Alcohol and Health. Fifth Special Report to the US Congress

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TITLE Alcohol and Health. Fifth Special Report to the U.S. Congress from the Secretary of Health and Human Services. INSTITUTION National Inst. on Alcohol Abuse and Alcoholism (DHHS), Rockville, Md. REPORT NO DHHS-(ADM)-64-1291 PUB DATE Dec 83 NOTE 170p. AVAILABLE FROM Superintendent of Documents, U.S. Government Printing Office, Washington, DC 20402. PUB TYPE Information Analyses (070)

EDRS PRICE MF01/PC07 Plus Postage. DESCRIPTORS *Alcoholism; Drinking; Etiology; Health; Heredity; *Physical Health; Pregnancy; *Prevention; Social Problems; Traffic Accidents

ABSTRACT This report is divided into an overview of alcohol and health, and eight chapters which deal with various aspects of alcohol use and abuse. The epidemiology e. alcohol abuse and alcoholism is discussed. Data are presented on self-reported consumption of alcohol among youths and adults; alcohol consumption during pregnancy; alcohol-related hospitalizations and mortality; alcohol problems in veterans and native Americans; and alcohol-related traffic fatalities. Early and recent studies on the heritability of alcoholism are reviewed, the environmental-genetic influences on alcoholism are considered, and human and animal studies on the genetic factors in physiological responses to alcohol are explained. In a discussion of psychobiological effects of alcohol, cognitive and neurophysiological effects, neuropathologic illnesses, electrophysiology, and neural and biochemical effects are considered, and theories of the effects of alcohol are reviewed. The medical consequences of alcohol are discussed in terms of alcohol and the digestive system, the liver, muscle systems, blood disorders, kidney disease, pulmonary disease, the endocrine system, and alcohol and cancer. The effects of alcohol on pregnancy outcome are discussed. Adverse social consequences of alcohol use and abuse are described, including alcohol-related accidents, crime, domestic problems, and suicide. Treatment trends in research and practice are discussed and preventive efforts are reviewed. (NRB)

*********************************************************************** * Reproductions supplied by EDRS are the best that can be made * * from the original document. * *********************************************************************** FIFTH SPECIAL REPORT TO THE U.S. CONGRESS ON ALCOHOL AND HEALTH FROM THE SECRETARY OF HEALTH AND HUMAN SERVICES

DECEMBER 1983

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DE Pat tMENT OF HEALTH AND HUMAN SERVICES Public Health Service Alcohol prim Abuse and Mental Health Admtntstrabon National Institute on Alcohol Abuse and Alcoholism 5600 Fishers Lane Rockville. Maryland 20851 This publicationmay be reproduced in any quantity desired.It is in the public domain and no permission is required.Citation of the source Is appreciated.(NIAAA)

DHHS Publication No. (ADM) 84-1291 Printed 1984

For sale by the Superintendent of Documents, U.S.Government Printingonto Washington, D.C, 20402 Contents Page Foreword

Preface vi vii Acknowledgments Contributors vii Reviewers viii

Introduction x

Alcohol and Health An Overview xiii Defining Alcoholism and Heavy Drinking xiii Alcoholism and Heredity xiii Alcohol and the Brain xv Other Health Hazards xvi Adverse Social Consequences xviii Treatment Trends xx Prevention xiii Future Directions xxiii

Chapter I. Epidemiology of Alcohol Abuse andAlcoholism 1 Consumption of Alcoholic Beverages Measured byAlcohol Sales 1 Surveys of Self-Reported Consumption Among Adults 2 Surveys of Alcohol Consumption Among Youthand Young Adults 3 Surveys of Alcohol Consumption During Pregnancy 5 Alcohol-Related Mortality Attributed to Alcoholism,Alcoholic Psychosis, and Liver Cirrhosis 6 Alcohol-Related Causes of Hospitalization 7 Alcohol-Related Problems in Veterans 8 Alcohol-Related Problems Among Native Americans 8 Alcohol-Related Motor Vehicle Fatalities 9 Summary 11 References 13

Chapter II. Genetics and Alcoholism 15 Heritability of Alcoholism--Early Studies 15 Heritability of Alcoholism -- Recent Studies 16 Environmental-Genetic Influence on Alcoholism 17 Genetic Factors in Physiological Responses toAlcohol 19 Potential Mechanisms of Genetic Influence 21 Summary 22 References 22

Chapter III. Psychobiological Effects of Alcohol 25 Cognitive and Neurophysiological Effects 25 Neuropathologic Illnesses 28 Electrophysiology 30 Neural and Biochemical Effects 31 Theories of Alcohol's Effects Summary 37 References 39 39 Chapter IV. Medical Consequences of Alcohol 45 Alcohol and the DigestiveSystem Alcohol and the Liver 45 Alcohol and Muscle Systems 48 Alcohol and Blood Disorders 51 Alcohol and Kidney Disease 53 54 Alcohol and Pulmonary Disease 54 Alcohol and the Endocrine System Alcohol and Cancer 55 59 Summary References 59 60 Chapter V. The Effects of Alcoholon Pregnancy Outcome Historical Perspective 69 69 Fetal Alcohol Syndrome andAlcohol-Related Birth Effects Prevalence 70 70 Problems with Human Fetal AlcoholStudies Animal Models 71 71 Specific Adverse Pregnancy Outcomes 72 Alcohol Use, Abuse, and Dependence and Pregnancy 75 Implications of Current Knowledge--Frontiers Summary 77 References 78 79 Chapter VI. Adverse Social Consequences of Alcohol Use and Alcoholism 83 Alcohol and Accidents Alcohol and Crime 83 87 Alcohol and the Family Alcohol and Suicide 89 92 Economic Costs of Alcohol Abuse 93 Summary 95 References 96 Chapter VII. Treatment: Emerging Trends in Research and Practice 100 Recent Advances in Diagnosis and Nomenclature 100 Screening and Early Detection of Alcoholism 104 Alcoholism Treatment: Programsand Therapeutic Approaches Therapeutic Approaches 105 109 Factors Affecting Treatment Outcome 113 Emerging Trends and Future Directions 115 Summary References 116 117 Chapter VIII. Prevention: A Broad Perspective Current Perspectives 122 122 Education, Information, and Training Law and Regulation 123 Current Activities 130 Summary 133 136 References 137 Index 142

5 iv Foreword

As thisreport so amply documents, the Interest to a few dedicated men and women price of alcohol abuse to the American people themselves often recovering alcoholics. Rppallingly high. And that price Is paid by Treatment now involves many thousands in the all of us. The cost to our economy has been helping professions as well. In industry, many, estimated at over $49 billion each year. But perhaps most, companies are coming to rec- the dollar cost is only the beginning. The cost ognize that losing a valued employee to alco- in human pain and misery, disease, and death holism Is costly--and that making provision for isstill more staggering. Accidents on our treatment just makes good business sense. streets andhighwaysclaimabout50,000 Many health insuranceplans are providing Americans' lives each year--leaving another benefits to treat alcoholismItself as they 150,000 permanently disabled. Half of those discover It costs much less in the long run than tragedies are alcohol related. Alcohol's role in treating its chronic health consequences. disrupting family life is less easily document- Perhaps the most encouraging sign Is the ed, but few doubt that it is significant. One in increasing awareness Americans are develop- three Americans surveyed last year felt that ing that we ourselves have a primary respon- alcohol caused problems in his or her family. sibility for preserving our well-being by prac- Fortunately,thislong-neglectedproblem ticing better health habits--including modera- has now become of increasing concern to many tion in alcohol consumption. Americans. As a result of citizen action, drunk This report deserves to be widely read--and driving, once largely ignored, is now being its implicationsthoughtfully considered. taken seriously. More and more States are Through our combined efforts, we can sharply enacting tougher laws to discourage driving reduce alcohol abuse and its devastating con- after drinking. Treating alcoholics once was of sequences.

Margaret M. Heckler Secretary of Health and Human Services December 1983

6 v Preface

Thishas been a centuryofimpressive Implicated in a wide range of other illnesses as achievement In public health. The &hien'. of well. vaccines against such diseases as stud! 'pox, As this and previous Alcohol and Health diphtheria, and polio and their widespread ap- reports indicate, the increased Federal role. in plication have virtually eliminated those once this area has markedly altered an earlier pes- dreaded Illnesses. Tuberculosis, the cause of simistic outlook with respect to treating those one In eight deaths In 1900, is now uncommon dependent on alcohol. We no longer believe and still more rarely 'fatal. Antibiotics have that the alcoholic must reach the late stages made most infectious diseases easily curable. of the Illness before he or she can benefit But the devastation of one disease has not yet from help. On the contrary, as in other ill- been significantly eroded. It plays a role in 10 nesses, there is good evidence that the earlier percent of all deaths in the United States. In treatment begins, the greater is the likelihood some segments of the population, it produces of successful recovery. still higher mortality. It is the principal cause Alcoholresearchhasprovideduswith of deaths through accidents among those aged greater insight into the underlying mechanisms 15 to 24. That malady is, of course, alcohol of alcohol dependence.ItIs by no means abuse. visionaryto say that our enhanced under- Alcohol abuse during pregnancy has been standing holds the promise not only of im- found to cause fetal alcohol syndrome and proved treatment, but of preventing alcohol other alcohol-related birth defects. Fetal al- dependence before it develops. We may not be cohol syndrome appears to be one ofthe far from the day when simple laboratory tests leading known teratogenic causes of mental can determine those who are at greatest risk retardation. There is reason to believe that of becoming alcoholic -- before they take that alcohol may be injurious to the developing first drink. fetus at dose levels no higher than those often The Fifth Special Report, together with Its consumed by those who drink moderately. predecessors, provides valuable insight Into In adults, alcohol abuse is the leading cause the impressive progress that has been made-- of liver cirrhosis (the eighth leading cause in and the distance yet to be traveled before we the United States), the leading contributing resolve this major public health problem. factor for chronic pancreatitis, and has been

Edward N. Brandt, sr., M.D. Assistant Secretary for Health

vi Acknowledgments

This Fifth Special Report on Alcohol and Health is the productof many people's efforts in reviewing and summarizing hundreds of scientific papers,begun shortly after the Fourth Special Report was forwarded to the U.S. Congress in 1981.The chief contributors, many of whom also contributed to previous reports, include some of the mostdistinguished scientists and knowledge- able alcoholism researchers and medical authoritiesin the world today. Equally important roles were played by individuals whoprovided professional review of the preliminary report. The combined efforts are reflected in every chapterof the report. Contributors Harold L. Altshuler, Ph.D. Ting-Kai Li, M.D. Texas Research Institute of MentalSciences Indiana University Texas Medical Center School of Medicine Houston, Texas Indianapolis, Indiana

Thomas F. Babor, Ph.D., M.P.H. Henry Malin Department of Psychiatry Acting Chief University of Connecticut Surveillance Branch School of Medicine Division of Biometry and Epidemiology Farmington, Connecticut National Institute on Alcohol Abuse and Alcoholism Herbert Barry III, Ph.D. Rockville, Maryland Department of Pharmacology and Toxicology University of Pittsburgh Peter R. Martin, M.D. Pittsburgh, Pennsylvania Acting Chief Section of Clinical Science Ralph Hingson, Sc.D. Laboratory of Clinical Studies School of Medicine National Institute on Alcohol Abuse Boston University and Alcoholism Boston, Massachusetts Rockville, Maryland

Paula I.. Hoffman, Ph.D. Barbara S. McCrady, Ph.D. Department of Physiology and Biophysics Center of Alcohol Studies University of Illinois at the Medical Center Rutgers University Chicago, Illinois Piscataway, New Jersey

Ronald Kadden, Ph.D. Roger E. Meyer, M.D. Department of Psychiatry Department of Psychiatry University of Connecticut University of Connecticut School of Medicine School of Medicine Farmington, Connecticut Farmington, Connecticut

Charles Kaelber, M.D. Peter E. Nathan,Ph.D. Division of Biometry and Epidemiology Alcohol Behavior Research Laboratory National Institute on Alcohol Abuse Rutgers University and Alcoholism New Brkinswick, New Jersey Rockville, Maryland

vii Robert J. Sokol, M.D. David H. Van Thiel, M.D. Wayne State University University of Pittsburgh Department of Obstetrics and Gynecology School of Medicine Detroit, Michigan Pittsburgh, Pennsylvania

Boris Tabakoff, Ph.D. Diana Walsh, Ph.D. Department of Physiology andBiophysics School of Medicine University of Illinois at the Medical Boston University Center Boston, Massachusetts Chicago, Illinois

Reviewers

James Beard, Ph.D. Donald W. Goodwin, M.D. University of Tennessee University of Kansas College of Medicine School of Medicine Memphis, Tennessee Kansas City, Kansas

Linda J. Beckman, Ph.D. Richard Jessor, Ph.D. University of California at Los Angeles University of Colorado Department of Psychiatry Institute of Behavioral Sciences Los Angeles, California Boulder, Colorado

Henri Beg leiter, Ph.D. Benjamin Kissin, M.D. Department of Psychiatry State University of New York SUNY Downstate Medical Center College of Medicine Brooklyn, New York Department of Psychiatry Brooklyn, New York Nancy L. Day, Ph.D. Department of Psychiatry and Epidemiology Gerald E. McClearn, Ph.D. Western Psychiatric Institute and Clinic Pennsylvania State University University of Pittsburgh College of Human Development Pittsburgh, Pennsylvania University Park, Pennsylvania

Richard A. Deitrich, Ph.D. William C. McCready, Ph.D. University of Colorado National Opinion Research Center Health Sciences Center University of Chicago Denver, Colorado Chicago, Illinois

Ivan Diamond, M.D., Ph.D. Marlene Oscar-Berman, Ph.D. University of California School of Medicine School of Medicine Boston University San Francisco, California Boston, Massachusetts

Herman Diesenhaus, Ph.D. Carrie. Randall, Ph.D. Colorado State Department of Health Medical University of South Carolina Denver, Colorado Charleston, South Carolina

Terry! T. Foch, Ph.D. Theodore Reich, M.D. Pennsylvania State University Psychiatrist-in-Chief College of Human Development Jewish Hospital University Park, Pennsylvania St. Louis, M4souri

viii Robin Room, Ph.D. Don Walker, Ph D. Pacific Medical Center University of Flo: Ada San Francis,:-,, California College of Medicine Gainesville, Florida Steven Schenker, M.D. University of Texas James R. West, Ph.D. Health Science Center University of Iowa San Antonio, Texas Iowa City, Iowa

Brian Suarez, Ph.D. Sharon Wilsnack, Ph.D. Washington University University of North Dakota Jewish Hospital School of Medicine St. Louis, Missouri Grand Forks, North Dakota

A significant number of NIAAA staffmembers made major contributions tothis report as technical reviewers and consultants.These individuals included LoranArcher, Deputy Director, NIAAA; Lois Chatham, Ph.D., KennethWarren, Ph.D., Helen Chao, Ph.D.,Tina Vanderveen, Ph.D., Mark Green, Ph.D., Albert Pawlowski,Ph.D., Daniel Lettieri, Ph.D., NathanRosenberg, Ph.D., Norman Chang, Ph.D., and ElsieTaylor, Division of ExtramuralResearch; Henry Malin, Division of Biometry and Epidemiology;William Gregory, Rita Albery, andJudi Funkhouser, Division of Prevention and ResearchDissemination; Susan Farrell and JoanWhite, Office of Policy Analysis; and Brenda Hewitt,Special Assistant to the Director,NIAAA. Ph.D., who served Other individuals who made significantcontributions were Robert Petersen, overview and other front matter, as a writer and providedtechnical assistance, particularly in the and Samuel Rosenfeld, a sciencewriter who participated during theearly draft stages of the report.

10 ix Introduction

To know where you are, it is often usefulto It is ironic that it tookso long for public look back at where you've been. Less than 13 policytoreflectaninformedconsensus. years ago, a major U.S. Government publica- Nearly 200 years ago, one ofour country's tion described the problem of alcohol abuse in most distinguished physicians, Dr. Benjamin America as follows: Rush, labeled alcohol abusean "addiction and a disease."2 He also provided the first epi- No other national health problem hasbeen demiological estimate of the number of deaths soseriouslyneglectedasalcoholism. each year from alcohol abuse. His estimate of Many doctors decline to accept alcoholics 4,000 deaths annually In a population of 6 as patients. Most hospitals refuse to ad- million (66.7 per 100,000) is surprisingly close mitalcoholics.Availablemethodsof to present estimates (as highas 93.2 per treatment have not been widely applied. 100,000). Research on alcoholismandexcessive While the problems associated with alcohol drinking has received virtuallyno sig- are still very much with us, we at the Institute nificant support.' take satisfaction In what has been achievedin the 12 years since NIAAAwas established. The It went on to laud the transition froman "at- first edition of the Alcohol and Healthreports mosphere of moral disapproval" in which al- (1971) referred to alcoolisr-6-7-11as an 'iceberg coholics were treated as "sinnersor criminals" problem," because social pressures causedso to the recognition that alcoholism isan illness. many with the disease to deny it. In the years Only 3 years before, a U.S. Court of Appeals, since, the hidden portion of that iceberg has In a precedent-setting decision, held thata become more and more exposed. There have homeless alcoholic's public drunkennesswas been important shifts inour attitudes toward involuntary. Up until then, nearly half of all drinking. Removing the moralonus from al- arrests (excluding traffic offenses) were re- coholism made it easier for alcoholicsto ad- lated to drunkenness. By 1968, Congressen- mit to having a disease rather thana defect of acted the Alcoholic Rehabilitation Act (P.L. will. Organizations that previously stressed 90-374), declaring that "alcoholism isa major anonymity in their rehabilitation efforts have health and social problem" and that"the become more sympathetic to individual self- handling of chronic alcoholics within thesys- disclosure. Many of our leading citizensare tem of c.irninal justice perpetuates and ag- now willing to "come out"to acknowledge gravates the broad problem ofalcoholism their own hard-fought battles with alcohol whereas treating it as a health problemper- addiction. Their courage has made it easier for mits early detection and prevention... and others to recognize that they too have alcohol effective treatment and rehabilitation. ." problemsand to do so at an earlier stage. This Act and subsequent legislation (P.L. There have been other benefits ofmore 91-616) establishing the National Instituteon honestly recognizing that problems from al- Alcohol Abuse and Alcoholism (NIAAA) cohol abuse can occur at all levels of drinking translated the long-held position of knowl- and of the society. The still prevalent myth edgeable professionals that alcoholismwas a that drinking is "sophisticated,"a necessary treatable disease Into national public policy. It part of the "successful" life, is slowly being officially declared, "Our task is not topunish, eroded. It now requires less socialcourage to but to heal." refuse a drink or to requesta nonalcohol sub- stitute. The belief that drinking is essentialto masculinity has been very mucha part of U.S. Department of Health, Education, and Wel- 2 fare. Alcohol and Alcoholism. National Clearing- Rush, 8. An Inquiry into the Effects of Ardent housefor Mental HealthInformation Pub. No. Spirits upon tbs. Human Body and Hinds wan ...y.1 5011. Washington, D.C.t U.S. Government Printing Office, 1969. tisompLaLitturslAg1124.162110. 11115) Brookrie'"ierriagn* at h "*-81 14. American folklore. It is being supplanted by an determine what works best with whom and increasing recognition of the health hazards of under what circumstances.Innovative em- alcohol abuse and a new commitment to af- ployee assistance programs are now chal- firmation of good health practices. A public lenging the traditional belief that treatment health revolutionis underway with official must be completely voluntary to be successful. recognition that the individual can do more for There is evidence that job-based referrals to his or her own health than any doctor, hospi- treatment, provided early and in lieu of distal, drug, or other medical innovation. The ciplinary action on the job, can be as effective past decade has clearly shown thathabits as as treatment sought on one's own.Treating basic to personal health as smoking, diet, and alcohol dependence early is far more likely to exercise can be changed--and in a remarkably succeed and is less costly to treat than in- short time. Our success in changing behaviors tervention when this insidious disease is far that were once thought immutable provides advanced. good reason for optimism about alcohol abuse. The fact that treating alcoholism within the As has become true of smoking, not drinking framework of health insurance plans is cost- of drinking more moderately maybecome the effective has now been proven repeatedly. "in" thing. There is no question that this leads to lower The carnage on our highways documented long-term health costs to the individual and here and in earer reports has also led to a the plan. Encouraging expansion of health innew public appreciationofthegravityof surance coverage to include adequate treat- mixing drinking with driving. Citizen groups ment of alcohol dependence is an important have been impressively effective in changing and continuing priority of the Institute. public attitudes toward drinking and driving, The high costs of medical care are coming making individuals more aware of just how under more careful scrutiny. While a hospital much alcohol impairs driving skill. was once thought to be the onlysuitable set- Primaryprevention--beforedrinkinghas ting for detoxifying alcoholics, other settings even begun--may be one key tosharply re- may beequally effective- -and much more ducing the high casualty rate from alcohol cost-effective. Alternative treatment models described in this report. Early intervention, employingcf.: *Hied alcoholismcounselors between the sixth and ninth grades, is one have had dem.trated success. As the capa- means of educationally "inoculating"children bilities of these less expensive alternatives against alcohol (and tobacco) abuse. Such ef- become apparent, health insurance programs forts to teach good health habits early need to shouldincludethemwithintheirbenefit be carefullyevaluated. As indicated here, structure. most alcohol education efforts at older ages A lack of agreement as to just what is and havebeenmoresuccessfulinincreasing meant by such terms as "alcohol abuse" knowledge about the drug, possibly altering "alcoholism" has plagued us for many years. expressed attitudes, but not in changing actual Because of it, comparing research and treat- drinking. ment outcomes has sometimes beendifficult. Drinking during pregnancy is now known to We now recognize that alcohol abuse and al- pose risks for the health of the newborn.Pro- coholism are both multidimensional with mul- grams directed toward womenwho have al- tiple causes. The newer modes of classifi- cohol problems could sharply reduce the num- cation described in this report attempt to take ber of newborn who suffer such serious con- this complexity into consideration. sequences of maternal drinking asthe fetal One of the most satisfying developments in alcoholsyndrome andotheralcohol-linked recent years has been research innovation. birth anomalies. Federal support for alcohol research, once Treatment of alcoholism has come of age. almost nonexistent, has had significant Im- Once largely confined to dedicated members pact. By its very nature, basic research is a of groups like Alcoholics Anonymous and a few long-range enterprise, and its practical im- committed professionals, treatment efforts in plications are often not immediately apparent. recent years have grown ai -1,7,st exponentially. But studies of the ways in which alcohol alters Treating alcoholics is nowespectable"--and the cellular anatomy and neurophysiology of training for physicians and others to treat the the brain are already enlarging our under- alcohol-dependent personreflectsthisnew standing in ways that have practical "payoffs." found status. A sensitive measure of the brain's electrical There is an increased willingness to subject respcnses to sound and light stimulation may therapeutic efforts to research scrutiny--to prove useful in determining those at greater

xi 10 riskof becoming alcohol dependent. Other percentage of problem drinkers of all ages by indications of the effects of alcoholon chem- 20 percent. The increased healthawareness in icals that govern nerve transmissionare pro- our country should facilitate achieving that viding better explanations of juot why certain goal. At the same time, we hope to attainre- symptoms of alcohol abuse occur. Newneu- ductions In alcohol-related accidents ofover rophysiological explanations of how alcohol 20 percent and decrease cirrhosis mortalityby and other dependency-producing drugs operate 10 percent. offer the tantalizing possibility ofsome form The risk of women's drinking whilepregnant of chemotherapy to reduceor even eliminate.is now recognized by only three-quarters of the likelihood of becoming alcohol dependent. women of childbearing age. Raising thecon- While this is not a promise for the Immediate sciousness of women to the point whereat future, it is an example of the kind ofpayoff least 9 out of 10 are aware of the potential that is unpredictable in the initialstages of risk by the end of the decade isa realistic goal basic research. for our public information efforts. Biological markersdescribedhere--tests While over half of Fortune 500 firmsnow that distinguish heavy drinkers from others by have alcohol prevention and referralprograms, measuring effects on the bloodor other bio- we believe that a heightened awareness of the logical variables--are becoming valuable in the value of employee assistanceprograms will early diagnosis of those with drinking prob- increase their numbers of 70 percent by 1990. lems. Used in many kinds of settings,such Building on the significantly improved epi- tests can serve to alert the individual to the demiological effort the past decade,it reality that he or she has an alcohol problem. should be possible by 1990 to collect farmore There is now evidence that making patients comprehensive data on the impact of alcohol aware of the results of such tests, together abuse on American society that will enableus withlimitedfollowuptreatment,canbe to better monitor what is happening- -andto effective. modify our programs as we becomemore Advanced computer technology appliedto aware of changing national needs. brain scanning has also shown evidence of If this edition of Alcohol_and Health,pro- alcohol-inducedbrain damage--eveninthe vides some grounds for optimism,t is absence of obvious clinical signs. little basis for complacency. Alcohol continues In earlier reports, the significance of her- to exact a fearsome toll. We sometimes forget editya biological predisposition toward al- that the cost of alcohol abuse to American coholismwas in doubt. A substantial body of society is highethan that for cancer, and at animal and human research now leaves little least equal to that for heart and vascular dis- question that heredity plays a roleIn sus- ease(Alcoholism and Related Problems: ceptibility to some of alcohol's effects and in Opportunities for Research. Report of the some individuals increases their likelihood of Institute of Medicine of the National Academy becoming dependent on it. The distinctpos- of Sciences,Washington, D.C.,1980).The sibility of identifying such potential alcoholics amount of our national resources devoted to early may enable us to focus prevention ef- reducing these costs is still modest compared forts on those at high risk. with that earmarked for more "acceptable" Our advances in knowledge have led toa disease. The moralistic stance ofan earlier measure of optimism in dealing with alcohol era, to that extent at least, is still with us. abuse. The 1990 Objectives for the Nation Many--perhaps most of us--continue toexper- cited in this report reflect this. Weare hope- ience conflicts about our use of alcohol. Aswe ful, for example, that, by 1990, 80percent of resolve those conflicts, a more rational indi- high school seniors will feel, as onlya third vidual and collective approach becomes now do, that there is "great risk" in becoming possible. intoxicated. It may be possible to reduce the

