. A randomized trial of treatment options

for alcohol-abusing workers. N Engl J Med 1991;325:775-782.

 	93. O'Malley SS, Jaffe AJ, Chang G, et al. Naltrexone and coping skills therapy for alcohol

dependence: a controlled study. Arch Gen Psychiatry 1992;49:881-887.

 	94. Volpicelli JR, Alterman AI, Hayashida M, et al. Naltrexone in the treatment of alcohol

dependence. Arch Gen Psychiatry 1992;49:876-880.

 	95. Fuller RK, Branchey L, Brightwell DR, et al. Disulfiram treatment of alcoholism: A

Veterans Administration study. JAMA 1986;256:1449-1455.

 	96. Cross GM, Morgan CW, Mooney AJ, et al. Alcoholism treatment: a ten-year follow-up

study. Alcohol Clin Exp Res 1990;14:169-173.

 	97. Bunn JY, Booth BM, Loveland Cook CA, et al. The relationship between mortality and

intensity of inpatient alcoholism treatment. Am J Public Health 1994;84:211-214.

 	98. Thurstin AH, Alfano AM, Sherer M. Pretreatment MMPI profiles of A.A. members and

nonmembers. J Stud Alcohol 1986;47:468-471.

 	99. Emrick CD. Alcoholics Anonymous: affiliation processes and effectiveness as treatment.

Alcohol Clin Exp Res 1987;11:416-423.

	100. Smart R. Spontaneous recovery in alcoholics: a review and analysis of the available

research. Drug Alcohol Depend 1975/76;1:277.

	101. Saunders WM, Kershaw PW. Spontaneous remission from alcoholism: a community

study. Br J Addict 1979;74: 251-265.

	102. American Medical Association, Council on Scientific Affairs. Guidelines for alcoholism

diagnosis, treatment and referral. Chicago: American Medical Association, 1979.

	103. American Academy of Family Physicians. Age charts for periodic health examination.

Kansas City, MO: American Academy of Family Physicians, 1994. (Reprint no. 510.)

	104. Canadian Task Force on the Periodic Health Examination. Canadian guide to clinical

preventive health care. Ottawa: Canada Communication Group, 1994:52-61, 826-836.

	105. American Academy of Pediatrics, Committee on Adolescence. Alcohol use and abuse: a

pediatric concern. Pediatrics 1995;95:439-442.

	106. American Medical Association. Guidelines for adolescent preventive services (GAPS):

recommendations and rationale. Chicago: American Medical Association, 1994.

	107. Green M, ed. Bright Futures: guidelines for health supervision of infants, children

and adolescents. Arlington VA: National Center for Education in Maternal and Child Health, 1994.

	108. Surgeon General's Advisory on alcohol and pregnancy. FDA Drug Bull 1981;11:9-10.

	109. American Academy of Pediatrics and American College of Obstetricians and

Gynecologists. Guidelines for perinatal care. 3rd ed. Washington, DC: American Academy of

Pediatrics and American College of Obstetricians and Gynecologists, 1992.

	110. American Academy of Pediatrics, Committee on Substance Abuse and Committee on

Children with Disabilities. Fetal alcohol syndrome and fetal alcohol effects. Pediatrics

1993;91:1004-1006.

	111. National Institute on Alcohol Abuse and Alcoholism. Moderate drinking. Alcohol Alert

no. 16. Bethesda: U.S. Department of Health and Human Services, 1992.

	112. U.S. Department of Health and Human Services. The Surgeon General's report on

nutrition and health. Washington, DC: Government Printing Office, 1988. (Publication no.

PHS-88-50210.)

	113. U.S. Department of Agriculture and U.S. Department of Health and Human Services.

Dietary guidelines for Americans. Washington, DC: Department of Agriculture, 1990.

	114.  Dietary Guidelines Advisory Committee. Report of the Dietary Guidelines Advisory

Committee on the dietary guidelines for Americans, 1995, to the Secretary of Health and Human

Services and the Secretary of Agriculture. Washington, DC: U.S. Department of Agriculture, 1995.

115. Secretary of State for Health. The Health of the Nation: a strategy for health in England.

London: Her Majesty's Stationery Office, 1992.

	116. Chen K, Kandel D. The natural history of drug use from adolescence to mid-thirties in

a general population sample. Am J Public Health 1995;85:41-47.