Robert G. Niven, M.D., Director National Institute on Alcohol Abuse and Alcoholism Alcohol and Health An Overview

Alcoholisundoubtedlythe most widely consequences of alcohol abuse. These conse- used- -and abused--drug in America. In1981, quences can be summarized mostsuccinctly by the latest year for which figures are available, saying that there is much evidence--on many the equivalent of2.77 gallons of absolute grounds- -forconcludingthatalcohol used (pure) alcohol was sold per person over age 14. heavily is costly in human as well as economic Translated into alcoholic beverages, thisis terms. New evidence of that costwill be dis- about 591 12-ounce cans of beer or 115 bottles cussed here. But the question of how much (fifths) of table wine or 35 fifths of 80 proof must be used to produce a giveneffect is far whisky, gin, or vodka.1 However, Americans more difficult to answer.Research on humans are far from equal in their drinkinghabits. In and animals indicateslarge individual dif- national surveys, a third of adults report they ferences in susceptibility to the drug. don't drink. Another third report drinking just When the term "alcoholic," "alcohol abuser," over 2 drinks per week(0.21 oz. absolute al- or "problem drinker" is used todesignate an cohol/day), and the remainingthirdreport alcohol abuser, It must be kept in mind that consuming an average of 14 drinks per week. these designations are somewhat lessthan But such averages are deceiving - -a tenth of precise. What is usually meant by an alcoholic the drinking population consume half the al- is an individual who has been formally diag- coholic beverages sold. nosed as such or has (or has had) serious al- While drinkingisnominally restricted to cohol problems that meet implicit or explicit adults,itactually begins much earlier. By criteria of alcoholism, whether or not these ninth grade, more than half (56percent) of have ever been formally diagnosed. It ishoped high school seniors responding to an annual that, in this report, context will clarify mean- 1982 natioml survey had tried alcohol. Butby ing. Similarly, the term "heavy use" sometimes their senior year, more than 9 out of 10(93 means use that is statistically morefrequent percent) had done so. Almost all seniors (90 than is true of American users generally(as in: percent) had drunk alcoholic beverages in the "The heaviest using third of the population previous year. Two out of 5 seniors (41 per- consume an average of 14 drinks perweek."). cent) reported they had had five or more More often, it is used to indicate a level at drinks -- enough to become drunkon a single whichpathological(oradversebehavioral) occasion in the 2 weeks prior to the survey. changes occur more frequently. Some types of Six percent reported drinking on a daily or episodic or binge drinking may fit neither def- near daily basis. High schooldrinking patterns inition of heavy use, but may nevertheless over the 7 years sampled havechanged very have serious implications (e.g., drunk driving). little. Male seniors drink more often than While we have indicated the drink equiva- females and are more likely to do so daily. lent of a particular amount of absolute alco- A third(31percent) of the high school hol, in reality typical drinks are by no means seniors did not disapprove of drinking one or uniform, and we are forced to rely on rough two drinks daily, although two-thirds(65 per- approximations. As in describing other areas cent) felt that as many as four or five drinks of real life (e.g., smoking habits), we are per day would be harmful. obliged to accept a certain lack of precision. But within those limits, meaningful observa- Defining Alcoholism and Heavy tions are possible, as this and earlier reports Drinking demonstrate. Previous editions of this report, likethis one, describe in detail manyhealth and social Alcoholism and Heredity Assuming 0.6 oz. absolute alcohol 21.5 oz.80 Is alcoholism inherited? New evidence con- proof spirits 2 Soz.table wine (12 percert alcohol) A 12 oz. beer (5 percent alcohol). cerning genetic susceptibility to alcoholism is

14 one of the exciting developments In recent Whiletheresearchjustdescribedhas research. The belief that alcoholism somehow stressed the importance of genetics in "runs in families" the is an old one. But growing up eventual development ofalcoholism,itis with an alcoholic parent as a role model Sias certainly not a simple matter of "naturevs. been the traditional explanation for the higher nurture." Other studies suggest thatwith a than normal rate of alcoholism in children of genetic susceptibility toward becomingalco- alcoholics. Evidence that alcoholics' children, holic, the additional factor ofnurturance by despite having been raised by nonalcoholics, an alcoholic parent doubles the chances of the still have a higher rate of alcoholismis per- child's becoming alcoholic.Butformany, suasive that genetics plays an important role. probably most, alcoholics, genetic factorsare Moreover, specific biochemical andphysio- not apparent in their immediate family's his- logical characteristics in which heredityap- tory. However, this does not rule out heredity. pears to be important have recently been Since studies have not been made of identified in alcoholics. multiple generations,thereisno way ofknowing A pioneering study of ,*coholicswho had whether such a biological tendencywas pres- half-siblings(i.e.,brothersorsisterswith ent in earlier generations. whom they had onlyone biological parent in Animal researchin which systematic in- common) found that half-siblingswho were breeding for several generations has beendone also alcoholic were three timesmore likely to clearly indicates the important roleof genet- have had an alcoholic natural parent than tt.) ics in determining individual susceptibilityto nonalcoholic half-siblings. many of alcohol's biological effects. Strains of Research on children adopted atan early animals can also be selectively bred to prefer age also helps to clarify the role of heredity drinking alcohol while other strains donot. and environment.Researchers studied a Assuming that some inherited tendency in- matched sample of naturalsons of alcoholics creases the likelihood of a person's becoming who were then adopted by others,comparing alcoholic, there are manyways in which it them with the natural sons of nonalcoholics might operate. To name a few: The individual who were also adopted. Bothgroups had been could be more sensitive to certain kinds of raised by nonalcoholic adoptiveparents. The stimulus overload, and alcohol may blunt this alcoholics' sons proved to be three timesmore sensitivity - -a mode of self-medication. The likely to become alcoholics than thesons of central nervous system might neurochemically nonalcoholic parents. When thesons of alco- function in a way that makes itmore readily holics were compared with their brotherswho dependent on the drug. It could alsoaccount had remained in their alcoholic families ofor- for a more rapid development oftolerance igin, the two groups had thesame rates of al- (the need for greateramounts to produce a coholism, a finding that heredity playsan im- given effect) and physical dependence.There portant role in the development of alcoholism. is some evidence for all of these andother Although too few femaleswere considered mechanisms as well. in the above studies to drawany conclusions Studies of human twins suggest thatas much about a genetic factor inwomen alcoholics, a as half the variation in the rate at which al- more recent study of adopted women found cohol is eliminated from the bodymay be that those whose natural mothers were alcohol geneticallydetermined. The otherhalfIs abusers were four times more likely to become probably related to how alcohol andother alcoholics than those whose motherswere not. drugs are used, diet, and other personal Alcoholic fathers did not habits. seem to have the Twin studies also indicate geneticallybased same effect on their daughters. Interpreting variationinsusceptibilityto such medical this study is complicated by the possiblerole complications as cirrhosis of the liver andal- of the mothers' alcoholuse while pregnant in cohol-induced mental disorders. affecting their daughters' later alcohol prob- Researchers have recently found thatone lems. While it Is the first studyto suggest a form of the genetically determined liveren- biological predisposition inwomen alcoholics, zyme aldehyde dehydrogenaseisabsentin there is no way of knowing whether thepre- many Orientals. This likely accounts for the disposition is on an in utero developmental higher rate of facial flushing observedafter basis or a hereditary basis--or both. drinking among many of these individuals. The A more recent study identifieda male lim- facial flushing is often accompanied bynau- ited form of alcoholism wheresons of alco- sea, vomiting, and a drop in blood pressure. holic fathers are at ninefold higher riskfor These unpleasant symptomsare similar to the developing alcoholism themselves. reaction that occurs when aperson taking

xlv 15 disulfiram consumes alcohol.Suchbuilt-in Alcohol and Brain Damage negative responses to alcohol may partially explain why individuals from similar back- Chronic brain injury caused by alcohol is grounds often differ so widely in their alcohol second only to Alzheimer's disease as a known consumption. cause of mental deterioration inadults. Many The certainty that heredity plays a signif- of the symptomsloss of ability to think ab- icantroleinthe development of harmful stractly, speech difficulty, and decreased co- drinking behaviors and in affecting individual ordination--are similar in the two types of sensitivity to alcohol's injurious effects offers disease. Both groups of patients show brain the possibility of better defining biological atrophy (shrinkage) and similar abnormalities subtypes of alcohol abusers. If the initial op- in brain electrical functioning. However, Alz- timism about finding biochemical markers is heimer's diseaseisinvariablyprogressive, justified by further research, it may be pos- whereas alcoholic mental deterioration is not. sible to identify potential alcoholics early- - If the patient stops drinking, the deterioration before they develop serious alcohol problems is arrested and substantial recovery can occur. or alcoholism. (Even in alcoholics without obvious evidence ofmental deterioration, CAT scanscom- puterizedtechniquesforvisualizingand measuring the brainhave revealed abnormalities).Anotheradvancedcomputerized Alcohol and the Brain method (average evoked response orAER) measures the response of thebrain to light and Alcohol's effects on the brain are among its sound stimulation. Recent work indicates that mostseductive--anddestructive -- properties. alcoholics respond differently than do non- Its pleasure-giving potential, along with many alcoholic persons. Alcoholics are more sensi- of its behavioral hazards, has been recognized tive to the stimulation. One theory is that since antiquity. Its natural occurrence through their sensitivity leads them to drink in anef- spontaneous fermentation probably makesit fort to reduce their stimulus overload. Pos- our most ancientmind-altering substance. But sible evidence of this is the recent discovery it Is only very recently that we are beginning that those with family histories of alcohol to understand the complexityof alcohol's ef- use --even though they were notthemselves underlying neuroanatomical alcoholicswere different in their AERs from fects and their family. If and physiological basis. those who had no alcoholics in the thisfindingisconfirmed,it may provide another means for early identification of those at risk of becoming alcoholics. Effects of Alcohol on SkilledPerformance Other advances in brain measurement have Amounts often drunk socially (two or three found that alcohol alters brain activity in drinks in an hour) can cause significant im- parts of the brain involved in memory, emo- pairment intheskillsrequiredindriving, tion, and higher level functioning. Microscopic flying, and other complex performance. Re- study of the brains of patients who havedied cent evidence also indicates thattime of day with Korsakoff's syndrome, an alcohol-induced can make a difference in howseriously one's disease characterized by severe memory loss performance is affected. Decrementstypically and impaired learning, has disclosed brainin- persist for many hours after drinking inthe jury near nerve pathways involved in these evening. Alcohol combined with fatigue has a functions. These brain lesions are very like more pronounced effectthan either alone. those found in patients who have died of acute Recent evidence also suggests that alcohol and vitaminBi(thiamine)deficiency,possibly tobacco have a greater combined effect on indicating that a similar vitamin deficiency auditory alertness than when used separately. occurs after chronic heavyalcohol use. Overall, there is compelling evidence that Debate took place in the past over whether alcohol alone and in combination with other the brain injury found in alcoholics isthe re- commonly used drugs has seriouseffects on sult of alcohol as such or of the dietarydefi- many kinds of performance.The decrements ciencies that are so common in advanced al- are generally dose-related--thegreater the coholism. It is now known that alcohol itself amount consumed, the greater theimpairment Injures brain tissue, although the combination that results. Further documentationof this of excessive drinking and poor diet may ac- can be found in earlier editionsof this report. celerate the process. "16 Neurochemistry--the study of minute quan- All of these preliminary neurophysiological tities of chemicals in the brain that govern observationsfallshortofadequatelyex- how nerve cells transmit their messages--is plaining the action of alcohol. Additionalre- also advancing our understanding of alcohol. search is needed to sort out some of these But the effects of the drug on theseneuro- conflicting--andstillclearly incomplete- - transmitters is not simple. They seem tovary explanations. depending on the part of the brain involvedas well as the dose. Dose-related opposing effectshave been Other Health Hazards found on the neurotransmitter norepinephrine. At low doses alcohol increases norepinephrine Even a casual observer notices some of the release, but at higher doses release of the effects of heavy drinking on the brain and the chemical is inhibited. This seems tocorres- complex behavior it controls. But thereare pond to the everyday observation that alcohol other, more insidious, consequences for other is initially stimulating in small amounts but parts of the body as well. And many of these has a depressant effect as more is consumed. arenotapparenteventoknowledgeable Another neurotransmitter, GABA, Inhibits drinkers. neuronal firing and can control the tendency toward certain types of convulsions. Animal research indicates that animals chronically The Digestive Tract given 4Icohol have a reduced number ofre- Cancers of the mouth, tongue, pharynx, and ceptor sites for GABA. This suggests that esophagus are more common in alcoholics than GABA may play a role in the seizures often in nonalcoholics. While the exactcause or seen in alcoholics. causes are unknown, alcohol's direct irritation Other research, on the neurocellular level, of mucous membranesiswellestablished. is probing alcohol's effects on cell membranes. This, combined with the known carcinogenic It may explain how tolerance for alcohol- -its properties of tobacco so often smoked by decreasedeffect when used regularly- - heavy drinkers, is likely to be jointly respon- develops and the neurocellular basis for phys- sible. Vitamin A and B deficiencies because of ical dependence. poor diet and/or alcohol's interference with Earlier research has found that alcoholcan the vitamins' absorption may also play a role. affect parts of the brain Involved in rewardor Animals that are vitamin A deficient are pleasure. There is now heightened interest in known to be more susceptible to skin, mouth, other mechanisms by which alcohol and similar and esophageal cancers. dependency-producingdrugsoperate.Natu- Alcoholaltersstomachacidsecretion, rallyoccurring opiate-like compounds have which along with its irritating gastric lining been found in the brain. Both these chemicals probably accounts for the stomach problemsso and externally derived opiates seem to have common in alcoholics. It weakens the stomach similar sites of actionthe opiate receptors. wall, making it more susceptible to bleeding. Chronic doses of alcohol in test animals may The use of aspirin by drinkers may increase alter the function of these opiate receptors. the likelihood of bleeding from the already This finding has led scientists to speculate weakened wall, sometimes leading to that alcohol and other psychoactive drugs may hemorrhage. act similarly in the brain. Some support for Alcohol has multiple effects in the intes- this theory comes from the observation that tines. It impairs vitamin absorption, isan ir- narcotic antagonists--drugs that can block the ritant, and results in increased gastrointestinal effects of an opiate by occupying opiate re- motility. This often leads to diarrhea in heavy ceptor sites- -also block some, but not all, of drinkers, which may contribute to theirpoor alcohol's effects. nutritional state. Another provocative preliminary hypothesis Chronic pancreatitisis common inalco- is that a group of chemicals called tetrahy- holics. Seventy-five percent of thecases in droisoquinolines, or TIQs, may play a role in the United States are believed to occur in al- habitual heavy drinking. TIQs are formed when coholics. Although pancreatitis often results in alcohol is metabolized. In some animal ex- abdominal pain and vomiting, half the alco- periments, when these chemicals were in- holic population show alteration in pancreatic jected into the brains of animals, their pref- function without obvious symptoms. Recent erence for alcohol increased significantly. evidence suggests that alcoholics may have

xvi 17 more of a specific geneticallydetermined an- Alcohol and the Blood tigen--a chemical that activates the immune system, which suggests a genetic mechanism Excessive drinking causes blood abnormali- behind the vulnerability to this disorder. Pan- ties. Both enlarged red blood cells and anemia creatic cancer is also twice as frecluent in are produced. These are probablythe com- alcoholics--75 percent of those who contract bined result of vitamin deficiency, alterations the disease are moderate to heavy drinkers. in fat metabolism (because of liverdamage), Perhaps the best known effects of excessive and other still unknownor poorly understood alcohol use are those on the liver. These range mechanisms.Abnormally large cells are so from fatty liver, the most common--and re- common (found in 90 percentof alcoholics) versible--problem, to cirrhosis, which is life - that a measure of this, the mean corpuscular endangering andirreversible.Whileitwas volume or MCV, has been suggested as a once thoughtthatliver damage couldbe means of detecting alcoholism.Four or more averted by an adequate diet, it is now known months of abstinence may be required before that damage occurs regardless of how nour- the MCV returns to normal. ishing the heavy drinker's dietis. Alcoholic Many alcoholics also have reduced white hepatitis also results from heavy drinking. The blood cell counts. These cells play an impor- inflammation and later destruction of liver tant role in the body's immune response.A cells from this disease kills 10 to 30 percent of diminished immune response has now been those who develop it. Alcoholic cirrhosis is the reported in alcoholics. The higher rates of most dangerous consequence to the liverfrom infectious disease common in this group are drinking, causing at least 11,000 deaths annu- probably attributable to this lowered ally in the United States. resistance. Alcohol and the Heart Alcohol and Sexuality Alcohol when used heavily may have det- Alcohol interferes with male sexual func- rimental effects on the heart. Cardiac myop- tioning.That was known inShakespeare's athy--damage to the heart muscle--often oc- time--and probablybefore.But recentre- curs after 10 or more years of heavydrinking. search provides both confirmation and an ex- Symptoms of this disorder range from chronic planation. Impotence and/or reduced sexual shortness of breath and ankle swelling to heart drive are found in from 70 to 80 percent of failure. Degenerative changes in heart muscle alcoholics. The same percentages have been cells can be seen with the electron micro- reported to show testicular atrophy and in- scope. If the damage is not tooextensive, re- fertility. Alcoholics have much lower levels of covery is possible, although it mayrequire 5 or the principal male hormone testosterone than more years of abstinence. do nonalcoholics, along with increasedlevels Alcoholalsointerfereswiththeheart's of female hormones. Because of this, 50 per- ability to contract. Heart beat irregularities cent of male alcoholics developfeminine pubic (cardiac arrhythmias),which can lead to heart hairpatterns, and 20 percent have breast failure, are common in alcoholics. Two ounces enlargement. of whisky drunk by an individual whoalready Like other effects of alcohol,these changes has heart disease can suppress theheart's in sexuality were once believed to arisefrom pacemaking abilities. liver injury. More recent evidence clearly in- dicatesthatalcoholreducestestosterone levels and causes direct gonadal injury. It also Effects on Other Muscles affects sexual functioning indirectly through Its impact on the brain's hypothalamus andthe The effects of alcohol on muscle tissue are pituitary, the so-calledmaster gland. Recent not confined to the heart. Muscularweakness research suggests that the increase in estrogen and severe pain from muscle cramping are levels found in alcoholic men is also partly due fairly common In heavy imbibers. Mild symp- to adrenal changes. The adrenal glands pro- toms of these myopathies, which may notbe duceestrogenprecursors--chemicalsfrom severe enough to come to medicalattention, which estrogens are laterformed, although the occur in about a thirdof alcoholics. Alcohol mechanisms involved are not yet known. also affects involuntary smooth muscle con- The alcoholic female's sexuality is also af- tractions. fected by her drinking.Severe gonadal fall-

xvii 16 ure--an inability to produce adequate quanti- will result In congenital anomalies cannot be ties of female hormones--leads to loss of such specified with precision. secondary sexual characteristicsas fat de- One somewhat encouraging finding is that posits in the breasts and other parts of the many women who usually drink heavily mark- body, reduced (or absent) menstruation, and edly decrease their drinking while pregnant. infertility. As with men, the control of hor- Such a reduction might be expected to demone production by the brain and the pituitary crease the risk of congenital defects. gland is affected. Current estimates arethat FAS affects somewhere between 1 and 3 births per 1,000, but other alcohol-related birth defects prob- Alcohol and Pregnancy ably add significantly to that number. Are- cent calculation suggests that 5 percent of Clinical and experimental researchover the total birth defects may be alcohol related. past decade underscores the threat to the de- Animal research, which can be morecare- veloping fetus that maternal alcohol misuse fully controlled than that on humans, leaves represents. The term fetal alcohol syndrome littledoubtthatalcoholingestionduring (FAS), first used 10years ago to describe a set pregnancyhasserious consequences.Birth of symptoms in the newborn infant believedto defects closely ;esembling those found in hu- be caused by heavy maternal alcohol abuse, mans have beerproduced In many animal has recently been more carefully standardized. species. Scientists who administered two doses The new standard demands that three kinds of of alcohol to mice on one day early Lipreg- characteristics be found in the newborn to nancy (an animal model resembling human justify being classified as a case of FAS: (1) binge drinking) found abnormal facial features growth retardation before or after birth, (2) in offspring like those reported in human FAS. abnormal features of the face and head such Extensive animal--and human--findings amply as unusually small head circumference and/or justifydiscouraging women fromdrinking flattening of facial features, and (3) evidence while pregnant. of central nervous system abnormality (e.g., Lowered birth weight is the most consistent mental retardation, abnormal behavior, etc.). result of alcohol use during pregnancy. Since Other birth anomalies are regardedas allow birth weight is associated with more fre- cohol related If there Is evidence of heavyor quent neonatal deaths and is frequently asso- frequent maternal drinking duringpregnancy ciated with mental retardation and neurolog- and if the specific anomalies occur In greater ical defects, this finding is important. frequency, after control for confounding var- Several studies have found low IQ and motor iables, among the children of heavier than development scores related to maternal al- lighter drinkers or abstainers. Some studies cohol use. Most recently (1983), 4-year-olds suggest a riskfor outcomes including de- whose mothers drank during their gestation creased birth weight and increased spontane- were found to have decreased attention spans ous abortion at levels of alcohol consumption and slow reaction times. Children with FAS as low as two drinks per day, although some and animals prenatally exposed to alcohol have investigatorsquestionwhethertheseself- been found to show hyperactivity. reported consumption levels are not in actu- alityhigher.Isolatedinstancesofheavy Paternal Drinking drinking may also pose significant hazard. Women's alcohol use during pregnancy has Although It is known that long-term alcohol been described by one research group as "the use by men can lead to reduced sperm counts, most frequent known teratogenic cause of decreased sperm motility, and higher rates of mental retardation inthe Western World." sperm abnormalities, thereisno evidence However, theprevalenceoffetalalcohol from either animal or human studies that syndrome or of other alcohol-relatedbirth heavy alcohol use leads to congenital defects defects Is not easy to specify. Moreover, since in the children of such men. heavy drinkers often underestimate (orun- derreport) levels of drinking, It is difficultto be certain how much alcohol consumption Is required, at what point or points in pregnancy, Adverse Social Consequences to produce abnormalities. Because developing fetuses probably differ in their sensitivityto Alcohol abuse plays a role In many kinds of alcohol as well, the pattern of alcohol use that social problems. In some--traffic accidents,

xvlli 19 for example--what is known about alcohol's the risk of being hit was twice as high at blood effects on complex skills makes it reasonable levels above 0.10 percent, five times higher if to ascribe a causal role to the drug. In other the BAC was above 0.20 percent. proble, s--child and spouse abuse, for example--excessive alcohol use is probably not the Industrial Accidents primary cause althoughitmay contribute significantly, perhaps by reducing inhibitions Less is known about the relationship of al- that might otherwise curb expression of anger. cohol to industrial accidents than to traffic accidents, although such a connection is pre- dictable. A 1982 Maryland study of workers Traffic Accidents who died in job-related accidents found that 11 percent had BACs above 0.08 percent. Traffic accidents are the fifth leading cause While this may not be nationally representa- of death in the United States and its leading tive, it indicates a relationship that should be cause among those under age 35. In the latest further examined. year for which data exist (1981), such tragedies killed 49,000 and permanently disabled Other Accidents another150,000 persons. The consensusis clear--alcohol is responsible for up to half of It is hardly surprising that the heavy imbiber these tragedies. A review of 23 studies found a is at greater risk in other types of accidents as third or more of drivers in fatal accidents had well. Accident statistics are 'consistent with blood alcohol concentrations (BAC) above the this expectation. Alcoholics are 5 to 13 times usual legal standard for drunk driving of 0.10 more likely to die from falls than nonalco- percent. Five or six drinksconsumedin the 2 holics. Alcoholics are also much more likely to hours before driving can cause this level in a die in fires--a tenfold increase over nonalco- 155-pound person. Drivers with blood alcohol holics. Heavy drinkers had 2.7 times the ac- concentrations above 0.10 percent have been cidental death rate (omittingtrafficacci- estimated to be 3 to 15 times more likely to dents) of other Kaiser-Permanente members have a fatal accident than nondrinking drivers. during a 10-year followup period. While such Other estimates have concluded that even statistics do not prove that alcohol played a lower BAC levelsfrom 0.05 to 0.099 per- direct role in the particular hazard, the pre- centIncrease theriskfrom1.25to3.25 sumption cannot be dismissed. times. This is the level that results when a 155-pound person has had three to four drinks Alcohol and Crime or a 120-pound person asfew as twoto three drinks within 2 hours.Unfortunately, many people are not aware of these risks. A recent Although many statistical associations have Massachusetts survey found that 17 percent of been made between alcohol use and criminal respondents believed the fiction that you can behavior, a direct causal link is more tenuous. have six or more drinks without becoming too One of the earlier homicide studies (1958) drunk to drive. (Six drinks ina 155-pound found that either the murderer or the victim person would result in a BAC above 0.10 per- had been drinking in two-third., of the slayings cent, even if the drinks were consumed during reviewed. Subsequent research has also found a 3-hour period before driving.) that a majority of murderers, their victims, or Pedestrians who have been drinkingalso both had been drinking prior to the crime. have a much higher risk of being Injured or Whatever the role of drinking in such studies, killed in a traffic accident than do nondrink- it is confounded by such factors as a failure to ers. In one recent study, more than a third(36 control for age, sex, and race, all of which are percent) of injured pedestrians and nearly half related to both violence and drinking. The (45 percent) of those who died from being most that can be concluded is that alcohol is a struck by a motor vehicle had blood alcohol contributing cause but is probably only one of concentrations above 0.10 percent. Only 13 several factors involved. percent of a control sample of uninjured pedestrians passing the same accident sites at a Rape similar time had that high a BAC. As with motorists, the higher thebloodlevel,the The role of alcohol in rape is even more higher the risk of accident involvement. Com- difficult to assess. Not only is rape very un- pared with that of the nondrinking pedestrian, derreported--authoritiesagreethatonly a

xix 20 minority of attacks are reported--but intox- Economic Costs ication may be offered as an excuse or ex- tenuating circumstance by the rapist. Studies General agreement exists that alcohol abuse of rapists, however, indicate that they often results in lost work productivity and an in- drank heavily prior to the crime, and that crease in industrial accidents. In one study of their rate of alcoholism is two to three times railroadcompanies,problemdrinkershad that of the general population. Whether alco- twice the absenteeism of other employees. hol plays a disinhibiting role, or serves as a Much less is known about the costs associated justification for the behavior, or plays some with episodic drinking on or off the job as it other part is unclear. affects work performance. Estimating the costofalcohol abuse to Alcohol and the Family American societyisdifficult. Many of the variables that should be taken into account are Alcohol abuse undoubtedly affects family simply not known with sufficient accuracy. life. It is noteworthy that a third of persons But even making very conservative assump- Interviewed in a 1982 survey felt that alcohol tions about these factors, a recent calculation caused problems in their families. But the places the annual national loss at about $49.4 precise ways in which it does so are more billion. The bulk of this amount$36.8 bil- difficult to document. The rate of separation lion--represents the value of lost productivity. and divorce among alcoholics is seven times The cost of various kinds of medical care for that of the general population. Two out of five alcohol-related illness and injury totals $6.4 domestic relations court cases involve alcohol. billion.The remaining $6.2 billionincludes While few doubt that heavy drinking plays such added costs as traffic accidents, fires, some role in family violence and the abuse of crime, and other miscellaneouslossesat- spouses and children, just how and to what tributable to alcohol. extent is again hard to specify. Most studies Perhaps the highest cost is the incalculable report that alcoholism or excessive drinking is pain and misery associated with alcohol abuse Involved in about half the cases of spouse for the abusers, their families, and the larger abuse. As with rape, drinking may be used as society. There is no disagreement that those an excuse for the violence involved. Early re- costs are profound. views of child abuse have described associations between it and alcohol in as many as 38 percent of cases. However, a recent review Treatment Trends has concludedthat alcohol Involvementin child abuse is no higher than in the general A basic problem in treatment is deciding population. just who is an alcoholic and just what is alco- A 1983 review of the effects of parental hol abuse. Failure to agree on definitions is alcoholism on children indicates that they are the basis for much of the confusion regarding more likely to have school problems and to the exact prevalence of alcohol abuse and its display antisocial behavior. Other studies re- implications. The latest revision of the Amer- port that such children have less self-esteem, ican Psychiatric Association's Diagnostic and more anxiety symptoms, more aggression, and Statistical Manual of Mental Disorders (DSM- more psychosomatic symptoms. illneirresents an important advance incon- ceptual and diagnostic clarity. Using a multi- Alcohol and Suicide dimensionalmatrix,ittakesintoaccount alcohol-induced symptoms, psychosocial Given the high rate of depression in alco- stress, the patient's level of adaptive func- holics, itis not surprising that they have a tioning, and related personality disorders. It is high rate of suicide. But here, too, itis un- hoped that the new manual will ensure uniform clear whether the depression contributes to standards that will in turn permit increased the drinking and suicide, or the alcohol use comparabilityoftreatmentandre earch causesthedepressionandensuingself- findings. destruction. Nevertheless, as the Fourth Spe- A related development in diagnosis is the cial Report noted, as high as four out of live improvement in relevant sections of the In- of those who attempt suicide had been drink- ternational Classification of Diseases (ICD) ing at the time. Alcoholics commit suicide resulting from collaborative effort between from 6 to 15 times more frequently than the the U.S. Alcohol, Drug Abuse, and Mental general population. Health Administration (ADAMHA) and the

xx World Health Organization (WHO). Central to worker has also shown definite promise. Sev- the WHO approach is the concept of a depend- eral studies have found that it works as well as ence syndrome, an interrelated cluster of cog- volz,ntarily sought treatment when measured nitive, behavioral, and physiological symptoms. by abstinence and improved job performance. One of the most promising new developments is the emergence of a group of bio- Detoxification chemical markers to assist in identifying alcoholics. While each of these tests has limi- Detoxification- -the process of withdrawing tations, several studies have now found that a the alcohol-dependent patient from alcohol profile of multiple blood tests can quite ac- and controlling his or her withdrawal symp- curately differentiatealcoholics from non- toms--has traditionally been done in a hospital alcohol ics. setting. In recent years, partly because of the The new Munich Alcoholism Test uses both high cost of in-hospital detoxification, other clinical signs and symptoms noted by the ex- settings have been tried. Although these al- amining physician. When combined with self- ternatives have not been systematically reportinginstruments and thebiological evaluated, a review of the evidence suggests marker approach, such testing promises to that detoxification can be done humanely, more usefully discriminate between different safely, and efficiently in nonhospital settings. types of alcohol-dependent patients. In pre- It may, however, be important to develop liminary trials of this approach, psychosocial clear criteria of what types of alcohol abusers problems were most evident in young abusers, are most successfullytreated by the new with clinical signs and symptortis toore com- alternatives. mon in older alcoholics. Treatment Benefits Early Intervention A number of studies testing the feasibility of treating alcoholics through medical insur- Early identification throughthesophisti- ance plans have now been completed. All have cated techniques now available offersthe found that alcoholics and their families are possibility of early intervention. And there is initially more expensive to treat, as they re- now increasing evidence that it works. Even a quire more care than those without alcohol 35-minutecounselingsessioninageneral problems. However, following treatment for hospital setting has been found to reduce alcoholism, demand for services drops, and the drinking in a significant number of newly treatment Is unquestionably cost-effective in identified problem drinkers who were followed reducing total medical expenses. The median up for 1 year. reduction in sick days and accident benefits A recent Swedish study using a biochemical was 40 percent in one review of 12 programs. marker--elevated GGTP scores--toidentify Research comparing Inpatient and outpa- heavy drinkers has also found that early in- tient treatment settings has not found sig- tervention can be valuable. Those identified nificant differences In treatment outcome. were told their GGTP results and their sig- Since patients are not usually randomly as- nificance. They were then repeatedly retested, signed to each type of setting, itis not yet given feedback on their progress, and encour- known whether differences in the types of aged to moderate their drinking. The group patients normally sent to these two settings had lower work absenteeism, fewer hospi- are important.(Seriously 111 patients with talizations, and a lower death rate during the medical complications may still be more ap- 6-year followup. propriately treated in a hospital.) In France, a combination of two biochemical tests and a clinical examination is now being Client-Program Matching used on a nationwide scale to detect early alcohol abuse in industrial, health care, and The problem of developing programs suited court settings. When a problem is found, the to special populations such as women, ethnic Individual is referred to local early interven- minorities, and the elderly has become im- tion clinics for care. The system, which has portant. As this and earlier reports indicate, yet to be evaluated, illustrates the feasibility groups such as Native Americans have much of large-scale intervention. higher rates of illness and death from alco- Work-basedalcoholismtreatmentinter- hol-related illness than does the general pop- vention as an alternative to disciplining the ulation. It is critical that treatment programs

xxi 22 be designed to overcome cultural, economic, Prevention and other barriers tiat deter some groups from seeking treatment. A survey of Cali- Alcohol abuse prevention is becoming more fornia facilities found that women alcoholics important as awareness grows that alcohol were less likely to seek treatment If programs problems are. present in the entire drinking lacked child care and aftercare arrangements population. While problems occur at lower and professional staff. More and more prog- rates In groups that drink less, they are rarely rams are being designed to meet these and totally absent other needs of special populations. There is little question that alcohol education programs can increase knowledge con- Treatment Approaches cerning alcohol and may also alter attitudes toward the substance. But the question of the Several experimental approaches to treat- extent to which they modify actual drinking ment have been extensively evaluated since behavior is not so easily answered. Even when the Fourth Special Report. Aversion therapy, such changes have been assessed--and most which links the sight, smell, and taste of al- programs have not tried to do so--they are cohol with a nausea-producing drug, appears to difficult to interpret. Changes in economic be effective with stable, well-motivated al- conditions, minimum ages at which drinking is coholics, while the same approach substituting permitted, and law enforcement policy are all electrical shock appears not to be. A related likely to overshadow program effects. technique -- covert sensitization--that pairs A 1982studyfoundthatteaching7th verbally induced nausea with imagined alcohol through 10th graders about alcohol improved consumption produces greater improvement their knowledge and also reduced their use. A than insight-oriented therapy, based on a 4- recent review of prevention programs em- year followup. phasizesthatimproveddecisionmakingis A recent study of disulfiram (Antabuse) not likely to lead to a reduction in pro-drinking discussed in the Fourth Special Report found attitudes, although itis overly optimistic to the drug slightly more effective in producing expect significant use reduction based on such abstinence after a year than a vitamin B limited interventions. preparation. Another study found that addi- Nontraditionalprogramsemphasizingin-) tional training in role playing, communication, teractive learning, which involves students in and stimulus control along with the use of di- the actual design of the prevention program, sulfiram was effective with married clients, seem to be most successful in altering atti- but not with the unmarried. Further training in tudes and possibly drinking behavior. drink refusal, social skills, muscle relaxation, Intervention--between 6th and 9th grades- - and job and recreational counseling for the to teach youngsters to develop resistance to single group raisedtheir abstinence levels, later use of alcohol (and tobacco) is a prom- however. Closely supervised use of disulfiram ising prevention strategy, although it has not in an industrial setting was effective in re- yet been followed up with longitudinal studies. ducing absenteeism. Because the college years are important in Traditional psychotherapy has been found developing long-term drinking habits, a num- not to be generally effective with alcoholics, ber of programs have been directed toward but may be useful with some types. Family these students. Improvements in knowledge therapy is also being tried, although it has not occur and thereis evidence that attitudes yet been fully evaluated. shift, but no changes in actual drinking have Early findings suggested that some "defi- been found. nitelyalcoholic"clientswerecapableof Increased sophistication is evident in pro- drinking moderately 6. months after treatment grams tailored to meet the needs of women and up to a year later. However, a followup 4 (especially during pregnancy), minorities, and years later has found that those who were ab- other special populations such as the elderly. stinent at 18 months were less likely to have These new programs need to be tested for ef- drinking problems at 4 years than those who fectiveness. drank moderately at 18 months. Mass media campaigns are probably too Patientsaffiliatedwithsuchaftercare weak an intervention to significantlyalter groupsashalfwayhousesandAlcoholics drinking behavior unless they are closely co- Anonymous have been found to have better ordinated with local education and training therapeutic outcomes than those who remain efforts. However, they can be useful in gen- unaffiliated. erating Ii8Otened interest in alcohol prob-

xxii lems and in mobilizing community resources to cally more vulnerable becoming alcohol de- deal with the problem. pendent. It may also enable them to drink Lowering alcohol consumption levels is as- moderately with less hazard. sociated with reduction in a number of adverse New evidence of the serious threat alcohol effects of drinking such asalcohol-related poses to the developing fetus argues persua- traffic accidents (especially by youth) and sivelyfor enhancedeffortsatpreventing diseases such as cirrhosis of the liver. Some maternal drinking by making women more effectiveefforts,documented throughre- fully aware of the risk. The evidence that search, are: many individuals are many times more vulnerable to alcohol's destructiveness demands Increasing taxes on alcoholic beverages that better prevention and treatment be developed for those at high risk. Better targeted Increasing the legal age for purchase of prevention efforts are also implicit in early alcoholic beverages detection of genetic vulnerability to alcohol through the use of biological markers. Altering the number and location of out- Treatment offers many opportunitiesfor lets for purchase of alcoholic beverages. increased innovation. One is to tailor programs to fit the needs of different types of clients. Many approaches that have been used with Future Directions reported success have not been adequately evaluated. The cost-effectivenessofearly New directions are evident in many parts of intervention in health maintenance organiza- this report. Among the most promising are tions and industry argues for more aggressive Improvedearlyidentificationofpotential efforts by both. problem drinkers and alcoholics and expanding Alcohol problems have plagued most soci- present basic knowledge of just how and why eties throughout history.But never before alcohol abuse is so destructive. Basic research have we had as much basic knowledge as we may result in developing strategies that re- now possess, with the promise of still greater duce the likelihood of those who are geneti- understanding to come.

24 Chapter I

Epidemiology of Alcohol Abuse and Alcoholism

Epidemiological research is useful in iden- 1969, and 14 years of age or older for years tifying many ofthe social, environmental, 1970 through1981. For1981, the average behavioral, and biological factors associated estimated consumption is 2.77 gallons per year with alcoholism and alcohol abuse. New in- or approximately 1 ounce of absolute alcohol sights and understanding of these factors are per day for each person in this population. complicated by the lack of standard and uni- Fifty-one percent of the absolutealcohol formly applied definitions. Terms such as al- consumed in 1981 was beer (1.40 gallons per cohol abuse, alcohol misuse, problem drinking, person), 36 percent distilled spirits (1.01 gal- alcoholism, and alcohol dependence are often lons per person), and 13 percent wine (0.35 usedinterchangeably. The developmentof gallons per person). uniform operational definitions should lead to Figure 2 displays estimated per capita con- continued advances in the epidemiology of sumption in 1981 for the three alcoholic bev- alcohol-relatedconditions.Meanwhile,re- erage types combined for each State and the searchers and policymakers must rely on cur- District of Columbia (NIAAA 1982a, d, e). This rent terminology and the best data available map indicates that substantial variation exists to understand the problems associated with across States in quantity of alcohol sold. Sta- alcohol abuse and alcoholism. The data pre- tistical data for each State also indicate con- sented here indicate the scope and magnitude siderable variation in the relative sales of of alcohol abuse and alcoholism in this country each type of alcoholic beverage. A number of and provide a framework for discussing the factors may Influence the variation in bever- effects of the excessive consumption of al- age sales and apparent per capita consumption coholic beverages. across States, Including: Difference In State taxes for each type of beverage Consumption of Alcoholic Beverages Measured by Alcohol Sales Differenceinthelegaldrinkingage within each State Sales of alcoholic beverages are often used as an Indirect measure of alcohol consumption. Differences in State legislation regarding But per capita consumption figures based on the location, type of outlets, and hours of sales and excise tax data do not take into ac- operation for selling alcoholic beverages count the amount of alcohol consumed in one State but purchased in another, the amount of Differences in cultural and social habits alcohol purchased but not consumed in any across geographic regions. given year, sales of alcohol that go unreported, and the consumption of Illegally produced U.S. alcohol per capita sales have increased alcohol (e.g., moonshine). approximately 35 percentsincetheearly Figure 1 shows the estimated per capita 1960s, but only 7 percent since 1971. While alcohol sales for beer, wine, distilled spirits, estimated per capita sales of beer rose 22 and the three beverage types combined. The percent and of wine rose 13 percent, sales of estimates are expressed In gallons of absolute distilled spirits have dropped 10 percent since alcohol per person, per year, for the United 1971. Considerable variationInsales rates States. For statistical purposes, this popula- occurs among States,e.g.,a decrease of 17 tion Is defined as the estimated population 15 percent In the District of Columbia and an years of age or older for years up through Increase of 36 percent In Hawaii. These data

1 2 5 must be interpreted cautiously, however, be- light drinkers (consuming up to 0.21 ounces of cause the States are differentially affected by absolute alcohol per day on the average), while such factors as drinking age, degree of urban- the remaining third were moderate (0.22-0.99 . Ization, tourism, and out-of-State purchasers. ounces) or heavier drinkers (1.0 ounces or more), the latter (heavier drinkers) consuming the equivalent of approximately two drinks or Surveys of Self-Reported Consumption more every clay. Among Adults Men drink significantly more than women, and younger adults more than older adults (see The National Institute on Alcohol Abuse and figure 3). The most recent national survey Alcoholism (NIAAA) has sponsored a series of (1979) confirms these sex and age variations. national surveys that characterize the self- In addition, the 1979 data indicate that ab- reported drinking patterns of the U.S. adult staining from alcohol Is less common In the population. Results across these surveys con- New England and Pacific regions and more ducted in the 1970s are similar. Approximately common in the South, and that the proportion one-third of the adult population described of abstainers falls as Income rises and years of themselves as alcohol abstainers (consumed schooling Increase. not a single drink in the year prior to the Findingsfromothernationalhousehold survey). Another third described themselves as surveys also confirm that alcohol consumption

Figure 1. Apparent U.S. Consumption of Alcoholic Beverages In Gallons of Ethanol Per Capita 1950-1981

I2_1_ I 1 3 I 1 -1.I1 11 2I 1 1 t.I

2.8- 4.1. 2.6- 00°. 6..6° TOTAL **- 2.4- 00' 2.2-

1.8- 1.6- 1.4- ...... BEER 1.2- ... 1-' de al . IP= oft SPIRITS 0.8 0,6- 0.4- ""'"'"' I alinsmo0 Mfla ONIMIIIIM, WINE

0 I ,rwl 2,1-21-21221.1211,2.1122r11.22 1950 1955 1960 1965 1970 1975 1980 1985 Age 15 andolder_.1 L.Age 14 and older) SOURCE Data from NIAAA 1982b.e.f

2 is greater among younger adults than among patterns and trends among the youth and older adults. During the years 1974 through young adult population. Two NIAAA surveys In 1982, the annual prevalence of alcohol use 1974 and 1978 (Rachal et al. 1975, 1980) were among younger adults, 18 to 25 years old, was followedin1980 bythe NIAAA-sponsored approximately 22 percent greater than among Gallup Youth Survey. In addition, the National adults 26 years and older. Overall, the annual Institute on Drug Abuse (NIDA) sponsors an prevalence of alcohol use reveals a slight but annual survey of high school seniors and a bi- gradual increase between 1974 and 1982. ennial household survey (NIDA 1983a)that The survey data suggest that a substantial collects data on alcohol consumption of the proportion ofall alcoholis consumed by a youth population. These surveys showed a relatively small fraction of the total drinking small decrease in the drinking levels among population (see figure4).This figure shows 16- to 18-year-olds for the years 1974, 1978, that 50 percent of the alcohol is consumed by and 1980 (Zucker and Harford in press). The 10 percent of the population. NIAAA data reveal some increase in the number of abstainers and a slight decrease in the proportion of moderate and heavy drinkers Surveys of Alcohol Consumption Among between the years 1978 and 1980. Youth and Young Adults Similar conclusions can be drawn from the national surveys of high school seniors spon- NIAAA has also sponsored a number of sored by NIDA since 1975 (NIDA 1983b). In a national surveys to assess alcohol consumption sample of approximately 130 public and pri-

Figure 2. Apparent Consumption of Ethanol from All Alcoholic Beverages in U.S. Gallons Per Capita of the Population Age 14 and Older, 1981

U.S. = 2.77

92 3.200 2.8'1'7 2 93 90

3 2 1 . 5 6 0 QUARTILES L f 1 70 2 24 2 25-2 79 111111111111112 80-3 20

SOURCE NIAAA 1982a,d,3.

3 27 Figure 3. Percentage of Drinkers by Age Group and Sex Averaged for the Period 1971-1976

90 - LEGEND 80- 444; MtVe.ONMALE HEAVIER DRINKERS

I MALE DRINKERS 70- FEMALE HEAVIER DRINKERS

60- \\ \FEMALE DRINKERS

50 -

40 -

30-

20-

10-

0 18-20 21-34 35-49 50-64 65+ AGE GROUP

SOURCE: Data from Clark. W.B. and Midanik. L. Alcohol Use and Alcohol Problems Among U S Adults: Results of the 1 979 National Survey. Alcohol and Health Monograph No1 NIAAA. 1982 DHHS Publication No (ADM) 82-1190

vate high schools selected to produce national In general, young males report more drink- estimates of drug-taking behavior among high ing episodes and more daily use than females, schoolseniors,alcoholconsumption among and consumptioo of larger quantities of alco- high school seniors has remained relatively hol on a single drinking occasion. High school stable from 1975 through 1982. The data on seniors from the South and the West appar- specific consumption show that more than 90 ently consume less alcohol than do those from percent of surveyed seniors reported having the Northeast and the North Central regions. used alcohol at least once during their life- These surveys of high school seniors also times, and almost 90 percent reported using it identified the grade at which an alcoholic In the past year. Six percent reported daily or beverage is first consumed. Approximately 10 nearly daily use during the month prior to the percent of those surveyed had their first drink survey, and a significantly greater percentage by the 6th grade. About 30 percent began reported occasional heavy drinking. Approxi- drinking by the 8th grade, about 56 percent by mately 41 percent of the 1982 sample of high the 9th grade, and about 75 percent by the school seniors stated that, on at least one oc- 10th grade. By senior year (12th grade), fully casion during the 2-week period prior to the 93 percent of those surveyed had had a drink. survey, they drank five or more drinks. The surveys show very little change in this

4 28 pattern over time. gave birth to live Infants in 1980, as well as a The surveys collected attitudinal informa. sample of married women whose pregnancies tion about alcohol consumption. In the 1981 terminated In a reported fetal death. These survey, 22 percent believed consumptionof two surveys conducted by the National Center one or two drinks daily to beharmful; 36 per- for Health Statistics (NCHS) collected infor- cent saw significantriskin having five or mationfrommarriedmothees, hospitals, more daily drinks once or twice eachweekend; physicians, and the birth or death certificates and 65 percent believed that consumption of (Prager et al. In press). Data were collected on four or five drinks daily would result in sig- prenatal care, previous pregnancies, diagnostic nificant harm. Thirty-one percent of the 1981 and other procedures performed during preg- high school seniors did not disapprove of tak- nancy, and drinking and smoking behaviorbe- ing one or two drinks nearly every day. Little fore and during pregnancy. (Additional data variation in these attitudes occurs over the and discussion are included in the chapter on 1975-1981 period (NIDA 1983a). alcohol and pregnancy outcome.) Finally, the NIDA survey data show a steady Preliminary analysis of 4,405 mothers giving decline (except for the year 1979) in the 12- to live births show that women substantially re- 17-year-olds who reported taking a drink in duce their alcohol consumption after they be- the 30-day period prior to the survey. The drop come pregnant (table 1). While 45 percentof from 37 percent in 1979 to 26 percent in 1982 these women abstained from alcohol use be- may reflect recent changes in the legal age forepregnancy, approximately 61 percent forpurchasing alcoholinthemajorityof abstained during pregnancy. The percentage of States. Future monitoring of the trends In al- all mothers who were moderate/heavy drinkers cohol consumption among teenagers and young (Level 2) declined from 12 percent before adults will clarify these findings. pregnancy to 2 percent during pregnancy. More detailed results of the NIDA surveys Table 1 also shows changes In drinking from are summarized in Alcohol and HealthMono- before pregnancy to during pregnancy. Of the graph No. 1 (Rachal et al. 1982). 516 women who drank 0.25 ounces or more of absolute alcohol per day (Level2)before pregnancy, only 16 percent continued to con- Surveys of Alcohol Consumption sume that amount during pregnancy,while 67 During Pregnancy percent consumedlessthanthatamount (Level 1), and 17 percent stopped drinking al- Recently, national surveys have been con- together. Similarly, of the 1,908 light drinkers ducted of a sample of married women who (Level 1), 66 percent remained light drinkers,

Table 1. Number and percentage distribution of change indrinking behavior from before to during pregnancy, 1980

(Married mothers giving live births)

Before pregnancy During pregnancy Number Percent Nondrinker Level 1 Level 2

Nondrinker 1,981 45 99 1 1 Level 1 1,908 43 33 66 1 Level 2 516 12 17 67 16

Total 4,405 100 61 37 2

than NOTE: Nondrinkers consumed less than one drinkless than once a month. Level 1 drinkers consumed less 0.25 ounces or absolute alcohol per day on the average.Level 2 drinkers coneumed 0.25 or more ounces per day. Source: Prager et al. in press.

2 Figure 4. Cumulative Distribution of Alcohol Consumption

100

0 0 20 40 60 80 - 100

CUMULATIVE POPULATION (%)"

'Drinkers only, aggregated from several U S national surveys. 1971-1975

SOURCE AEDS data from HANES I Medical History Questionnaire and Louis Harris and Associates Surveys for 1972-1974

while 33 percent stopped drinking. These data Alcohol-Related Mortality Attributed to confirm other research showing similar de- Alcoholism, Alcoholic Psychosis, and creases (Little et al. 1976; Rosett et al.1983). This research also describes drinking behav- Liver Cirrhosis ior before and during pregnancy for several sociodemographic characteristics of married Three important causes of death attributed mothers giving liv4! births. Black mothers drink to excessive alcohol consumption are alco- less before and during pregnancy than white holism, alcoholic psychosis, and cirrhosis of mothers. Hispanic mothers drink less than non- the liver. By definition, all deaths from alco- Hispanic mothers. Women with less education holism and alcoholic psychosis are alcohol and from families with lower incomes drink related; however, alcohol is not the exclusive lessthan women with more education or cause of cirrhosis of the liver. The 1979 U.S. higher family incomes. mortality rate foralcoholism was1.8 per

.011VAVAd03 1S39 6 30 100,000 population, or approximately 4,000 Alcohol-Related Causes of deaths. The mortality rate in 1979 for alco- Hospitalization) holic psychosis was 0.2 per 100,000 population, or about 440 deaths. Cirrhosis of the liver, the The national vital statistics record system eighth leading cause of death in the United of the National Center for Health Statistics States in1979, accounted for about 29,000 (NCHS)collects and tabulatesmortality deaths, or 13.2 deaths per 100,000 population. information by cause of death for the entire Since 1949, the death rates attributed to U.S. population, but no comparable data sys- alcoholic psychosis and alcoholism have re- tem exists to collect and tabulate statistics on mained relatively stable, while the death rate morbidity (disease) for the entire population. attributed to cirrhosis of the liver rose until The Hospital Discharge Survey (HDS) operated about 1973 and then began to decline (see by NCHS approximates a national morbidity figure 5). The U.S. mortality rate for cirrhosis surveillance system by sampling more than decreased 12 percent between 1973 and 1979. 225,000 records from over 400 participating The overall decline in the cirrhosis death rate hospitals on an annual basis.

appeals to be due to factors other than alco- 1 hol; alcohol-related cirrhosis death rates have This section summarizes various reports prepared by the National Center for Health Statistics. remained stable at approximately 5 deaths per These reports have been cumulated in the 100,000 population (Malin et al. 1982a). references.

Figure 5. Trends in Cirrhosis Mortality Rates With and Without Mentionof Alcohol in the United States, 1949-1979

150

CIRRHOSIS WITHOUT ALL CIRRHOSIS MENTION OF 100 ALCOHOL

...no/46v

50 CIRRHOSIS SPECIFIED AS ALCOHOLIC

0 .1.1.1.1111111111.1.1i 50 52 5456586062 6466 6870 7274 76 7880

YEAR

SOURCE Malin (1982) and personal communication with Mortality Branch.National Center for Health Statistics

BEST COPY AVAILABLE

7 31 National estimates have been made for the Since 1970, the proportion of VA patients years 1971 through 1980 on the numbers and with alcoholism or problem drinking has more rates of patients discharged with diagnoses of than doubled for those under age 35 (15 per- alcoholism, alcoholic psychosis, and cirrhosis cent to 35 percent). This marked increase re- of the liver. Because of sampling variability in flects the growth in alcohol-related disabil- the HDS from year to year and the relatively ities from, the Vietnam era. The reasons for low frequency of some diagnoses, monitoring this substantial increase remain to be iden- trends over time must be viewed with caution. tified. It is not clear whether (a) this increase Nonetheless, the data suggest a significant is specific to the VA beneficiary program, (b) increase in the number of persons hospitalized the statistics reflect a more general increase for alcoholism during the 1970s. For example, among all men of comparable age, (c) younger there were an estimated 200,000 alcoholism veterans have a greater proportion of alcohol discharges in 1971 compared with an estimate problems simplybecause the incidence of of 519,000 alcoholism discharges in 1978, an other health conditions such as cancer or increase of more than 160 percent. During this stroke is less in this population, or (d) the in- same period, the national mortality rates re- creases are attributable to some combination mained relatively stable. of these and other reasons. The trend over When HDS data are considered by sex, the time does reflect, in part, the aging of this rates for discharges with alcoholism are 3-1/2 group,increased years ofdrinking,and a to 4-1/2 times greater for males than for fe- greater probability of being diagnosed as al- males. While the numbers and rates of dis- coholic. In' response to alcohol problems, the charges with alcoholism have increased for VA has promoted specialized alcohol depend- both sexes,thisratio has remainedfairly ence treatment programs, which have multi- constant. The male rate for hospital discharges plied from 8 in 1970 to 100 in 1980. for cirrhosis of the liver has remained stable through the 1970s at about 1-1/2 times the female rate. Alcohol-Related Problems Among Native Americans Alcohol-Related Problems in Veterans Alcohol-related mortality is a major prob- Data from the Veterans Administration (VA lem among Native Americans, with cirrhosis 1982) show that a substantial fraction of the of the liver the fourth leading cause of death. nearly 1 million discharges from VA hospitals Accidents are the leading cause, and the con- in 1980 had an alcohol-related disorder, in- tribution of alcohol to fatal mishaps is sub- cludingalcoholicpsychosis,alcoholism,or- stantial. Death rates attributable to major ganic brain syndrome, and alcoholic cirrhosis alcohol-related causes of death (alcoholism, of the liver. Such disorders constitute the alcoholic psychosis, and cirrhosis of the liver second largest category of diagnoses (next to with mention of alcoholism) are about eight heart disease) among patients discharged from times greater among Native Americans than VA hospitals. The proportion rose from 15 per- for the U.S. population as a whole (Indian cent in 1970 to 19 percent in 1974 and 1975 Health Service 1982a). and has dropped slightly to 17 percent in 1977- Hospital discharge rates from the Indian 1980. Nearly two-thirds of these discharges HealthServices(IHS)hospitalsystemfor had a principal diagnosis that was alcohol alcohol-relateddiagnosesareaboutthree related. times the rates for the entire United States Periodically, the VA conducts a census of and double the rates for races other than hospitalized patients (VA 1982). During the white. This higher IHS alcohol-relateddis- 1970s, the rate of patient hospitalizations with charge rate applies to both males and females. analcohol-relatedprincipaldiagnosiswas For ages 15 to 44 years, generally years of relatively stable at about 8 to 10 percent each high productivity, the IHS hospital discharge year. In some years, the VA has also estimated rate for alcohol-related diagnoses is more than the number of problem drinkers, who consti- four times that of the rate for thetotal tute an additional 5 to 6 percent of the patient United States (Indian Health Service 1982b). census. When problem drinkers are added to Table2 shows age-specifichospitaldis- those patients identified as alcoholic, about 25 charge rates for the IHS and for the United percent of the entire VA patient load have States as a whole in 1981. INS discharges are alcohol-related problems that contribute to from IHS and general hospitals under contract their medical disabilities. to the IHS, while U.S. discharges are from

8 32 non-Federal short-stay hospitals. The alcoholic veillance of all traffic crashes involving one or psychosis rate for all ages for IHS discharges more fatalities, the Fatal AccidentReporting is four times as great (11.8 vs. 2.9 per 100,000) System (FARS). For everyfatalaccident, as the discharge rate for the UnitedStates as FARS provides data on each vehicle, each a whole. The discharge rates fornondependent driver, and each person involved in the acci- abuse of alcohol and for alcoholic liver disease dent, including a subjective characterization are 3.4 times as great (5.8 versus 1.7 and6.4 of alcohol involvement when itis known. In versus 1.9, respectively), and the alcoholde- 1981, the blood alcohol concentration (MC) pendence syndrome rate is nearly double that was known for only 30 percent ofthe 62,120 for the total United States (35.8 versus 19.7). drivers involved in fatal traffic crashes (see The table also shows these comparisons for table 3). Among these 18,540 drivers, 6,349 (34 specific age groups where the differences are percent) had no detectable BAC at the time of even greater. the testing; 2,450 (13 percent) had BACs between 0.01 and 0.09 percent; while the remaining 9,741 (53 percent) had BACs of 0.10 percent or higher, the level of legal intoxi- Alcohol-Related Motor Vehicle Fatalities cation in all but three States. In addition, of the 48,069 deaths thatoccurredin1981, Motor vehicle accidents have claimed be- 20,658 (43 percent) were known to involve tween 45,000 and 55,000 lives annually over alcohol. the past decade. While the death rate per 100 Alcohol involvement in accidents is espe- million vehicle miles has in general declined cially common in single-vehicle crashes,in by more than 25 percent (perhaps as the result which young people aredisproportionately of the post-oil-embargo lower speed limit and involved (see table 4). The 16- to 24-year-old more rigorous enforcement), motorvehicle age group accounts foronly 16.5 percent of crashes have become one of the Nation's lead- the U.S. population but 41percent of the ing causes of death for all age groups and the single-vehicle accident fatalities and 45 per- leading cause of death for persons aged 15 to cent of all single-vehicle fatal accidentsin- 24 years. Inthis age group, motor vehicle volving alcohol. In contrast, the 55-and-older fatalities account for about 40 percent of all age group represents 21 percent of the popu- deaths. lation but accounts for only 11 percent of all The National Highway Traffic Safety Ad- single-vehicle accident fatalities and 5.5 per- ministration (NHTSA) maintains national sur- cent of the single-vehicle accidentsinvolving

Table 2. Discharge rates per 10,000 from Indian Health Serviceand contract general hospitals and from non-Federal short-stay hospitals by first-listeddiagnosis andage,1981

Alcoholic Alcoholic Age at Alcoholic dependence nondependent Liver admission psychosis _syndrome abuse of alcohol disease

IHS rateU.S. rateIHS rateU.S. rate IHS rateU.S. rateIHS rateU.S. rate

All ages 11.8 2.9 35.8 19.7 5.8 1.7 6.4 1.9 Under 15 years 0.0 0.0 0.6 0.6 0.9 0.4 0.0 0.0 /15-44 years 19.0 3.1 50.5 22.6 8.6 2.1 8.0 1.1 45-64 years 20.1 6.3 83.2 38.3 8.9 2.3 18.9 5.2 65 years and over 4.9 2.0 21.7 13.6 4.4 1.6 4.2 2.4

Source: Indian Health Service 1982b.

9 33 Table 3. Alcohol Involvement by performancemeasure and by alcohol test results (BAC) of drivers in fatal traffic accidents, 1981

Alcohol involvement Drivers In determined by Alcohol test results (BAC1 Persons tested fatal performance measures 0 .01.09 .10 and + Number Percent accidents

No 6,136 2 2 6,140 14 42,878 Yes 213 2,448 9,739 12,400 64 19,242 Total 6,349 2,450 9,741 18,540 30 62,120

a When suspected of drinking by an investigating officer, a driver'spoor response to performance measures, such as the ability to walk a straight line, generally leads toa label of "alcohol involvement" on the investigative report. Source: NIAAA 1983.

Figure 6. Percentage of Drivers With Positive Blood Alcohol Concentration (BAC)by Age Group in Single Vehicle Accidents, 1981

10-

0 .- .05 .10 .15 .20 25 .30 OVER .30

BAC LEVEL

SOURCE Maim et al 1982b dispro- Alcohol-andnon-alcohol-relatedtraffic alcohol. Young drivers are even more monthly portionately involved in single-vehicleacci- fatalities appear to follow similar dents when other factors such as average variations.Forbothgroups,fatalitiesare drive higher in summer months when morevehicle miles driven and proportion licensed to tend to are considered. Fewer youngdrivers areli- miles are driven, while in winter they and they fall below the average monthly rate. censed than their older counterparts Figure 7 displays the day of week and the drive less on average. 1981. Fatali- Figure 6 shows the percentage ofdrivers in time of day for all fatalities In accidentsineach age ties In accidents with no knownalcohol in- single-vehiclefatal 8 p.m. group at various levelsof BAC. Greater per- volvement peaked between 4 p.m. and lower BACs on Sunday throughThursday. In contrast, the centages of young drivers have alcohol-related fatalities peaked later in the than older drivers. This suggeststhat younger drivers become Involved in fatalaccidents at evening (8 p.m. to 4 a.m.) forMonday through Saturday, lower BAC levels than olderdrivers (Malin et Thursday. Similarly, on Friday and the greatest number ofnon-alcohol-related al. 1982b). fdtalities occurred between 4 p.m. and4 a.m., Driversinvolvedinalcohol-relatedfatal previously while alcohol-related fatalitiesoccurred later crashes have a higher frequency of higher recorded accidents, license suspensionsand (midnight to 4 a.m.) and were much driving while than the weekend maximumsforfatalities revocations, and convictions for (NIAAA intoxicated (DWI), as well as a higher propor- with no known alcohol involvement tion of previously recorded speedingconvic- 1983). tions and "other harmfulmoving violations." For the 62,120 drivers involved(but not nec- essarilykilledthemselves) infataltraffic Summary their crashes in 1981, data were collected on that the acqui- previous convictionsforDWI. Among the In summary, it can be said have no sition of new knowledge aboutthe epidemi- drivers who were tested and found to abuse and al- detectable BAC, 2 percent had a previousDWI ologic factors affecting alcohol knowledge conviction. Among the drivers whoseBAC was coholism is increasing. Advances in 5 per- have been hampered by a lackof uniformly in the range from 0.01 to 0.09 percent, alcoholism cent had a previous DWIconviction. Among applied definitions of terms such as the drivers with BACs of 0.10 orgreater, 11 and alcohol abuse, but there areencouraging percent had previous DWIconvictions, a rate signs of progress. without de- The per capita alcohol consumption con- 5.5 times greater than the group steeply as In tectable BAC (NIAAA 1983). tinues to rise, although not as

Involvement, 1981 Table 4. Fatal single-vehicle accidentsby age of driver and alcohol

Number single- Number accidentsAlcohol-involved accidents U.S. populationvehicle accidents Total with alcohol Age group (percent) (percent) (percent)

41.0 3,190 44.6 16-24 16.5 10,295 27.8 2,193 30.6 25-34 16.8 6,977 902 12.6 35-44 11.5 3,165 12.6 8.0 476 6.6 45-54 9.9 2,002 10.6 397 5.5 55+ 21.1 2,656

7,158 100.0 Totals 25,095 100.0

Source: Malin et al. 1982b.

11 35 Figure 7. Number of Fatalities by Day of Week, Time of Day, andAlcohol Involvement, 1981

ALCOHOLRELATED ACCIDENTS

NONALCOHOIRELATED ACCIDENTS

;/000 -

500

1 000

IS Si ( i

M4 8N48 M48N48M48N48M48N48 M48N48M48N4HM4HN4I1. MONDAY TUESDAY WEDNESDAY THURSDAY FRIDAY SATURDAY SUNDAY DAY OF WEEK AND TIME OF DAY

SOURCE AEDS data from NHTSA Fatal Accident Reporting System (FARS)for 1981

earlier decades. About a third of the total substantially. Alcohol-related problemsamong population abstains from alcohol consumption Native Americans continue to bea major during the typical year, another thirdcon- source of both morbidity (disease) and mor- sumes an average of less than one drink every tality, with alcohol-related disordersamong other day, while the remaining third drinks Native Americans being several times higher more heavily. than for the U.S. population asa whole. Women substantially reduce their alcohol A substantialfractionoftheNation's consumptionaftertheybecomepregnant. traffic fatalities continuesto be associated While 43 percent abstain beforepregnancy, 61 with alcohol consumption. More than halfthe percent are abstainers during their pregnancy drivers involved in fatal accidentsare intox- period. Similarly, 12 percentare moderate to icated.DrinkingdriversinvolvedInfatal heavy drinkers before pregnancy, while only 2 crashes tend to have poorer driving records, percent continue drinking to' this extent after including a higher frequency of previouslyre- they become pregnant. corded accidents, a higher frequency ofpre- Overallmortalityfrommajoralcohol- viouslyrecorded license suspensions and/or related causes of death has remained rela- revocations, and a higher proportion ofpre- tively stable. Alcohol-related diseaseappears viouslyrecorded speeding convictionsthan to have fallen from a high point in 1973, but nondrinking drivers in similar accidents. liver cirrhosis has decreased only slightly. Epidemiological research continues to W'thin the Veterans Administration hospital clarify the nature and extent of alcohol abuse system, alcohol-related disorders have dropped and alcoholism. Increased knowledge andap- from previous high levels In the 1970s. How- plication of that knowledge to prevention and ever, the proportion of veterans underage 33 treatment could help reduce the individual and with alcohol-related problems has increased social costs of alcohol abuse and alcoholism.

12 36 References

Clark, W.B., and Midanik, L. Alcohol use and al- National Center for Health Statistics. Utilization cohol problems among U.S. adults. Results of the of short-stay hospitals: Annual summary for the 1979 national survey. In: National Institute on United States, 1979. Vital and Health Statistics, Alcohol Abuse and Alcoholism. Alcohol Con- Series 13: Data from the National Health Survey, sumption and Related Problems.Alcohol and No. 60. DHHS Pub. No. (PHS) 82-1721; 1980. Health Monograph No. 1. DHHS Pub. No. (ADM) Vital and Health Statistics, Series 13: Data from 82-1190. Washington, D.C.: Supt. of Docs., U.S. the National Health Survey, No. 64 DHHS Pub. Govt. Print. Off., 1982. pp. 3-52. No. (PHS) 82-1725.Hyattsville,Md.: NCHS, Indian Health Service. Analysis of Fiscal Year 1981 1981, 1982. IHS and U.S. Hospital Discharge Rates by Age National Institute on Alcohol Abuse and Alcohol- and Primary Diagnosis.Rockville,Md.: IHS, ism, Alcohol Epidemiologic Data System. Anal- August 1982a. ysis of Data From FARS for the Year MT. Indian Health Service. "Chart Series" Tables. FY Rockvrtle, Md.: NIAAA, April 1983. 1983 ed. Rockville, Md.: IHS, Office of Program National Institute on Alcohol Abuse and Alcohol- Statistics, March 1982b. ism, Alcohol Epidemiologic Data System. U.S. Little,R.E.;Schultz,F.A.;andMandell,W. Apparent Consumption of Alcoholic Beverages Drinking during pregnancy. Journal of Studies on Based on State Sales, Taxation, or Receipt Data. Alcohol 37:375-379, 1976. U.S.AlcoholEpidemiologicDataReference Malin, H.; Coakley, J.; Kaelber, C.; Munch, N.; and Manual,Section 1.Rockville,Md.: NIAAA, Holland, W. An epidemiologic perspective on 1982a. NTIS No. PB-82-187-113. alcohol use and abuse In the United States. In: National Institute on Alcohol Abuse and Alcohol- National Institute on Alcohol Abuse and Alco- ism, Alcohol Epidemiologic Data System. Cir- holism. Alcohol Consumption and Related Prob- rhosis of Liver Mortality in the United States, Each State and County and Selected SMSAs. U.S. lems.Alcohol and Health Monograph No.1. IHS Pub. No. (ADM) 82-1190. Washington, Alcohol Epidemlologic Data Reference Manual, D.C.: Supt. of Docs.,U.S. Govt. Print. Off., Section 2. Rockville, Md.: NIAAA, 1982b. NTIS 1982a. pp. 99-153. No. PB-82-187-097. Malin,H.J.;Trumble,1;Kaelber,C.T.;and National Institute on Alcohol Abuse and Alcohol- Lubran, B. Alcohol-related highway fatalities ism, Alcohol Epidemiologic Data System. Hos- among young drivers-United States.Morbidit pital Discharges With Alcohol-Related Coa- and Mortality Weekly Report 31(48 :641 -644, tions.Hospital Discharge Survey,1975 -1977. DataReference 1982b. U.S.AlcoholEpidemiologic National Center for Health Statistics.Detailed Manual,Section4.Rockville,Md.: NIAAA, diagnoses and surgical procedures for patients 1982c. NTIS No. PB-82-187-121. dischargedfromshort-stayhospitals:United National Institute on Alcohol Abuse and Alcohol- States, 1977, DHHS Pub. No. (PHS) 79-1274; ism, Alcohol Epidemiologic Data System. U.S. 1977, DHHS Pub. No. (PHS) 80-1274. Washington, Apparent Consumption for Calendar Year 111M D.C.: Supt. of Docs., U.S. Govt. Print. Off., AEDS WorkingPaper#50.Rockville,Md.: 1979, 1980. NIAAA, June 1982d. National Center for Health Statistics. Inpatient National Institute on Alcohol Abuse and Alcohol- utilization of short-stay hospitals by diagnosis: ism, Alcohol Epidemiologic Data System. U.S. United States, 1971. Vital and Health Statistics, Apparent Consumption for Calendar Year 1981. Series 13: Data from the National Health Survey, AEDS WorkingPaper#55.Rockville,Md.s No. 16. DHEW Pub. No. (HRA) 75-1767;1972. NIAAA, June 1982e. Vital and Health Statistics, Series 13: Data from National Institute on Drug Abuse. National house- the National Health Survey, No. 20 DHEWPub. hold survey on drug abuse. NIDA Capsules C83- No. (HRA) 76-1771; 1973. Vital and HealthSta- 1 :1 -3, February 1983a. tistics, Series 13: Data from the National Health National Institute on Drug Abuse. Student Drug Survey, No. 25 DHEW Pub. No. (HRA) 77-1776; Abuse in America, 1975-1982. DHHS Pub. No. 1974. Vital and Health Statistics, Series 13: Data (ADM) 83-1260. Rockville, Md.: NIDA, 1983b. from the National Health Survey, No. 30 DHEW Prager, W.; Malin, H.; Graves, C.; Spiegler, D.; Pub. No. (HRA) 77-1785; 1978. Vital and Health Richards,L.;andPlacek,P."Smoking and Statistics, Series13: Data from the National Drinking Behavior Before and During Pregnancy Health Survey, No. 55 DHHS Pub. No. (PHS) 81- of Mothers of Live-born Infants." U.S. Depart- 1716. Hyattsville, Md.: NCHS, 1974, 1975, 1976, ment of Health and Human Services. National 1977, 1981. Center for Health Statistics, Health U.S. 83, in National Center for Health Statistics. Standardized press. microdata tape transcript.1975 Hospital Dis- Rachal, J.V.; Guess, L.L.; Hubbard, R.L.; Maisto, charge Survey.Hyattsville, Md.: NCHS,n.d. S.A.; Cavanaugh, E.R.; Waddell, R.; and Benrud, NTIS No. PB-270-773; 1976 Hospital Discharge C.H. AdolescentDrinking Behavior *M-1978, Survey. Hyattsville, Md.: NCHS, n.d. NTIS Order Vol. 1. Rockville, Md.: National Institute on Al- No. PB-82-179-227. cohol Abuse and Alcoholism, 1980.

13 3 7 Rachal, 3.V.; Maisto, S.A.; Guess, L.L.; and Hub- alcohol consumption and fetal development.Ob- bard, R.L. Alcohol use among youth. In: National stetrics and Gynecology 61 (5)039-546, 1983. Institute on Alcohol Abuse and Alcoholism. Al- U.S. Department of Health, Education,and Wel- cohol Consumption and Related Problems. Al- fare. Third Special Report to the U.S. Cowen cohol and Health Monograph No. 1. Dill-13 Pub. on Alcohol and Health. Noble, E.P., ed. DHEVi No. (ADM) 82-1190. Washington, D.C.: Supt. of Pub. No. CADM) 79-832. Washington, D.C.:Supt. Docs., U.S. Govt. Print. Off., 1982. pp. 55-95. of Docs., U.S. Govt. Print. Off., 1978. Rachel, IV.; Williams, 3.R.; Brehm, M.L.; Cava- Veterans Administration. Office of Reportsand naugh, B.; Moore, R.P.; and Eckerman, W.C. A Statistics.Alcoholism and ProblemDrinking, National Study of Adolescent Drinking Behavior, 1970-1975: A Statistical Analysis of VAHospital Attitudes and Correlates. Rockville, Md.: Na- Patients. 1980 Supp. Biometrics MonographNo. tional Institute on Alcohol Abuse and Alcohol- IrVirshington, D.C.: VA,1982. ism, 1975. NTIS No. PB-246-002. Zucker, R.A., and Harford, T.O. A nationalstudy Rosen, H.L.; Weiner, L.; Lee, A.; Zuckerman, B.; of adolescent drinking practices In 1980.Journal Doo ling, E.; and Oppenheimer, E. Patterns of of Studies on Alcohol, In press.

14 Chapter!! Genetics and Alcoholism

One of the most keenly debatedissues in tients to report parental al -olism. Thus, the alcoholism research has been whethergenetic high rate of parental alcoh m appeared to factors play an important part in thedevel- be not a general characterisc of adisturbed opment of alcoholism. In otherwords, is sus- population but a specific correlate of alco- ceptibility to alcoholism inherited, at '.,st in holism. Alcoholism was more prevalentin some individuals? If so,what are the predis- male relatives, in the families offemale al- posing factors? To what extent doenviron- coholics, and in near relatives than in distant mental influences determine theexpression relatives. and severity of the disorder? The results of family studies do not un- An affirmative answer to the firstquestion equivocally support genetic transmission.A began to emerge 10 years ago with theGood- family shares a common environment as well win et al. (1973) study on adopted-out sonsof as common genes, andfamilial patterns of alcoholics, although the results wereinitially alcoholism can be explained just as readily by evidence behavioral and sociocultural theories asby greeted with skepticism. Impressive of now indicates that heritablefactors influence genetic ones. Although evidence in support susceptibility to alcoholism as well as to a environmental theories is tenuous, suchfac- number of physiological and biochemical re- tors cannot be ignored. Itis notable that, in Cotton sponses to alcohol consumption.Furthermore, the familystudies summarized by research has documented thatenvironmental (1979), 45 to 80 percent of the alcoholicsub- other and hereditary factors interact toproduce the jects did not have an alcoholic parent or individuals alcoholic state in some individuals. relative. This suggests that in many environmental factors influence the expression and severity of the disorder. To separate the influence of heredity from Heritability of Alcoholism that of environment, studies are needed com- Early Studies paring special populations in whichthe influence of either heredityor environment The notion that alcoholism runs infamilies differs (e.g., comparing rates of alcoholism dates back centuries. Reportsbefore 1900 on among identical versusfraternal twins or be- the familial nature of alcoholism werepri- tween half-siblings, or comparingsuch rates marily anecdotal. In the past 80 years,how- among adopted children ofalcoholics versus ever, more than 100 studieshave examined the those who are raised by their biological par- ofalcoholism(Goodwin ents). All of these special population groups familialincidence A 1971). In reviewing 39 studies conducted over have been used in alcohol-related research. and the past four decades, Cotton(1979) summar- number of studies have compared identical 6,251 alco- fraternal twins with regard to alcohol-drinking ized statistics on the families of effect holicsand4,083nonakoholics.Themost practices, alcohol metabolism, and the striking finding was that, regardlessof the of alcohol on brain waves asmeasured by nature of the nonalcoholiccomparison popu- electroencephalogram (EEG). Nonespecifi- lation, alcoholics were more likely than non- cally investigated clinically defined alcohol- alcoholics to have an alcoholic father, mother, ism, however. sibling, or distant relative. Onthe average, In 1972, Schuckit and coworkers reported on alcoholics a study of alcoholismin half-siblings. The 69 almost one-third of any sample of their had at least one parent with analcoholism probands (alcoholic subjects who brought six times families into the study) were hospitalized pa- problem. Alcoholic patients were di- more likely thannonpsychiatric patients and tients who had half-siblings and had been two times more likely thanpsychiatric pa- agnosed as having primaryalcoholism,i.e.,

Is 39 alcohol abuse without preexisting psychiatric the potentialforalcoholismingenetically disorder. Thirty-two of the 164 half-siblings susceptible individuals. Adopted-out daughters were alcoholic. It was found that 62 percent of of alcoholics and of nonalcoholicswere also the alcoholic but only 20 percent of thenon- compared (Goodwin et al.1977), but because alcoholic half-siblings hadat least one alco- so few alcoholics were found in eithergroup, holic biological parent. This differencewas no conclusion could be drawn regarding ge- statisticallyhighlysignificant.Further, the netic predisposition in women. alcoholic half-siblings had not lived inan alcoholic environmentany more frequently than hadthenonalcoholichalf-siblings.Half- Heritability of Alcoholism siblings who shared the childhood environment Recent Studies of the alcoholic proband did not havean in- creasedrateofalcoholism.Theseresults Confirmation of the findings of Goodwin and suggestedthatgeneticpredispositionwas coworkers came quickly from researchers in more important than childhood environment in Sweden and the United States. Bohman (1978) influencing the development of alcoholism. compared the rates of alcohol abuse in 2,324 A cleaner separation of geneticand envi- adoptees (1,25 men and 1,199 women) and in ronmental factors can be achieved by studying their biological parents (2,261mothers and subjects who were adoptedor placed in foster 1,902 fathers of established paternity). The homes at an early age. Suchan approach was adoptees had been born in the Stockholmarea first employed by Roe (1944), but thestudy between 1930 and 1949 and had been placed in was flawed by its small sample size and by adoptive homes before theage of 3. Histories uncertainty about the validity of the diag- of alcohol abuse were sought in the records of nostic criteria used to indicate alcoholism. the excise board, the health insurance office, The study by Goodwin and associates (1973) and other public agencies. The excise board's of adopted sons of alcoholics in Denmarkdrew register contained informationon fines im- from a larger sample population, 5,483non- posed for intemperance, treatment for alco- blood-relatedadoptioncases,anduseda holism, and supervision of chronically alco- stringent set of criteria for diagnosingalco- holicpersons.(Scandinaviancountriesare holism. The probands were 55 adopted-outsons ideally suited for large studies of thissort, of alcoholics and the controlgroup consisted owing to their systems of public recordkeeping of78 adopted-outsonsofnonalcoholics, and the accessibility of these records forre- matched to the probands bycurrent age and search use.) age at adoption. Alcoholism was definedas The Bohman study showed that adoptedsons heavy drinking leading to problems in at least whose biological fathers were alcoholicwere three of four areas, two social and two medi- three times as likely to become alcoholicas cal and physiological. Sons of alcoholicswere were the adopted sons of nonalcoholic fathers. found to be more than three timesas likely to Adopted sons whose biological motherswere become alcoholic as were sons of nonalco- alcoholic were twice as likely to become al- holics. They were also more likely to be alcoholic as were the adoptedsons of nonalco- coholic at a relatively early age and to havea holic mothers. Registration rates for alcohol form ofalcoholismsufficientlyseriousto abuse were the same among adoptedwomen, warrant treatment. Sons of alcoholicswere regardless of their biological parents' records shown as no more likely to be heavy drinkers of alcohol abuse. The findings suggested that than were sons of nonalcoholics, and havingan genetic factors influenced the occurrende of alcoholic biological parent did notappear to alcohol abuse in men, but the study'ssmall predispose individuals to psychiatric disorders. samplesizeprecludedajudgmentabout Some of the probands had brothers who had women. been raised by their alcoholic biologicalpar- Some of the data were also analyzed in the ent. A second phase of the Danish adoption manner of a control study, comparable to that studies compared the rate of alcoholismin employed by Goodwin and coworkers (1973). these adopted and nonadopted siblings (Good- From the 2,324 adoptees, 192 probands whose win et al. 1974). Nonadopted siblingswere no parents had the most frequent or seriousrec- more frequently alcoholic than were their ords of alcohol abuse were selected. These adopted-out brothers who were raised in probands included 50 men and 50women whose nonalcoholic environment. The investigat, biological fathers had been reported forre- therefore concluded thatexposure to an al- peated and severe alcohol abuse and had been coholic family environment did not Increase hospitalized for treatment of alcoholism. An

id 40 occurring with additional 42 men and 50 women whosebio- ondary alcoholism (alcoholism for alcohol and preceded by adult psychiatricdisorders), logical mothers had been reported biological abuse were included as well. The subjects were but none of them had alcoholic selected parents. Adoptee alcoholism wasfound to be compared with four control groups biological from the same population on the basisof age, unrelated to psychiatric diagnoses in parents or to a variety ofpsychosocial and sex, age at adoption,occupational category of It the adoptive parents, and ages of thebiolog- environmental variables in postnatallife. correlatedwith ical and adoptive parents when thechild was was, however,significantly childhood conduct disorders in theadoptees born. abuse In the Male adoptees whose fathers were reported and with alcoholism and alcohol as having severe alcoholismshowed a 20 per- biological parents. compared with In the second Iowa study, only maleadop- cent incidence of alcohol abuse sample was en- 6 percent in the controls. In theadopted men tees were studied, but the whose biological mothers had beenreported largedto includeadoptees whose second- for alcohol abuse, 33 percent were reported degreerelatives(e.g.,grandparents,aunts, behavior for alcohol abuse as compared with 19 percent uncles, cousins) had psychiatric or in the control group -- however, thedifference disturbances. A matched control group was is not statistically significant. On thewhole, also recruited. Out of the 167male adoptees thedataof 18 years and older thus identified,data were thesefindingsagain confirm Interview Goodwin and coworkers (1973) concerning a collected on 92 men (55 percent) by influence on alcoholism oralcohol with the adoptee, the adoptive parent, orboth. genetic The studies were marred byhigh dropout abuse in the sons of male alcoholics. available information on Adopted women whose biologicalparents rates; as measured by alcohol abuse, as well as participantsand nonparticipants,however, were reported for sample bias in the two studies wasestimated adopted women with non-alcohol-abusing biological parents, had low rates ofalcohol to be minimal. Of the 92male adoptees, 23 abuse. Because of this outcome, aconclusion were alcoholic and22 had experienced child- genetic influ- hood conduct disorders. Evidencefor alco- about the presence or lack of 15 first and second- ence on alcohol abuse in womencould not be holism was present in degree relatives. Statistically significant made. alco- ResearchersattheUniversityofIowa associations existed between adoptee 1980) holism and an alcoholic family(biological) (Cadoret and Gath 1978; Cadoret et al. disorder have contributed two reports onalcoholism in background and between childhood and the development of alcoholismin adult- American adoptees. The first studyfocused on factors, in- male and female adoptees who had been sep- hood. None of the environmental who cluding psychiatric or alcoholproblems in the arated at birth from biological parents socioeconomic showed evidence of psychiatric orbehavior adoptive family as well as its control status, predicted alcoholism. disturbance. Biological parents of the conclusions of group adoptees were notmentally disturbed. Both studies confirm the The experimental and control groups were Goodwin and coworkers "thatgenetic factors matched on age, sex, time spentinfoster importantly affect alcoholismdevelopment." mother at birth of But both failed to demonstrate anindependent care, and age of biological the devel- her child. Data were collected on84 of 173 effect of environmental factors in with the opment of alcoholism. Also, theassociation of adult adoptees by interview, either alcoholism in adoptive parents or with bothadoptee and childhood conduct disorders with of the iden- adult life is in accord with previousreports adoptive parents. The remainder disorder and tified adoptees (51 percent) eithercould not suggesting that childhood conduct hyperactivity may predict subsequentalco- be located or refused to beinterviewed. Goodwin et al. Two or more social or medicalcomplica- holism (Schuckit et al. 1972; tions of excessive alcohol use orhospitali- 1975). zation for detoxification constituted adiag- nosis of alcoholism (Feighner etal. 1972). The alcoholism rate was low in both theexperi- mental and control groups.Three adoptees Environmental-Genetic Influence with primary alcoholism wereassociated with onAlcoholism 1 alco- 6 alcoholic biologic! .1parents versus here clearly biologicalparents The adoption studies described holicadopteefrom78 predisposition is an without alcoholism. Seven adopteeshad sec- demonstrate that genetic

17 41. Important determinant of alcoholism insome Type II alcohol abuse occurred In 4percent individuals. What then is the contribution of of the adopted men. It represented, therefore, environmental influences to the expressionof about 25 percent of the alcohol abusers inthe alcoholism in other individuals? Dothine in- study. Their biological fathers, butnot their fluences affect severity of the disorderIn the mothers, had severe alcoholism requiringex- genetically susceptible individual? tensive treatment. Postnatal environmenthad In other words, are subtypes ofalcoholism no effect on the expected numbers of abusers and alcohol abuse each affected to different but may have Influenced severity. Alcohol extents by genetic and environmental vari- abuse in the susceptible sonswas usually re- ables? To study these questions,researchers current and moderate, although sometimes it from Washington University in St.Louis and was severe. An estimated ninefold increase In from Sweden collaborated to analyzefurther risk of developing alcohol abuseor alcoholism the population of adoptees studied byBohman was evident in the affected individuals, (1978). re- This research teamfirst examined gardless of postnatal environment. Thechar- adopted men withalcoholabuse problems acteristics of this type ofalcohol abuse/ (Cloninger et al. 1981). Out of 1,125adopted alcoholism are similar to those described in men in the Stockholm adoption study reported the Danish adoption studies (Goodwinet al. by Bohman, 862 subjectswere selected whose 1973). paternity was known and whowere adopted It is notable that an average of 60percent before the age of 3 by nonrelatives. of the men in all three categories of alcohol These adoptees werefirstdividedinto abuse had no family history of abuse. Their groups according to severity of alcohol abuse. alcohol abuse may have been caused byother Mild abuse was definedas one registration for disorders, such as psychiatricor behavioral. abuse (by the excise board) without treatment. Alternatively, they could represent, inpart, a Moderate abusers had two or three registra- group whose parents were geneticallysus- tions withouttreatment,whereassevere ceptible to alcohol abuse but lacked thenec- abusers had at least four registrations and essary environmental provocation to become compulsory treatment or psychiatric hospi- abusers. This issue remains unresolved: talization for alcoholism. The characteristics Bohman et al. (1981) studied adoptedwom- of the biological parents (e.g., severity ofal- en, using a similar statistical analysis. From coholabuse,occupationalstatus)andof the1,199 adopteesoriginallyreported by postnatal environment (e.g.,occupational Bohman (1978), 913 satisfied theentry cri- status of adoptive father, age at adoptive teria. Because only 31 women (3.3 percent)out placement) were analyzed to findwhich fac- of this sample were alcohol abusers, theywere tors would best distinguish onegroup from not grouped by severity of abuse. A fourfold another. The discriminant characteristicsof increaseinalcohol abuse occurredinthe each group were then applied to the total adopted women iftheir biologicalmothers population to measure the extentto which were alcohol abusers. A relationship between these characteristics contributed to thenum- alcohol abuse in the biological father and that ber of individuals with alcohol problems. in the daughter was less clear-cut.Itap- As a result of these statistical analyses,two peared, therefore, that in daughters maternal heritable subtypes of alcoholismwere iden- alcohol abuse was a more significant predictor tified, which the authors named TypeI(or of abuse than was paternal alcohol abuseor milieu-limited) and Type II (or male-limited). alcoholism. Both biological parents of alco- Type I alcohol abuse occurred in 13percent of hol-abusing female adopteeswere mild alcohol the adopted men. Both their biological fathers abusers who usually did not require extensive and mothers typically exhibited mild alcohol treatment. When young, the alcohol-abusing abuse requiring no treatment, and postnatal female adoptees were frequently placedin environment determined both the frequency rural homes in which adoptive fathers had low and the severity of alcohol abuse in thesus- occupational status; the women generally had ceptible sons. The sons' alcohol abusewas had contact with their biological mothers be- usually mild or isolated, but could besevere, fore final placement. Alcohol abuse inthe depending upon the nature of theenviron- adoptive home did not modify the risk ofal- mental provocation. With such provocation, cohol abuse in the daughters. As with the the relative risk of developing alcoholabuse in study on male adoptees,many women came congenitally predisposed individualswas in- from families with no history of alcohol abuse. creased twofold; without it, the riskwas the The most remarkable finding of this study same as that in the general population. was the strong component ofmother-and-

18 42 daughter transmission in the adoptee daugh- rate of acquisition of tolerance toalcohol ters. But the Influence may not bepurely genetic, since alcohol abuse by the pregnant rateof development andseverityof mother may have affected the growing fetus physical dependence on alcohol (thelatterwould, of course, be true for mother-daughter or mother-sontransmission). susceptibility to the medical complica- In the adopted women, both the severityof tions of chronic alcohol consumption. alcohol abuse and the characteristics of their biological parents resembled those of the Type Studies in humans and in experimental ani- Imale alcoholabusers. The influenceof mals have shown a tremendous degree of in- postnatal environment on frequency and se- dividual variation in their biological responses verity of abuse could not be conclusively es- to alcohol. A considerablebody of evidence tablished, however, because of the limitations now shows that much of thisvariation Is ge- of the sample population or thefailure to netic in origin (McClearn and Erwin1982). The identify the relevant variables. Both of these findings in humans and in experimental ani- unresolved issues will require further inves- mals will be described separately as they use tigation. Nevertheless, the study demonstrated different experimental approaches and design. for the first time the existence of agenetic or congenital determinant for alcohol abuse In Human Studies women. The demonstrationthatsocioculturalin- Because genes cannot be manipulated in fluences are critically important in the ma- humans, studies have been limited to the com- jority of genetically predisposedindividuals parison of fraternal and identical twins and of suggests that changes in behaviorand social different ethnic groups. Identical twins have attituaes by and toward individuals at high risk identicalsetsofgenes, whereas fraternal or, can alter both the courseand the prevalence twins do not. By comparing variability of alcohol abuse and alcoholism.Potential conversely, similarity in the expression of a alcohol abusers could be identifiedthrough trait within sets of identical andfraternal herit- sensitiveandaccuratephysiological,bio- twins, researchers can determine the chemical, and behavioral predictors of alco- ability or the importance of genes in the ex- holic vulnerability. These recentdiscoveries pression of that trait. Twin studies are not are significant forfuture treatment and pre- perfect, however, since the environment of vention strategies as well as forfuture re- identical twins tends to be more similar than search on this important healthproblem. To that of fraternal twins. Hence, the extent to this end, prospective and longitudinalstudies which genetic factors affect that trait cannot with children of alcoholics, severalof which be established with absolutecertainty. A are in progress, offer apromising approach similar limitation pertains to the comparison (Schuckit 1980; Gabriel li et al. 1982; Elmasian of different ethnic populations:They differ allcandidate et al. 1982). socioculturally.Accordingly, genetic traits predisposing to alcoholabuse should be studied in experimental animals so Genetic Factors in Physiological that environmental Influences can beexperi- mentally controlled. Responses to Alcohol Several twin studies have been performed on al. A number of biological responses toalcohol drinking behavior (Kaij 1960; Partanen et 1972; potentiallyhavepathophysiologicalsignifi- 1966; Jonsson and Nilsson 1968; Loehlin cance for alcohol abuse,including Kaprio et al. 1978). General agreement pre- vails that genetic factors Influence the quan- cravingoralcohol-seeking be- tity and frequency of drinking as well assuch alcohol hangovers and havior symptoms of heavy drinking as loss of control. Identical twins are morealike sensitivity of the central nervous system than fraternal twins in their drinkingbehavior, (CNS) to alcohol but the environment may play aconsiderable role. sensitivity of other body systems(sys- Twin studies have also been used to demon- temic sensitivity) to alcohol strate that neurophysiologicalsensitivity to alcohol and alcohol elimination rate are ge- rate of alcohol metabolism orelimination netically controlled. Propping(1977) showed

19 43 that alcohol's effects on brain-wavefunction example, approximately half of the are nearly identical in identical twins, whereas Japanese population exhibit the reaction, whichhas they are disparate in fraternal twins.Alcohol been linked to elevated blood acetaldehyde elimination rate varies bya factor of 2 to 3 levels after alcohol intake (Mizoiet al. 1979). among individuals, even after adjustment for Alcohol flush was once thought to be thecon- body weight (Bennion and Li1976). Several sequence of an overproduction of acetaldehyde studies have compared identical and fraternal (Stamatoyannopoulos et al. 1975). Morerecent twins to determine how much geneticfactors research, however, indicates that thereaction contribute to this variation (Vesellet al. 1971; may result from the absence of a particular Kopun and Propping1977). Genetic factors form of aldehyde dehydrogenase, thereby af- account for about 40-50 percent of thevari- fecting the oxidation of acetaldehyde (Inoue ation in alcohol elimination et rate. Daily alcohol al. 1980; Agarwal et al. 1981; Teng 1981).In- intake, smoking, diet, and druguse are some direct evidence suggests that acetaldehyde of the environmental factors thataccount for can cause the release of histamine and perhaps the remainder. othersubstancesaffectingbloodvessels; A potentialbiochemicalexplanationfor hence, the flush reaction. genetic variation in human alcoholelimination Finally, studies of twins have shownthat rate has recently been discovered. AlcoholIs some individuals may be genetically suscept- eliminated from the body primarilythrough ible to certain medical complications ofpro- metabolism. The enzymes or proteincatalysts longed alcohol abuse, namely liver cirrhosis responsible for this processare alcohol dehy- and psychosis (Hrubec and Omenn 1981). Also, drogenase and aldehyde dehydrogenase. The some people may be susceptible to developing first enzyme oxidizes alcohol to acetaldehyde the Wernicke-Korsakoff syndrome dueto an and the second enzyme oxidizes acetaldehyde inherited metabolic defect involvingone of to acetate. Acetate then enters the general the thiamine (vitamin B1)-requiringenzymes metabolic pathway for sugars and fats andis (Blass and Gibson 1977). Studiesto confirm oxidized further to carbon dioxide andwater theseImportantobservations areclearly (Li 1977). The amount and propertiesof alco- needed. hol dehydrogenase in the liver determinethe rateofalcohol metabolism--and thereare many genetically disparate forms of this enzyme in human livers, varying among individ- Animal Studies uals. The individual molecular forms of hu- Animals, like humans, vary in their man liver alcohol dehydrogenase havenow responses to alcohol. Genetic factors are re- been isolated, and many of them differ mark- sponsible for some of the differences, includ- edly In their catalytic properties (Bosron and ing such responses to alcoholas the acquisition Li 1981). Since the combination offorms is of tolerance and physical dependence. Anim- determinedgenetically,thevariationin portant feature of animal experimentation, elimination rate among individuals can be Impossible with humans, is the ability toma- readily accounted for by the large differences nipulate the genetic background of the animals in the genetically determined properties ofthe through inbreeding,selectivebreeding, and different enzyme forms. No experimentshave other measures. It has been possible to develop yettried to correlate the specificenzyme lines or strains of animals with highor low makeup of individuals with their alcoholme- responsiveness to the various actions of alco- tabolism rates. However, It has been reported hol. Such animals can then be usedto study that Chinese and Japanese individuals,on the the biochemical and physiological mechanisms average, metabolize alcohol 30 percent faster underlying genetic variability andto discern than Caucasians do (Hanna 1978). More than how these developed traits and mechanisms 90 percent of Orientals possess the so-called affect alcohol-drinking behavior. Conversely, atypical alcohol dehydrogenase genetictrait breeders can develop animals that preferor (Bosron and Li 1981). The atypical alcoholde- disdain alcohol, and researcherscan test their hydrogenase enzyme formsare much more responsiveness to the various actions of alco- active than the forms present in Caucasians. hol. Such animal studies can suggest hypoth- Someindividuals,particularlyOrientals, eses and experimental approaches in human respond to alcohol with an "alcohol flush,"a research to learn what predisposes individuals systemic reaction consisting of facial flushing genetically to aberrant drinking behavior. Re- and rapid heart rate and, in severe cases, search with animal models thus providesa nausea, vomiting, and low blood pressure. For cornerstone offuturebiologicalknowledge

20 4 4 susceptibility to the chronic administration of alcohol(Grieve ...bout the nature of genetic al.1980). Inbred alcoholism. et al.1979; Tabakoff et pref- mouse stra!ns alsodiffer in the severity of Inbred strains of mice differ In their depend- erence for alcohol consumptionwhen food, withdrawal symptoms after physical water, and alcohol are madefreely available ence has been established.Goldstein (1973) bred mouse to them (McClearn and Rodgers1959). Inbred and Goldstein and Kakihana (1974) in "sleep time," that lines with those reactions. Thus, both the rate mouse strains also differ severity of is,the time required to recover fromthe of tolerance development and the hypnotic effects of alcohol(Kakihana et al. physical dependence caused by chronicalcohol 1966), and in alcohol metabolic rate (Sheppard ingestion are genetically determinedIn mice et al.1970). Inbred strains are developed by and possibly in humans. mating successive generations of closerela- tives. After about 20 generations ofsibling Potential Mechanisms of matings, the animals within each inbredstrain are almost geneticallyuniform and show the Genetic Influence traitreadily.The strains constitute prima facie evidence of genetic influence onthat Alcoholism and alcohol abuse lie at one ex- of drinking behavior trait. treme of a continuum be- whose opposite endrepresentsabstinence. A genetic influence on alcohol-drinking Is a havior, CNS sensitivity to alcohol, andalcohol Drinking behavior as a trait, therefore, weight. metabolic rate has also been demonstratedin continuous variable, as are height and selectively bred lines of rats andmice. Se- Such traits are usually determined by many which ani- sets of genes that sometimestend to appear lective breeding is the process by different mals showing achosencharacteristicare together or to be correlated. When order to traits can be influenced by common setsof mated in successive generations in called pleiotropy, true segregate the genes responsiblefor that trait genes, a phenurnenon genetic correlation has occurred.The asso- into one line of animals. Thus, if aquantita- trait tive trait is under genetic control, separate ciation may come about because one and the influences the expression of theother. For strains can be bred, one in the high Japan in- other in the low direction. Rats thatdiffer in example, preliminary reports from been raised dicate that, compared with thenormal popu- alcohol metabolic rate have also populations contain fewer through selective breeding(Thurman 1980). lation,alcoholic bred selectively individuals with deficiencies in themitochon- Lines of rats have now been that to differ in voluntaryalcohol consumption: the drial enzyme aldehydedehydrogenase and the oxidizes acetaldehyde (Harada et al.1982; alcohol-preferring AA and P lines is ANA and NPlines Yoshihara et al. 1982). When this enzyme alcohol-nonprefer ring high (Eriksson 1968; Li et al. 1979). Lines ofmice absent,alcohol consumption leads to sensitivity to the blood acetaldehyde levels and theunpleasant and rats that differ in CNS with sedative-hypnotic effects of alcoholhave also alcohol flush reaction. Thus, an Individual (LS) and short- the enzyme deficiency Is likely toavoid al- been developed: the long-sleep it brings. sleep (SS) mouse lines(McClearn and Kakihana cohol and the unpleasant reaction 1973) and the most-affected (MA) andleast- Animal studies have revealed other poten- affected (LA) lines of rats (Riley etal. 1977). tial mechanisms of geneticinfluence. Mice particularly that consume large amounts ofalcohol vol- Such selectively bred animals are acquire useful for studying the underlyingmechanisms untarily are more likely than others to that contribute to these geneticdifferences. tolerance rapidly (Erwin et al.1980). Alcohol- time be- preferring lines of rats recover morerapidly For example, the difference in sleep alcohol tween the LS and SS mice isrelated to a ge- from the sedative-hypnotic effects of netically determined difference in thebrain than do alcohol-nonpreferring ones(Lumeng et that is both region-specific anddrug-specific al.1982). These studies suggest an experi- 1981). New andexciting mentally verifiable hypothesis: Anability to (Sorensenetal. (tolerance) may pre- findings are likelyto emerge from further adapt quickly to alcohol studies with these animals that willimprove disposeindividual;topatternsofheavy reseachers' understanding of thedifferential drinking. Other mechanisms of alcohol preference are CNS sensitivity to alcohol in humans. which may Various inbred strains of mice aswell as the likely to be discovered, each of selectively bred LS and SS lines of micediffer contribute in some way to thetrait of high Animal 'exper- in how rapidly they developtolerance after voluntary alcohol consumption. iments can reveal such mechanisms ofalcohol Genetic factors also affect individualdif- consumption (NIAA A1981).Thisresearch ferences in response to alcohol,such as drink- approach may ultimately leadto an under- ing ixehavior, sensitivity of the brain andother standing of the nature of geneticheteroge- body systems to alcohol, alcoholelimination neity of alcohol abuse and alcoholismin hu- rate, the acquisition of tolerance, and the de- mans, thephysiological and biochemical velopment of physical dependencies. Muchof mechanisms underlying this problembehavior, this knowledge has been obtained fromex- and how environmental factors interactwith periments in laboratory animals specifically these inherited pathways. developedforthepurposeofalcoholism- related research. Collectively, the gains in research Inthe Summary past decade predict an excitingera of new discoveries In the next. Future research should focus on improving methodology fordetecting Great strides have been made inrecent subtypes of alcohol abuse andon developing years in researchers' knowledge and under- behavioral,physiological, and biochemical standing of the genetic factors contributingto predictors of genetic vulnerability. In this alcohol abuse and alcoholism. re- Ithas been gard, ongoing and future work inexperimental firmly established that heredity playsa role in animals can provide invaluable cluesfor hu- determiningindividualdifferencesinsus- man investigation. Existing animal models and ceptibility to the disorder. Genetic influence those yet to be developedcan be used not only is identifiable in at least 35to 40 percent of toidentifygeneticcorrelatesofalcohol- alcoholics and alcohol abusers, and it affects seeking behavior, but also to elucidatethe both men and women. People withfamily biological nature of the process. When this histories involving parental alcohol abuseface stage of knowledge is reached, the genetic increased risk. Furthermore,many types of subtypes of alcohol abuse and alcoholism will alcohol abuse may exist, each withits own be precisely defined as pharmacogenetic dis- genetic predisposition Interacting witha par- orders of behavior by the nature of theirun- ticular environment. derlying pathology.

References

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24 Chapter III Psychobiological Effects of Alcohol

Alcohol acts on virtually every cell of the only two to three alcoholic beverages on an body, but the central nervous system is the empty stomach. In addition, he found thatthe target most affected. Alcohol's influenceis same blood alcohol leveldecreased a driver's profound--from the personality disarray cre- ability to divide his attention amongseveral ated by chronicdrinkingtothedistorted stimuliwhilemaintainingacceptableper- judgment of the drunken driver. Current re- formance. Clayton suggested that the result- search is converging on explanations for some ing diminished performance could be caused by of these effects and their underlying biological a decreased ability to processinformation. mechanisms,butacomprehensiveunder- Driving a car is a learned skill that requires standing of an individual's response to alcohol good judgment based on experience and prac- is still elusive. tice. McNamee et al. (1980) examined how Because no unitary explanation of alcohol's alcohol affects experience and judgmentin effect on human behavior seems adequate, estimating the velocity of a moving objectan researchers continue to explore all levels of essential task for drivers. Initially, with low brain function and behavior. Accordingly, this doses of alcohol, the subjects actuallyim- chapter presents selected research findings at proved their estimates. But after continuing to four broadlevels -- cognition andneuropsy- drink (resulting in a blood alcohol concentra- chological effects, neuropathological illness, tion above .10 percent), their performance electrophysiology, and neural and biochemical declined dramatically. This biphasic phenome- effects. Finally, a brief overview of theories non, of initial stimulation orexcitation of the that may explain the'appeal of alcohol andthe central nervous system with low dosesfol- causes of alcohol addiction arediscussed. lowed by depression as the dose isIncreased, v ;II be encountered again laterin this chapter. In a study closely related to velocityesti- mates, Colins and Chiles(1980) investigated Cognitive and Neurophysiological how alcohol affects tracking skillsIn airline Effects pilots. The results confirmed McNamee'sstudy and showed, in addition, that thepilot's errors frequent during eve- Driving-Related Cognitive Skills were greatest and most ning hours. Thus, It appears thatbiological Our society has acknowledged the profound rhythms may influence alcohol's effects on and often harmful behavioral effects ofalco- judgment. The researchersalsofound that required to hol,especially asitinvolves drinking and many hours of abstinence are driving. Driving is a complex task requiring eliminate all such alcohol-induced errors. such skills as psychomotor coordination, re- Many people believe they can override or action time, memory, perception,judgment, control alcohol's negative effects onbehavior. information processing, and conscious control Young and Pihl (1980) evaluated the degree to of behavior. Not surprisingly, manyresearch- which volunteer subjetts could control their ers have chosen to investigatealcohol's cog- speech and behavior and prevent visible symp- nitive effects by measuring how it impairs toms of intoxication. Althoughthe subjects various driving-related skills. Such studies can varied greatly in their suppressionof symp- reveal- toms, none was completely successful. yield practical applications while also in ing more basic psychological mechanisms. Fatigue impairs cognitive performance Clayton (1980) found that driving skills are much the same way that alcohol does,leading impaired at blood alcohol concentrations(.04- some researchers toexamine the relationship (NHTSA 1981) .05 percent) one might observe afterdrinking between the two. Ryder et al.

25 49 reported that alcohol Increasedthe cognitive may drink more than those impairments produced by with high func- fatigue as deter- tioning; the former, dueto poor verbal skills, mined by driving performance.CaffeineIs may provide thought by many to lessvaliddrinkinghistories. counteract the effects of Heavy drinkers may be both alcohol and fatigue. more anxious and de- Moskowitz and Burns pressed perhaps due (1981), usinga driving simulator, evaluated to underlying problemsor the recency of drinking.Finally, individuals caffeine as a possible antidoteto alcohol In may have to consume tracking, searching, and a minimal amount of Information process- alcohol (threshold)before it has detrimental ing. They found that caffeinecould partially effects. counteract the behavioral effects of alcohol. As more sensitivetechniques for assessing However, since the effectswere marginal, neuropsychological functioninghave been ap- these findings should discouragethe folk belief pliedtoIndividualswithdifferingsocial that coffee Is an effectiveantidote to alcohol, drinking patterns and especially when driving. Ina study of another socioeconomic circumstances, It has become increasinglyclear that often-used combination, Tongetal.(1980) many questions must be answered. found that both tobaccoand alcohol individ- Specifi- ually diminished auditory cally, what are the limitsof normal function- vigilance (ability to ing? At what point shouldan individual be detect sound stimuli);taken together, they led to even greater impairments. considered impaired dueto alcohol use? Is alcohol, use a causativeor an exacerbating Using an animal researchdesign that Is factor, a complication of likely to reflect humanreactions, Moody et al. or simply coincidental to such measuredimpairments? The (1980) demonstratedthat alcohol significantly social use of alcohol is slowed monkeys' reaction sufficiently widespread time to sound sig- in our culture, and thedegree of behavioral nals. Recordings of electricalactivity in the impairment attributed to social brain's auditory pathwaysshowed that alcohol drinking is difficulttomeasure.Therefore,long-term had not impeded the signalfrom the ear to the studiesof brain. Rather, the impairment manyIndividualswithvaried seemed to be drinking patterns will be neededto clarify the caused by slow informationprocessing in the brain's "higher" centers. cognitive consequences of socialdrinking. Alcohol and Aging Cognitive Functioning in SocialDrinkers On average, olderpersons perform less well on standard psychological tests thanyounger Since this topicwas reviewed in previous ones with equivalent patterns of reports to Congress (USDHHS 1981; alcohol con- Parsons sumption (Car len etal. and Leber 1982), Mac Vane 1981b).However, et al. (1982) have people of the same chronologicage may age also found that performanceon some neuro- quite differently physiologically. psychologicaltestscorrelates withsocial Because young alcoholics resembleold peo- drinking patterns.Five studies have found ple In their performance some statistical relationships between alcohol on neuropsychological use and decreased cognitive performance tests, some researchers havehypothesized In that alcohol consumptionmay accelerate the social drinkers (Parker1982).However, as normal process of aging (Ryan 1982). Parsons and Fabian (1982)have pointed out, However, electrophysiologicdata,particularlybrain such relationshipswere not consistent for the evoked potentials (electrical same cognitive tests in each of these activity in re- studies. sponse to sensory stimulation),suggest that Furthermore, in the Mac Vanestudy, although the organic brain diseaseofalcoholicsis the 58 heavy social drinkersdrank three times caused by an underlying as often and twice as much mechanism different as did the 48 light- from premature aging (Porjeszand Beg leiter moderate drinkers, the performanceof the 1982). two groups on the cognitive tests was not Whether or not the twoprocesses share a significantly different. common cause, alcohol consumption Methodologic issuesmay partially explain may in- the lack of teract with aging In severalways (Freund and a dose-response relationship be- Butters1982). Changes intheir tweenconsumptionand abilityto cognitiveability metabolize alcohol and in theircentral ner- (Parker 1982). However,variables other than vous system function may make alcohol use, as yet unknown, the elderly may also be in- increasingly vulnerable to thedeleterious ef- volved (Parsons and Fabian 1982).Individuals fect of alcohol (Wood and Armbrecht with poor cognitive function, 1982). In for example, addition, alcohol may interfere withnormal 26 50 computer-assisted regenerative processes of thecentral nervous largest long-term study of tomography (brain scan) changesin alcoholics, system (West et al.1982). all brain scan measurementsdiffered significantly between alcoholics andcontrols. None Alcoholics Versus Nonalcoholics of the alcoholics had clinically overtsigns of brain damage, but all showed thesyndrome of Allofthepreviouslydiscussedhuman effects on the be- alcohol dependence (Ron et al.1982). studies examined alcohol's differed havior of individuals from thepopulation at Alcoholics over 43 years of age both alco- from their controls more markedlythan did large. But the population includes measure- holics and nonalcoholics, who mayrespond to the younger alcoholics. Brain scan has at- ments were significantlycorrelated with age, alcohol differently. Recent research of alcoholism as tempted to measure alcohol'scognitive and but not with such measures neuropsychologic effects on alcoholics com- length of drinking history, measuresof amount consumed, or scores on a "socialdecline scale." paredwith nonalcoholics.Further,ithas (short- In the older subjects, abnormalities seenby examined both the effects of acute those who had term) doses of alcohol and theimpact of brain scans were least severe in abstained longest before scanning.In addition, chronic drinking. it was noted that recoveryproceeded at a faster rain younger alcoholicscompared followup tests, from Cognitive Effects ofAlcoholism with older alcoholics. In 30 weeks to 3 years after initialexamination, alcoholics the largely abstinent patientsshowed signif- O'Leary et al. (1980) found that icant improvement over time inbrain scans, performed significantly worsethan did non- their ability to note while the continuing drinkersshowed little alcoholics when tested for change. The length of abstinence was corre- anddistinguishslightdifferencesbetween closely related objects. In a studythat could lated with the degree of improvement. The work of Ron and hiscolleagues (1982) explain the results obtainedby O'Leary and his deficits may be associates, Rubin (1980) foundthat, compared suggests that neuropsychologic exhibit various reversible. However, Adams etal. (1980) were with nonalcoholics, alcoholics improved neuropsy- autonomic nervous systemdifficulties,in- unableto demonstrate regulation of eye chological performance in patientsin their cluding poor physiological late thirties from analcoholism treatment pupil size and the rate atwhich pupils respond after their last drink to visual stimuli.Such poor regulation could program tested 3 weeks distinguishing between and again 1 year later.Posttreatment alcohol hamper alcoholics in consumption by 63 percent of thesepatients closely related objects. that while may have influencedthis study, however, as Several studies have suggested (1980) noted that abstainers alcoholism does impair cognitiveskills, alco- Eckardt et al. perform better than those who R. umealcohol holics regain such skillsquite rapidly after al. (1980) con- consumption. These resultsemphasize that they stop drinking. Chaney et if alcohol-related firmed the earlier studies,adding that younger total abstinence is desirable after cognitive deficits are to be reversed.Reviews alcoholicsregaintheirverbalskills that detoxification more rapidlythan do older ofexisting literature noted, however, many studies fail to assessalcohol intake ac- alcoholics. of abstinence Ryan (198.i found that, atthe beginning of curately during so-called periods (Orrego et al. 1979; Parsons and Leber1982). a testing session,alcoholics and nonalcoholics performed equally well in ashort-term memory test. But, whenasked to recall words after Nutrition and Alcoholism a 3-hour interval,the alcoholics remembered did the non- significantly fewer words than Because alcohol is a concentrated sourceof alcoholics, possibly as a resultof more mental energy (about 200calories per ounce), alco- fatigue. holics often find theircaloric needs largely satisfied by the alcohol they consumebut de- Neuropsychological Performancein velop deficiencies ofvitalnutritionalele- Alcoholics ments. Indeed, mostmedical textbooks recommend restoration of a properdiet with underlie cognitive im- vitaminsupplementationasafirst-order Brain abnormalities treatment of alcoholism.In particular, thia- pairment in alcoholics(Wilkinson 1982). In the 51 27 mine (vitamin B1) deficiencymay result In the Elect roencephalographic (EEG) abnormalities, damage to brain cells (Blass 1980), and alcohol cerebral and cerebellar tissue loss, and the Itself may interfere with thiamine's absorption enlargement of the fluid spaces in the Interior fromthegastrointestinaltract(Hoyumpa of the brain are also similar in thetwo dis- 1980). orders. But the overall course of the diseases A genetic enzyme abnormalitymay largely is potentially different. In alcoholic dementia, determine which individuals are most likelyto cognitive Impairment isreversible to some become thiamine deficient during periods of degree with abstinence,althoughcognitive poor nutrition (Leigh et al. 1981). Shaw and his decline usually occurs with continued drinking associates (1981) reported impaired learning in (Cutting 1978). Potential reversibilityclearly thiamine-deficient rats, but not In rats feda differentiates alcoholic dementia from Alz- balanced diet or an alcohol-containing liquid heimer'sdisease,whichisInvariablypro- diet. Thus, it appeared that thiamine defi- gressive. Gottfries (1980) suggests that alco- ciencyalone can causeneuropsychological holic dementia may be differentiable from damage. Alzheimer's disease on the basis of abnormal Other evidence (Walker et al.1981), how- acetylcholine neurotransmission in the latter. ever, suggests that, despite adequate diet, This may be difficult to demonstrate, how- chronic alcohol consumption is in itselfneuro- ever, due to the many areas of neurochemical toxic and causes learning deficitsas well as overlap among Alzheimer's disease, alcoholic long-lasting brain damage. Clearly, bothnu- dementia, and aging. trition and alcohol contribute to neurotoxicity, Patients withKorsakoff'spsychosis(see and their relative roles in alcoholic brain in- USDHHS 1981; Butters1982),unlike those jury remain to be resolved. with alcoholic dementia, suffersevere and oflen persistent memory impairment while other Intellectual functions remain relatively intact. There are marked deficits in acquiring Neuropathologic Illnesses new learning and amnesia for more recent events.. Unlike early-stage Alzheimer ,patients with superficially similar memory deficits, Chronic Organic Brain Syndromes Korsakoff patients can recall rules fororga- nizing Information and can recall previously Chronic consumption of harmful quantities acquired knowledge (Weingartner et al. 1983). of alcohol may lead to two clinically and At autopsy, Korsakoff patients have charac- neuropathologically distinguishable chronic teristic lesions that resemble those described organic brain syndromes: alcoholic dementia in patients who have died from acute thiamine and alcohol amnestic (memory loss) syndrome deficiency (Wernicke's encephalopathy). Those (also called Korsakoff's psychosis) (Wilkinson lesions,whose preciserelationshiptothe and Car len 1981; Lishman 1981). Korsakoff memory deficits is still controver- Chronic organic brain syndromes due to al- sial (Butters 1982), are near brain pathways coholism are the second most common of the that in animal studies have been implicated in known causes of dementia in adults (approx- learning, memory, drive, and reward. Mairet imately 10 percent) next to Alzheimer's dis- al.(1982) have found reductions inneuro- ease (40-60 percent) (Wells1979). Despite transmitters, which are correlated with the emergingtechnologicaladvances,alarge performance of Korsakoff patients on learning proportionofdementingillnessescanbe tasks. However, itIs unclear whether such diagnosed with certainty only by examining neurochemical changes are significantly dif- the microscopic structure of the brainat ferent from those seen In age-matched healthy autopsy. For example, alcoholic dementia is controls or in individuals with dementia due to characterized pathologically by destruction of other causes. cerebral cortical neurons, particularly those in Harper (1979) diagnosed 51cases with the the frontal lobes. pathological findings of Wernicke's encepha- The clinical picture of alcoholic dementia lopathy(thiamine-relateddegenerationof may be indistinguishable from that of Alz- neurons in the brain) or approximately 2 per- heimer's disease. Global intellectual decline, cent of the brains examined from diseased seen In both, Is characterized by deficits In alcoholics at autopsy In a 4-year study. These abstracting ability and problem solving, dys- findings were not appreciably different from phasia(deficitInverbalexpression),and those of similar prior studies (Cravloto et al. apraxla(diminishedskillinmotortasks). 1961; Victor et al. 1971). In only 7 of Harper's

28 52 51 cases had the clinical diagnosis ofWer- Relationship Between Alcohol Abuse and nicke's encephalopathy orKorsakoff'spsy- Psychiatric Illnesses chosis been considered during life. The majority of affected patients were known alcoholics; 10 had died suddenly and unexpectedly, apparently as a result of hemorrhages in the Drinkinginsufficient amounts to cause part of the brain that controls theheart rate serious medical, social, domestic, vocational, and respiration. or legal problems mayreflect, occur together Itis disturbing that Wernicke's encepha- with, or lead to various psychiatric Illnesses lopathy is so greatly underdiaposed because It (Martin 1981). Alcohol use itself may produce is treatable and preventable with adequate various forms of psychopathology as a direct thiamine supplementation. Harper(1979) and result of its pharmacologic actions (Behar and Lishman(1981)suggestthatthepresent Winokur 1979), through psychosocial conse- (Goodwin and Guze clinicalappearanceofWernickeencepha- quences of its chronic use lopathy and Korsakoff syndrome may have 1979), or by alteration of psychological equi- changed somewhat from classical descriptions librium during alcohol withdrawal (Hamm et because many alcoholics may now routinely al. 1979). Depression, anxiety, hysteria,soci- receive thiamine treatment before the clinical opathy, drug abuse, anorexia nervosa,and signs are obvious. Such treatment, while in- childhood hyperactivity are more common in sufficient to prevent the disease, masksthe alcoholics and In their family members than in classical syndrome, thereby making a tradi- the genoral population (Morrison andStewart tional diagnosis difficult. Thus,clinical symp- 1971; Overall et al. 1973; Goodwin et al. 1975; toms may develop after repeatedepisodes of Tarter et al.1977; Andreasen and Winokur barely detectable brain degenerationin which 1979; Eckert et al. 1979; Goodwin and Guze the usual signs of mental confusion,ataxia 1979; Munjack and Moss 1981; Wood etal. (loss of body coordination), ophthalmoplegia 1983). Whether psychopathology is the result of, or (eyeparalysis),nystagmus(abnormaleye movements), and memory loss are absent or the cause of, alcoholism is sometimesdifficult not readily recognized(Kearsley and Musso to determine. There are,however, definite eachalternative 1980). clinicalimplicationsfor (Andreasen and Winokur 1979; Hamm et al. Inalcoholics,Ailing and Bostrom (1980) have found damage to myelin, thecovering 1979; Weissman and Myers 1980; Linnoilaand sheaths that enhance electrical conduction in Martin 1983). For example, if alcoholism pre- from some nerve cells. Thedamage occurred in a dates psychiatric symptoms, abstinence part of the brain almost alwaysaffected in alcohol isindicated before beginning other alcoholism classicalKorsakoff'spsychosis.These ran- treatments (Schuckit 1982). If the domly selected alcoholics never hadWernicke follows psychiatric disease, it is important to in life diagnose the psychiatric Illness accurately so encephalopathy or Korsakoff syndrome the pa- anddidnotshowthetypicalpathologic that treatment may be tailored to changes ofthis disorder under microscopic tient's needs (Linnoila and Martin 1983). examination at autopsy. The considerable overlap between alcohol- Alcoholic dementia andKorsakoff'spsy- ism and the affective disorders(mania and chosis probably represent ends of a continuum, depression) has become an important area of with the majority of patients seenin clinical research. Alcoholism and depression arethe practice falling somewhere in betweenand two behavior-associatedIllnesseswiththe (Parsons highest rates of suicide (Tsuang 1977). Recent having some characteristics of both abnor- and Leber 1982; Butters 1982; Harper1982). It evidencesuggests possible common is not uncommon to find the symptomsof al- malitiesInmetabolism oftheneurotrans- coholic dementia (cortical atrophy,enlarged mitter serotonininalcoholism,aggression, fluid space in the interior of the brain,and suicide, and depression (Ballenger et al.1979; moderate intellectual decline) in patientswith Rosenthal et al. 1980; Brown et al.1982). Such Korsakoff's psychosis. Conversely, those with neurochemical similarities between alcoholism be a alcoholic dementia probably have some mem- and depression suggest that there may have microscopic common underlying mechanism.Tricyclic an- orylossandfrequently for findings that are characteristic ofKorsakoff's tidepressantsandlithiummedications alcohol depression and mania - -may offersignificant psychosis. Both nutritional deficits and de- neurotoxicity may contribute to eitherchronic therapeutic benefit to alcoholics who are organic brain syndrome. pressed (Coppen 1980).

29 Indirect Alcohol-Induced Neuroptithology probes that recorded only gross brain activities of thousands or even millions ofnerve cells. The recordings, called electroencepha- Liver diseaseassociates:with alcoholism lograms (EEGs), could indicate the results of may result in behavioral deficits ranging from either spontaneous brain activityor the brain's subtle neuropsychologic abnormalities (Smith responses to a stimulus such as a light flash and Smith 1977; Rehnstrom et al.1977) to (evoked potentials). More recent technological serious brain degeneration, delirium, andcoma advances allow microrecordings from single (Schenker et al. 1980). In addition,head trau- nerve cells. In today's research, both macro- ma and inadequate oxygen supply to the brain, and microrecordings of alcohol's effectsaug- frequently sustained during Intoxication,can ment one another to contribute toan under- become a recurrent theme in the life ofan standing that neither alone can provide. alcoholic, with cumulative and adverseneuro- In general, the electrophyslological effects logic effects (McLeod 1982). of alcohol are complex andvary at different Alcohol inhibits the respiratorycenter of sites within the brain. Most alcohol research the brain and renders the individualmore with these techniques has attempted to de- susceptible to obstructivesleep apnea(in- termine functionalcentralnervoussystem ability to breathe normally during sleep),an differences between alcoholics and nonalco- increasingly recognized condition thatcauses holics and, sometimes, to quantify theacute hypoxemia (reducedbloodoxygen content) effects of alcohol. during sleep (Guilleminault et al. 1978). Even mild hypoxemia may adversely affect brain EEG Studies function and lead to dementia, particularlyin individuals who have chronic obstructive lung Recent studies have compared EEGsac- disease, as is often thecase in alcoholics companying the loss of consciousness resulting (Blass 1980). from alcoholingestion,normalsleep,and Hillbom and Kaste (1982) have reported that barbiturates (Zornetzer et al. 1982). Although both occasional alcohol intoxication andreg- the loss of consciousness caused bymost bar- ular heavy drinking carry an increased risk of biturates and by alcohol superficiallyresem- stroke due to subarachnoid hemorrhage, but bles normal sleep, the conditionsare quite the mechanism for this is not yet clear. In different electrophyslologically. addition, alcohol withdrawal may beaccom- Surprisingly littledetailed information panied by serious metabolic disturbances that exists on how acute doses of alcohol affect the can impair cerebral function (Linnoila and EEG. Several recent studies have investigated Martin 1983). the relation between alcohol's effectson the The common useofotherpsychoactive cortical (outer brain layer) EEG and its effects drugs by alcoholics may also contributeto on EEGs from deep brain structures. Grupp behavioral deficits (Linnoila and Martin 1983). (1981) reported that alcohol altered theelec- Depression,whichfrequentlyaccompanies trical activity of both the hippocampus (a deep harmful alcohol use (Schuckit 1982),can also brain structure associated withmemory and impair cognition considerably (Weingartneret emotion) and the cerebralcortex (involved In al. 1981). Cognitive impairmentmay often high-level Information processing). Partlyon precede alcoholism, however. The highprev- the basis of such studies, Klemm and Sherry alence of attention disorders inyoung male (1981) proposed a brain model ofintoxication. alcoholics (Wood etal.1983), for example, They theorized that alcohol "scrambles" brain suggests that part of the cognitive impairment messages, thus disrupting normal communica- attributedto alcohol-relatedbrain damage tion within the centralnervous system. Be- was probably present before the use of alcohol cause Klemm and Sherry rely largelyon sup- (Parsons and Leber 1982). porting evidence recorded from the cerebellum (a part of the brain associated withpos- ture, movement, and balance), their model Electrophysiology may not account for the pervasive effects of intoxication on other brain structures. Increasingly over the pasthalfcentury, electrophysiologIcal recordings have been ex- Evoked Response Studies panding researchers' knowledge of thenervous system. Until about 25 years ago, such record- Electrophyslologicalresponsestosensory ings were limited to macroelectrodes, large stimuli reveal a great deal about the brain.

30 54 Because responses to individual stimuli are prove to be valuable in future research, espe- often lost in a sea of electrical "noise," how- ciallyinidentifyingspecificindicators or ever, researchers cf ten resort to atechnique markers of alcohol susceptibility. called the average evoked response (AER). In essence, a readable AER depends on a com- Neural and Biochemical Effects puter's averaging a large number of the brain's electricalresponsestorepetitivesensory stimuli.Individual responses that would be Behavior and thought, learning and memory, imperceptiblewithoutcomputerassistance sensations and movements, all of which are become magnified and visible when averaged affected by drinking alcohol, find their bio- together. logical basis in the nervous system. The in- Recently, several researchers have turned dividualunits ofthis system are neurons to the AER to investigate the brain's response (nerve cells). to sensory stimuli under various conditionsof Neurons are now known to be extraordi- alcohol use. Studies showed that alcohol dis- narily subtle electrochemical processors. New rupted (1) the normal AERs to visual stimuli knowledge of neurons, accompanied by new (Hetzler et al. 1980); (2) the normal patterns measurement techniques, has encouraged some of attention to visual stimuli (NHTSA 1980); optimism that a deeper examination of alco- and (3) the normal AERs to auditory stimuli hol's effects on neurons could reveal how al- (Pfefferbaum et al.1980), which were cor- cohol affects the nervous system and, in turn, related with slowed reaction times to sound how the nervous system affects behavior. Be- signals.Suchdisruptedelectrophysiological fore discussing alcohol's effects on neurons, it responses to perceptual stimulicould explain is necessary to understand what a neuron is alcohol's adverse effects on driving. and how it works. Many Investigators have attempted to de- Neurons are,in computer parlance, logic tect whether AERs in alcoholics differfrom elements.Theyconductinformationand, thosein nonalcoholics. A frequently cited based on a combination ofelectrical and study demonstrated that, compared with non- chemicalsignals,communicate withother alcoholics, alcoholics produce higher ampli- neurons, with muscles, andwith the body's tude AERs when presented with light flashes endocrine system hormones. of low intensity, even though these alcoholics A typical neuron (shown highly simplifiedin had been abstinent from alcohol for 1 week or figure1)usually receives chemical inputs, more (Buchsbaum and Ludwig1980). When the through its dendrites, from other neurons. It flash intensity was increased, alcoholics' re- changes the chemical signal into an electrical sponses increased more than thoseof norn signal, which travels to the other end of the end) subjects.Thus,the alcoholics' AERs were neuron (the nerve terminal or output somewhat greater than not.mals' at low in- where neurotransmitterchemicals,,which tensities, but much greater at high intensities. continue to carry thesignal,are released Buchsbaum and Ludwig (1980) noted that al- across a space called the synapse toadjacent coholics, in increasing their AERs at higher neurons. The process is usuallyrepeated many light Intensities, are more sensitive to higher times to create signal paths throughout the level stimuli. They speculated that alcoholics nervous system. Essentially, thetransmission may be neurophysiologicallyvulnerable to in- between neurons is chemical, while the trans- tense sensory inputs either bypredisposition or mission within neurons is electrical. as a result of the toxiceffects of alcohol, and If we probe into the nature of the electrical that perhaps they use alcohol to diminish their signal that is carried along the neuron, we find augmented sensitivity. that it is formed by the movement of sodium One provocative question is whetherdif- and potassium ions (charged particles) flowing ferences seen in the AER are consequent to, across the thin semipermeablemembrane en- or predispose for, alcoholism.Recent research closing each nerve cell and crossing back indicates that there may be inherited differ- again. When the flow of these ions reaches ences in the brain's electricalactivity. Elma- threshold conditions, an impulse is propagated sian et al. (1982) observed that AERs from down the neuron to its destination, the nerve groups of individuals withand without a family terminal. Instruments can detect these short signal history of alcoholism were markedlydifferent. electricalpulsesastheelectrical These differences were apparent whether or travels through each neuron. Alcohol could not theindividuals had consumed alcohol. affect the propagation of electrical pulses by Electrophysiological methods may, therefore, making the membrane more or less permeable

31 r: Figure 1. Typical Nerve Cell (Neuron)

DENDRITES

NUCLEUS U SIGNAL CELL FLOW BODY

AXON

pAiNERVE TERMINAL NEUROTRANSMITTER-7 ft0 )SYNAPSE RECEPTORS

32 56 to the charged particles.After a pulseis isnot simply a standard element repeated propagated, the neuron must be recharged billions of times in the brain. Rather, a wide before it can carry another electrical impulse. diversity exists among neurons--in speed of This process is regulated by an enzyme that conduction, size, number of inputs, and chem- moves ions that entered the neuron back out- ical makeup; therefore, the case for alcohol's side. Alcohol may also interfere with this ion effect on neurons' electrical activity was re- "pump"mechanism,which maintainsthe opened.Itwas realized that a differential electrical stability of each neuron. sensitivity to alcohol might result because of When theelectricalimpulsesreachthe differences between neurons. nerve terminal, calcium ions, acting as gate- Recently, researchers (Car len et al.1982; keepers of the synaptic membrane, enter the Shefner et al.1982) have demonstrated that neuron and allow tiny packets of neurotrans- alcohol diminishes electrical activity in parts mitter chemicals to be released across the of the brain of mice and rats. In particular, synapse. On the adjacent neuron, receptors neurons in the hippocampus and locus ceruleus, exquisitely matched to the neurotransmitter deep inside the brain, are affected by alcohol chemical characteristicswillrecognize the concentrations below those that might be ex- chemical message and unlock the membrane of pected in a person after several cocktails. the receiving neuron to allow the signal to The differential sensitivity of various brain continue. Continuation of the signal, Inside the areas to alcohol seems to be genetically in- receiving neuron, depends on increased flow of fluenced. In a line of mice (LS) bred for sen- sodium and potassium Ions to reach the thresh- sitivity to the effects of alcohol, the hippo- old conditions for generating anelectrical campus was less sensitive than another brain impulse and allowing the whole process to re- area, the cerebellum. These two brain areas peat.(Depending ontheneurotransmitter were equally sensitive, however, to the effects chemical, however, the receiving neuron may of alcohol in another line of mice (SS), bred be inhibited from firing,rather than being for resistance to alcohol's effects (Sorenson et fired. In this manner, the nervous system can al. 1981; Basile et al. 1982). Comparisons be- turn off, as well as turn on, the flow of in- tweenstrainsalsoclearlydemonstrated a formation.) This activity can occur hundreds genetically influenced differential response to of times a second and in billions of neurons in alcohol. Neurons in the cerebellum of the mice the brain. The resultisthoughts,feelings, resistant to the disruptive effect of alcohol learning, or the link between a red light and were less affected electrophysiologically by musclesflexing to step on the brake. Any inalcohol (Sorenson et al. 1980, 1981; Basile et terference with the neurotransmission process al. 1982) than were those from the sensitive could affect that link. mice. The nature of the effects of alcohol on Electrical Conduction electrical activity led Car len and his coworkers (1982) to postulate that alcohol altered, in In the late 1940s, it was found that sodium a complex way, the movement of potassium and potassium ions were responsible for the ions across the neuronal membrane. electrical conduction in the neuron. Research. Another neuronal component related to the ers interested in alcohol's effect on the brain electrical activity of the cells Is the enzyme hypothesized that alcohol could impede the sodium-potassium-ATPase. This enzyme, the movement of ions necessary to produce and ion "pump," is responsible for maintaining the conduct the electrical impulse. Early studies proper concenti itions of sodium and potassium on the squid's giant axon confirmed the hy- ions on either side of the neuronal membrane. pothesis, but only at alcohol levels four to five Alcohol alone in nonlethal amounts does not times the lethal concentration (Gal lego 1948). affect the enzyme activity. When combined Therefore, many researchers concluded that with the neurotransmitter chemical norepi- alcohol's Ionic effects could not explain why nephrine, however, brain alcohol concentra- or how drinking alcohol could affect the ner- tions that could be achieved by beverage con- vous system. The hypothesis seemed to lead to sumption can inhibit the enzyme. Such inhi- a dead end. With time, new technology and bition would be expected to affect the con- instrumentation have allowed a more detailed duction of electrical impulses (Rangaraj and view of the brain and individual neurons. After Ka lant 1979). Thus, alcohol's effects on the examining and recording the electrochemical locusceruleus,whichhas norepinephrine- activity of neurons throughout the brains of containing neurons, could be related to inhi- various mammals, it was found that a neuron bition of the enzyme.

33 5 As mice and rats become more tolerant to striatum and cerebellum (both associated with the sedative effect of alcohol, the sodium- movement) were more sensitive to alcohol's potassium-ATPase becomes more resistant to effects than were samples from the cortex and alcohol'sInhibitoryeffects(Leventaland brain stem. These results confirm again that, Tabakoff 1980; Rangaraj and Ka lant1982). even at the chemical level, different brain Such a change suggests that alcohol tolerance areas seem to respond according to their own may,Inpart,bebasedon neurochemical programs. changes in the brain. Clearly, more informa- Perhaps more Important, neuronal prepar- tion Is required to establish unequivocally the ations from mice chronically fed alcoholre- link between alcohol, electrical activity In the sisted alcohol's effects on calcium uptake, brain, and behavioral responses to alcohol. regardless of what the initial alcohol effects were. This evidence suggests a possible direct Neurotransmission link between behavioral tolerance of alcohol and the microenvironment of the neuron. Chemical messages carriedacross the syn- The aforementioned studies measured al- apsesthetinyspaces betweenadjacent cohol's effects on the uptake of calcium- -that neurons--are critical to brain function. Any is,the movement of calcium ions Into the interference with the release of neurotrans- neuron. Calcium isalso stored within cells mitters, their recognition by receptors,or the near the membrane in a kind of chemically development of the new signal In the adjacent adhesive process called binding, which Is also neuron will affect the flow of information in affected by alcohol. Low levels of alcohol in- thebrain.Withoutchemicaltransmission, creased the binding of calcium, whereas higher brain function stops. Therefore, various re- levels were not as effective (Michaelis and searchers have examined the chemical flow at Myers 1979). As with calcium uptake, alcohol the synapse to determine the potential effects had littleeffect on calcium binding when of alcohol on neuronal activity. Measurement added to neuronal preparations from rats feda of neurotransmitter release and metabolism chronic diet containing alcohol.Thus,this represents an alternative to direct measure- study also indicates a link between behavioral ment of electrical activity, since the rate of and biochemical tolerance.Itis,however, neurotransmitter release and synthesis usually premature to conclude that behavioral toler- reflects the electrical activity ofneurons. ance is the direct result of alcohol's effects on The release and recognition of chemical calcium--whether related to calcium uptake or neurotransmitters between neurons propagates binding. messages through the brain. Neurochemicals Evidence linking neurotransmitters to be- are allowed to pass through the nerve cell havior led alcohol researchers to investigate membrane by a mechanism that is dependent threeneurotransmittersystems:norepine- on the movement of calcium ions Into the phrine, dopamine, and GABA (gamma-amino- neuron.CouldalcoholInterferewiththis butyric acid). They found that alcohol affects process? Friedman etal.(1980) found that the release of the neurotransmitters as well as alcohol stimulated the initial rate of calcium their recognition by receptors at the post- accumulationinaspecialpreparationof synaptic membrane (Bacoupoulos et al. 1978; neuronal membranes deprived of calcium. In Ticku and Burch 1980; Rabin et al. 1980). another study on mice (Harris and Hood 1980), When alcohol is acutely given to an animal, alcohol inhibited the flow of calcium Into a the amount of norepinephrine released depends neuronal membrane preparation that wasen- on the level of alcohol in the brain. Moreover, riched with calcium. Furthermore, this latter the process is biphasic: It reverses with larger effect was detectable only under conditions amounts of alcohol (Hunt and Majchrowicz that mimic the electrical signals' arrival at 1974). That Is, a small amount of alcohol leads the synapse. In effect, when there was a mes- to anincreasedrelease ofnorepinephrine, sage and no calcium ions, alcohol quickly mo- while higher doses actually depress the release bilized a new calcium cadre. With an excess of of norepinephrine. Since release of a neuro- calcium ions, however, alcohol inhibited the transmitter reflects nerve activity, this sug- calciumstimulatedreleaseofneurotrans- gests that low doses of alcohol have an excit- mitter. ant or disinhibiting effect, while high doses Recent studies (Stokes andHarris1982) have an Inhibiting effect on neurons containing have found that the inhibitory effects of al- norepinephrine.These effects on norepine- cohol on calcium uptake depend on the part of phrine release may, In turn, be related to the the brain that is examined. Samples from rat behavioral changes produced by alcohol. Sim-

34 58 Ilar results were obtained when the effects of at the time of the most severe withdrawal alcohcrt on dopamine were examined in rats symptoms. (Hunt .981). In mice, however, the reaction is Clinical results demonstrate that benzodi- reversed (Kiianmaa and Tabakoff 1983). Low azepines suchas diazeaam(ValiumR)and doses of alcohol lead to low release of dopa- chlordiazepoxide (Librium t9 control the major mine, whereas higher doses lead to greater symptoms (especially convulsions) of alcohol release. The causes of these different reac- withdrawal. Specific receptors In the nervous tions to acute infusions of alcohol In closely system for the benzodiazepines are related to related species are not yet understood; they GABA receptors. Part of this relationship ap- may, however, be related to different organ- pears to be a common effect on the flow of ization of the nervous system of these species. chloride ions across the nerve membrane. It In both species, the effect of chronic doses of appearsthatalcoholdisturbsthenatural alcohol is consistent, leading to Increased re- linkage between GABA and diazepam. The lease of norepinephrine and decreased release strongest evidence for this effect comes from of dopamine (Hunt and Majchrowicz1974; studies in which the receptors were removed Pohorecky 1974). fromtheirnormal membrane environment Over the years, laboratory animals have (Ticku and Burch 1980). been bredwithspecificcharacteristicsin Recentstudieshavedemonstratedthat mind. One strain of mice has been developed chronic feeding of alcohol to animals affects for Its relatively high resistance t ) the be- the receptors for other neurochernical mes- havioral effects of alcohol. These mice are- sengers,Includingtheendogenousopiates also more resistant to the effects of alcohol (Hoffman et al. 1982), acetylcholine (Tabakoff on dopamine release (Kiianmaa and Tabakoff etal.1979),norepinephrine (Rabinetal. 1983). This finding suggests that some animals 1980), and dopamine (Barbaccia et al. 1982). may be genetically more tolerant of alcohol After the receptors have recognized the than others, and that differences in behavior neurotransmitter message, a new signalis may be related to differences in biochemistry. generatedwithinthereceivingneuron. A The preceding research collectively shows chemical (cyclic adenosinemonophosphate or that alcohol's effects on norepinephrine and cAMP) sometimes called the second messenger dopamine release, as well as on movement of carries the message from the receptors to the calcium ions, vary with dosage, species, ge- interior of the receiving neuron. Recent re- netic strain, and brain area. searchindicatesthatafterwithdrawalof The discussion thus far has focused on the animals from chronic alcohol treatment, the neurotransmitters at the transmitting neuron. release of the second messenger Is inhibited Across the synapse, the receiving neuron with (Tabakoff and Hoffman 1979; Luthin et al. its receptors must recognize the neurotrans- 1983). mitters. Much of the research at the receptor As the number ofidentifiedneurotrans- end has been devoted to GABA, a neurotransmitters increases (some researchers expect it mitter that inhibits firing in neurons and is of to go from the current 40 to as many as 200 or particular interest to alcohol researchers. By even more), and with growth in understanding inhibiting electrical impulses, it controls the how they work, neurotransmission is likely to tendency to convulsions, which are caused by help explain the nature of alcohol's biological uncontrolled electrochemical activity in the effects on the central nervous system. brain. Because the symptoms of alcohol withdrawal include convulsions, GABA is a prime The Membrane suspect as a cause of these symptoms. In fact, research strongly implicates GABA The transmission of information between receptors in alcohol withdrawal symptoms. In nerve cells is dependent upon the function of mice, an acute dose of alcohol results in an receptors, enzymes, and ion gates. All of these increase in the number of GABA receptor sites components are proteins located in and on the (Ticku and Burch 1980), suggesting lessened neuronal membrane. Changes in the physical neural activity. This finding is consistent with state of these membranes could have adverse alcohol's depressive effects. Chronic adminis- effects on the ability of the specialized pro- tration of alcohol results, conversely,in a teins to function normally. A number of re- decrease in the number of GABA receptor searchers are studying this problem and in sites--a finding that could explain convulsions particular are examining the lipids in mem- in withdrawals. Indeed, in rats, the decreased branes, which are the biochemically Important number of receptor sites was most pronounced elements in maintaining the structural integ- rity of the membrane. Results have clearly cording to this model, animals learn to asso- shown that membrane viscosity is decreased ciate environmental cues with the pharmaco- by acute treatment with levels of alcohol that logical effect of alcohol, much as Pavlov's can be attained through consumption of alco- famous dog associated a bell with food. In the holic beverages (Chin and Goldstein1977). presence of those cues, an animal may develop After chronic treatment of mice with alcohol, a response designed to counteract the effect however, it was folind that subsequent acute of alcohol. In essence, the Pavlovian model doses of alcohol would no longer change the suggests that animals learn to reduce their viscosity of neuronal membranes (Chin and response to alcohol in a particular context, Goldstein 1977). This suggests that bt. which provides the cues for their response. tolerance to alcohol may, in part, be auoci- Tolerance is reduced or absent, however, when ated with a tolerance of membrane lipids to the animal Is subsequently tested in a dif- alcohol-induced decrease in viscosity. ferent environment. Thus, in some cases, the Goldstein et al. (1982) compared alcohol's mere exposure of an animal to alcohol is not effects on neuronal membranes from two sufficient to cause tolerance development; the different genetic strains of mice: LS mice Initial environmental cues must be repeated (long sleep, with greater sensitivity to alcohol) (Crowell et al. 1981). and SS mice (short sleep, with less sensitivity Neurochemical studies have also suggested to alcohol). They found that neuronal mem- that the presence of alcohol, while necessary, branes taken from LS mice were more sensi- is not a sufficient condition for the develop- tive to alcohol than were membranes taken ment oftolerance; neurons containing the from SS mice. Another study (Lyon et al. 1981) neurotransmitters norepinephrineandsero- showedthatalcohol'swell-knownsedative tonin seem to play a role in developing tol- effect is correlated with its effects onneu- erance. When those neurons were destroyed, ronal membranes. In turn, these membrane ef- animals tended to retain their initial responses fects would be expected to influence the to alcohol (Tabakoff and Ritzmann 1977; Le et function of the specialized proteins that reside al. 1981) or to develop tolerance more slowly. in the membrane and are critical for proper Thus, the activity of specific neuronal sys- neuronal transmission. tems, in conjunction with alcohol, seems to be quite important for tolerance development. In Tolerance and Dependence addition to neurotransmitter systems, certain hormonal systems appear to affect the de- Alcohol produces toleranceinchronic velopment of tolerance. Vasopressin (some- drinkers--thatis,the subjective effects of times called antidiuretic hormone) can main- alcohol decrease with continued exposure. It tain an already developed tolerance, even in may take a chronic drinker a pint of whisky to the absence of continued exposure of the or- obtain the same effect that an occasional ganism to alcohol (Hoffman et al. 1978). Vas- drinker gets with a cocktail or two. Physical opressin's ability to maintain tolerance de- dependence--the need to continue to drink pends onthepresence ofintactnorepi- alcohol to prevent withdrawal symptoms--may nephrine-- and /orserotonin-containing neurobe related to tolerance, as it develops only nal pathways (Le et al. 1982; Hoffman et al. In after chronic ingestion of alcohol. press). Whether vasopressin playsa rolein At one time, it was thought that tolerance developingalcoholtolerance under normal and dependence woulddeveloponlyafter conditions is not clear, but in at least one relatively long periods of exposure. A recent study, a strain of rats lacking this hormone study (Gallaher et al.1982), however, found could not develop alcohol tolerance (Pittman that tolerance to alcohol's ataxic effects (loss et al. 1982). of muscular coordination) developed after only Changes in neuronal membranes could ac- 2 days. The fairly straightforward behavioral count for tolerance and physical dependence. effects of tolerance and dependence have yet Alcohol initially increases membrane fluidity, to be described fully; biological mechanisms but membranes from alcohol-tolerant animals underlyingthesephenomenaarecurrently are less sensitive to this effect. Also, enzymes even more obscure. in the membrane demonstrate a biochemical Recent studies suggest that learning may tolerance to alcohol (Levental and Tabakoff play an important role in developing tolerance, 1980; Rangaraj and Ka lant1982). Membrane andseveralinvestigatorshave proposed a fluidity could affect sodium-potassium- Pavlovian model of alcohol tolerance (Crowell ATPase activity and therefore,indirectly, et al. 1981; Melchior and Tabakoff 1981). electrical conduction in the brain. The mem- 60 36 brane's biochemical adaptation could be re- similarities between alcohol'sreinforcing lated to behavioral tolerance. properties and those of other drugs of abuse. Physical dependence,liketolerance, may But how does reinforcement work? Many re- result from an adaptation of neuronal mem- searchers have noted the similarity between branes during chronic alcohol exposure. This the reinforcing properties of alcohol and those adaptation might be expected to produce in- of opiate drugs (Altshuler1982; Amit and appropriate neuronal activity in the absence of Brown 1982). They have reasoned, therefore, alcohol. If so, when alcohol is withdrawn, the that drugs (opiate antagonists) that nullify the membranes of physically dependent animals brain's reaction to opiates may well block might be more viscous than normal. Although similar reactions to alcohol. The research re- initial studies did not reveal such changes in sults have been somewhat difficult to inter- animals'braincell membranesfollowing pret.In some cases, the opiate antagonist chronic alcohol consumption (Chin and Gold- blocked a specific effect of alcohol, while In stein1977), more recent studies have con- others the opiate antagonist was ineffective. firmed the expectations (Lyon and Goldstein Striking similarities have been reported be- 1983). Another study (Ingram 1982) also cata- tween the electrophysiological effects of al- loged a number of changes in lipid (fat) con- cohol and opiates, especially opiate peptides tent of brain cell membranes derived from naturally occurring in mammals (Siggins and chronically alcohol-fed animals, which could Bloom 1980; Siggins et al.1982; Hoffman et contribute to changes in fluidity. These adap- al.1982). Furthermore, inrats and mice, tive changes could well be responsiblefor chronicalcohol doses caused significant some aspects ofphysicaldependence and changes in the characteristics of opiate re- tolerance. ceptors (Hoffman et al.1982). All of these Toleranceanddependencearecomplex reports confirm the link between alcohol and phenomena, however, and may result from the opiate system in the central nervous sys- different but interacting biochemical mecha- tem. In general, it appears that, while opiate nisms. Astoleranceand dependenceare antagonists do not affect alcohol's depressive studied in more detail, it becomes increasingly properties, they can alter some of its stimu- clearthatthey are influenced by various lant or excitatory properties. neuronal and hormonal systems. Such findings suggest a possible relationship between alcohol's excitatory effects and the phenomenon known as reinforcement. Drinking studies conducted with almost every labora- Theories of Alcohol's Effects tory species have provided many demonstra- tions that alcohol is a reinforcer in animals as Alcohol as Reinforcer it is in humans. Some researchers contend that the most Since the publication of the Fourth Special appropriate way to study alcohol reinforce- Report (USDHHS 1981), a new hypothesis has ment in laboratory animals is to study their emerged to explain the mechanism behind al- voluntary oral alcohol consumption. Yet the cohol'sreinforcingactivity.Mostearlier usefulness of oral alcohol consumption studies studies focused on specific neurochernical and in animals for measuring alcohol preference or behavioral correlates of alcohol's depressive reinforcement has been a persistent source of effects. Although the stimulant effects had disagreement among researchers.Advocates been noted in the past (USDHEW 1974, 1978; contend that since humans consume alcohol by Hunt and Overstreet1977; USDHHS 1981), drinking it,oral studies are most likelyto most earlierstudies lacked the theoretical provide meaningful results. Opponents argue focus that has emerged in recent years. Now that when drugs, including alcohol, are taken much of alcohol's appealIs thought to be orally, animals will choose them based on directly related to its excitatory effects, and flavor rather than for their reinforcing ef- many current studies are attempting to verify fects.The problem of estimating or con- therelationship(Taberner 1980; Lindman trolling how flavor affects oral Intake studies 1982). has plagued researchers for many years, but a Essentially all studies of alcohol as a drug of recent study (Crawford and Baker 1982) sug- abuse are based on the premise that humans gests a method to distinguish between the re- and animals consume alcohol because ofits inforcing effects of firavor and alcohol. reinforcing(orrewarding)effects.Recent Because drinking studes in animals are of- years have seen considerable interest in the ten difficult to conduct, a technique called

37 61 self-administration was developed to substi- Alcohol Metabolism and TIQs tute for oral consumption. The technique al- lows animals to work for alcohol by pressing a lever to obtain intravenous (directly Into a Another theory about alcohol and its actions vein) or intragastric (into the stomach) alcohol is based on the hypothesis that biologically infusionsthroughsurgicallyimplanted can- active chemicals calledtetrahydroisoqulno- nulae (tubes). Early studies (Deneau etal. lines (TIQs) may be formed during alcoholme- 1969) demonstrated unequivocally thatmon- tabolism(Davis and Walsh1970).Interest keys would self-administer alcohol intrave- arose in these compounds because some of the nously. Altshuler (1982) showed that monkeys TIQs are structurally related to morphine (an would also self-administer alcohol intragas- opiate) and, therefore, could Involvea com- trically for extended time periods. Both in- mon addictive mechanism. vestigations showed that many animals would About 6 years ago, Myers and Melchior work for alcohol over time periods sufficiently (1977) proposed a provocative hypothesisre- long to develop tolerance, physical depend- lating TIQs and alcoholism. The hypothesiswas ence, and eventually, alcohol-related toxicity. based on the observation that infusions ofa Another less direct technique tomeasure TIQ,tetrahydropapaveroline(THP),intoa alcohol's reinforcing effects is the intracranial brain cavity changed an animal's drinking be- self-stimulation (ICSS) model.Stimulating havior fromrejectingalcoholto choosing electrodes are placed in parts of the brain moderate doses.It was speculated that ex- where electrical stimulation presumably pro- cessive drinking by human alcoholics could be duces pleasurablesensations.Theanimals, caused by metabolic abnormalities that result usually rats, are able to press a lever to ac- in the formation of TIQs. They reasoned that tivatethestimulatingelectrodeintheir becausedrinkingcreatesTIQs,andTIQs brains. Most animals will press the lever fre- stimulate drinking, the positive feedback loop quently to obtain the apparently pleasurable could explain uncontrolled drinking by alco- sensation that follows. This ICSS phenomenon holics. That conjecture generated both support is thought to be associated with many dif- and disagreement, which continue unabated to ferent reinforcers, perhaps through a common this day. Several research groups (Sinclair et pathway or center of reinforcement. Indeed, al. 1982; Tuomisto et al. 1982) attempted to most addictive drugs seem to affect ICSS. replicate the initial studies with, at best, only Because alcohol (and other reinforcing drugs) mixed results. Myers et al. (1982), however, changes the rate at which animals will press reported recently that TIQ infusions produced the lever during ICSS, a number of researchers outcomes in monkeys identical to those in (Wise 1980; Amit and Brown 1982) havecon- rats,and that THP infusions producedin- cluded that the drugs were acting as rein- creased alcohol drinking by monkeys. How- forcer s. ever, these infusion studies use TIQ that is A controversy has emerged over the neuro- synthesized in the laboratory. While it is the- chemical mechanism responsible for alcohol's oretically possible that TIQ Is formed in the reinforcing properties in the ICSS model. Most brain, a great deal of controversy remainsas researchers agree that alcohol is a reinforcer to whether TIQs are in fact formed in the and that reinforcement is controlled by the brain, or if the concentrations of these chem- brain's reward system (Wise 1980; Amit and ical compounds are increased following alcohol Brown 1982). Wise (1980) hypothesized that ingestion. A number ofinvestigatorshave alcohol affects dopamine's role in information searched for these compounds using increas- transfer within the reward system. Amit and ingly sophisticated and sensitive techniques, Brown (1982) suggested that norepinephrine with only limited success (Bloom et al. 1982). rather than dopamine is affected.In either A less controversial hypothesis relatesen- event, alcohol reinforcement Is probably as- dogenous (naturally producedInthebrain) sociated with a specific cluster of neurons opiatemechanisms toalcohol'sbehavioral that may also be the site of the reinforcement effects. These studies have Investigated pos- produced by several drugs and ICSS. The ex- siblepharmacologicalrelationships between perimental evidence implicates several neuro- TIQs, endogenous opiate compounds, and the transmitters, includingdopamine, norepi- reinforcing properties of alcohol. Most have nephrine, and opiate peptides, as the neuro- reported that the reinforcing properties of chemicalsresponsibleforthereinforcing alcohol and opiates could be related to TIQ properties of alcohol. mechanisms. 62 38 Infuturestudies, many researcherswill mentia and Korsakoff's psychosis. probably turn their attention to the biphasic Alcohol may be the indirect cause of other effects of alcohol and may reexamine many neuropathology. Liver damage, head trauma, assumptions aboutitseffects onbehavior. malnutrition, and breathing impairment during Additional research about alcohol reinforce- sleep, resulting from alcoholism, can lead to a ment, preference, and voluntary consumption range of adverse effects from behavioral def- is likely to illuminate the role of the TIQs, icits to serious brain damage. opiate mechanisms, and alcohol-induced In an effort to understand the neuropsy- stimulation. These data may provide an un- chological effects of alcohol, researchers have derstanding of the underlying biological mech- examined the effects of alcohol on structures anisms that contribute to alcohol abuse. and neurochemicals in various regions of the brain. Chronic drinking seems to cause several biochemical adaptationsin nerve cells that Summary could partially explain why alcoholics become tolerant to alcohol and why they suffer with- Alcohol affects every level of the nervous drawal symptoms after sudden abstinence. system--from the neurochemicals within single In a search to explain why people drink al- cells to the macrofunctions governing thought cohol to excess, researchers have proposed processes and behavior. Research on cognition several theories. One theory suggests that and brain responses to various stimuli con- alcohol's appeal stems from its initial excit- tinues to expand the inventory of alcohol's atory effects. Animal research tends to sup- effectson humans.Driving-relatedstudies port the theory, as animals will work to re- have shown thatalcohol impairs judgment, ceive infusions of alcohol--thus meeting one attention, information processing, and reac- criterion of reinforcement. tion time. Alcohol also alters the brain's re- Another provocative preliminary hypothesis sponses to visual and auditory stimuli. Chronic is that tetrahydroisoquinolines, or TIQs, may drinking affects memory and the ability to play a role in habitual heavy drinking. TIQs are detect small differences and creates such au- formed when alcohol is metabolized. In some tonomic difficulties as lack of proper eye pupil animal experiments,when these chemicals control.Abstinencecanreversealcohol's are injectedintothe brainsofpreviously cognitive effects more easily in young drinkers abstinent animals preference for alcoholis than in older ones. increased. Social drinking appears to resultin some Empirical and theoretical progress over the cognitive impairment, but methodologic issues past decade offers encouragement that re- cloud the picture. Alcoholism, on the other search will continue to acquire fundamental hand, definitelyimpairs cognitive perform- knowledge essential to understanding how hu- ance. Late stages of alcoholism may also re- mans react to alcohol and what makes them sultinorganic brain damage--alcoholic de- drink excessively.

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44 Chapter IV

Medical Consequences ofAlcohol

For most of us, alcohol conjures up pleasant more susceptibleto cancersoftheskin, social occasions- -wine with a good meal, beer mouth, and esophagus than are nondeficient at a ball game, or cocktails during a party of animals. friends. Rarely do we consider the harmful effects ofalcohol. Even many experienced drinkers who know every vineyard, vintage The Esophagus year,distillery, and brewery are relatively unaware of the basic medical andbiological The occurrence of nonmalignant esophageal consequences of drinking. disease such as esophagitis has been associated This chapter follows the trail of adverse with chronic alcohol abuse (Shiraz' and Platz effects of alcohol throughout the body and its 1978). In normal human volunteers, alcohol has impact on various organ systems. been shown to interfere with acid clearing mechanisms and to irritate the mucous membranes (Mayer etal.1978). Mucosal tissue -Alcohol and the Digestive System tends to be abnormal in alcoholics (Zeus 1970). Moreover, there is an increased risk of Bar- rett's esophagitis (a premalignant lesion) in The Mouth alcoholics when compared with nonalcoholics The application of dilute alcohol and a num- (Martini and Wienbeck 1974). Esophageal var- ber of alcoholic beverages to the tongue and icose veins, which can develop in cirrhotic mucous membranes of the cheekstimulates patients, can be eroded, resulting in bleeding the flow of saliva (Martin and Pangborn1971). Into the gastrointestinal tract (Chaput et al. However, after a short time, the secretion 1974). rate of saliva is inhibited for 60 to 90minutes beforereturningtonormal(Winsorand Strongin 1933). Enlargement of the parotid (a The Stomach specific salivary gland) is common in alcoholics (approximately 12 percent), butitis The effect of alcohol on gastric emptying uncertain whether it occurs as a result of al- largely depends on the concentration of alco- cohol use or is due to the protein deficiency hol in the stomach (Cooke 1972). Gastric emp- frequently seen in alcoholics (Bode 1981). tying is slowed when alcohol concentrations Inflammation of lips and soft tissue of the are greater than 6 percent(Pirola and Davis mouth, common in alcohol abusers, is thought 1970). to occur as a result of nutritionaldeficiency, While it has no effect of the muscle that particularly of the various B vitamins and iron empties the stomach, alcohol has been shown (Larato 1972). to produce a diminution in the sphincter mus- Cancers of the mouth, tongue, pharynx, and cle response to acidity in the duodenum(Pho- esophagus occur more often in alcoholics than sawasdi et al. 1979). In nonalcoholics. Wynder (1975) has suggested Chronic consumption of alcohol causes a that a synergistic effect between alcoholand diminution of gastric acid secretion in humans tobacco may be responsible. Other factors (Cooke 1972). Furthermore, alcohol increases that may contribute to such carcinogenesis the formation of prostaglandins, which are include deficiencies of vitamin A, vitamin B, known toinhibit acid secretion (Main and and zinc that may occur in the alcoholic Whittle 1976). Such an increase may account (Wynder and Chan 1970). Sporn et al. (1976) for the reduced stomach acid observed in in- found that vitamin A deficient animals are dividuals who have abused alcohol for 5 or 69 45 more years. Acute administration of alcohol intestinal lesions occur within 10 minutes of Into the mouth, stomach, or blood, however, alcohol ingestion, are well developed withinan stimulates secretion of gastric juice. These- hour, and disappear after 4 to 16 hours (Bar- cretion appears to be maximalat alcohol aona et al. 1974). This same study found that concentrations between 8 and 16 percent,ap- animals that chronically consumed alcohol did proximately the concentration found In wine not respond with such lesions. (Elwin 1969). Decreases In Intestinal enzymes, Including Acid often Injures the mucous membranes of those that act on milk, arecommon in exper- the stomach (Gottfried etal.1976). Thus, imental animals and man after alcohol Inges- drinkingcanproducegastrichemorrhage. tion. Thus, milk intolerancemay be exagger- While alcohol alone does notcause gastric ated in alcohol abusers (Per lowet al. 1975). bleeding in normal subjects,itsignificantly When applied directly to small intestinal Increases blood loss in persons with aspirin- membranes, alcoholdecreases the sodium- derived mucous membranes injury (DeSchepper potassium-ATPase activity from 94 percent to et al. 1978). Therefore, the aspirin commonly 17 percent of control values (Hoyumpa et al. taken by alcohol abusers to alleviate discom- 1977). As a result of this effect, alcohol in fort may aggravate further stomach injury excess of 2 percent can Inhibit the transport (Robert et al. 1980). ofelectrolytes, amino acids,and glucose Alcohol abuse as a cause of gastric ulcer across the small intestine (Kuo and Shanbour disease, however, remains controversial. Al- 1978). Thus, both in animals and in humans, though the Incidence of peptic ulcer has been alcoholinhibitsthetransportofessential reported to be as high as 20.6 percent inpa- amino acids (Israel etal.1968).Although tients with alcoholic liver disease,an associ- tissue damage resulting from largeamounts of ation between the two disease conditions has alcohol can Inhibit amino acid transport, the never been proven (Bode 1981). fact that it is rapidly reversible suggeststhat There is conflicting evidence concerning the a physiochemical change rather than a toxic role of alcohol in stomachcancer, with most injury is responsible (Israel et al. 1968). studies showing no clear association. However, Vitamin absorption is adversely affected by a limited number of studies have shown a alcohol. Alcoholics have showna significant positive correlation between alcoholuse and reduction in the absorption of folic acid (a thedevelopmentofgastriccancer(Bode vitamin) into the jejunum, anotherpart of the 1981). Whether alcohol-induced gastritisis a small bowel (Halsted et al.1973). However, premalignant lesion, particularly ifit occurs after 2 weeks of nutritional supplementation, repeatedly, is an important question for which the folic acid absorption of alcoholics im- sufficient evidence is not yet available (Bode proves despite continued use of alcohol. This 1981). suggests that,inalcoholics, impairedfolic acid absorption may be primarilya result of poor nutrition rather than a direct toxic effect The Intestine ofalcohol.Insupport ofthiscontention, studies of acute alcoholadministration to normal subjects have shown a decreased folic The intestine is an important site for the acid absorption in only 20 percent of the sub- absorption of nutrients into the blood stream. jects studied (Halsted et al.1967). However, The major focus of research in thisarea has folic acid deficiency is the mostcommon nu- been on the small intestine. This site isex- tritionaldeficiencypresentinalcoholics posed to higher concentrations of alcohol than (Leevy et al. 1965). There also is evidenceto any other organ in the body except the stom- suggest that liver tissue is less able to takeup ach. After either acute or chronic alcohol folic acid from blood after acute alcohol ad- consumption, the small intestine may demon- ministration to either normal or alcoholic In- strate structural injury. dividuals (Lane et al. 1976). In humans, a single small dose (1 gm/kg body Thiamine (vitamin B1) is absorbed much like weight) of alcohol can produce lesions inthe folic acid. The active absorption of thiamine duodenum, apartrfthesmallintestine by cells lining the small intestine is not af- (Gottfried et al. 197 \dditional studies with fected by alcohol (Hoyumpa et al. 1974). How- human volunteers: I that the structural ever, thiamine movement out of the Intestinal changes that occurr,:a upon consumption of cell is impaired by alcohol (Hoyumpa et al. alcohol disappeared once alcohol consumption 1975). Both human and animal studies ceased (Rubin et al. 1972). Similarly, In rats, suggest that alcohol Inhibits the mechanism 70 46 for absorption of thiamine at normal levelsof the relationship of these findings to the clin- the vitamin (Thomsor et al. 1970), but has no ical condition of alcohol-induced hyperlipid- effect on the diffusion mechanism that comes emia (excess lipids in the blood) remains un- intoplayathighthiamineconcentrations clear (Baraona et al. 1975). (Hoyumpa et al. 1974). The effect of alcohol on the motility of Alcohol'seffectonironabsorptionis different small intestine segments is variable, unclear. In one human study (Charlton et al. but the net effect Is to shorten the transit 1964), a single dose of alcohol increased ab- time through the intestine. Initially, when in- sorption of a dietary form of iron,ferrous travenous alcohol is given to volunteers, mo- chloride, while others have found no effect of tilityincreases, particularlyInthe second either acute or chronic alcohol administration portion of the duodenum (Piro la and Davis on iron absorption(Murray and Stein 1965). 1970). This increased motility is characterized Adding further confusion to this issue are the by an increase in intestinal pressure and in the studies that showed that ferrous iron absorp- number of contractile waves generated. Later, tion is inhibited rather than enhanced by al- there is a decrease in duodenal activity with a cohol (Tapper et al. 1968). gradual return toward normal. Moreover, al- Although high levels of zinc are commonly cohol depresses nonpropulsive motility of the found in the urine of alcoholics, ithas not colon in both dogs and humans. It should be beenestablishedthatalcoholconsumption noted that these changes in small and large produces zinc deficiency by Increased urinary intestinal motor activity may contribute, at zinc losses (Sullivan1962). While alcohris least in part, to the diarrhea commonly seen metabolized by a zinc-containing enzyme, zinc following excessive drinking (Martin etai. deficiency is not known to decrease alcohol 1980). metabolism (Wang and Pierson 1975). The mechanism involved in calcium trans- The Pancreas port by the small intestine has not beenelu- cidated. An animal study showed that alcohol Excessive alcohol use can cause chronic inhibits calcium absorption (Krawitt 1975), but pancreatitis, in which lesions and functional the mechanism of such inhibition is not en- impairment persist even in the absence of al- tirely clear. In contrast to animal studies, one cohol (Sarles 1974). This contrasts with gall- study of nonalcoholics given short-term alco- stone-induced acute pancreatitis in which the hol showed no adverse effect on calcium ab- pancreas returns to normal aftereach episode. sorption (Verdy and Caron 1973). Others, how- More than 75 percentofthe cases of ever, have reported a doubling of fecalcal- chronic pancreatitis in the United States occur cium in human volunteers after drinking, sug- in alcoholics. Moreover, pathologic changes or gesting a reduced calcium absorption (Krawitt alterations in pancreatic function can be de- 1975). tected in half the alcoholics without pancre- Alcohol has multiple effects on lipid me- atitis symptoms (Reber 1978). Steady alcohol tabolism within the small intestine. In general, consumption over about 6 to 12 years is nec- alcohol increases triglyceride synthesis in in- essary before pancreatic symptoms occur. testines and in mucous membranes (Baraona et Acute pancreatitis usually does not occur in al. 1975). It also causes a decrease in fatty the iiolidlcoholic who occasionally drinks ex- acid oxidation. cessively (Strum and Spiro 1971). On the other After exposure to alcohol, the intestinal hand, alcoholics develop symptoms of acute lymph glands produce more cholesterol and pancreatitis,but onlyafter functional and triglyceride, an effect seen only when alcohol histologic (tissue) changes of chronic pancre- is present within the intestine (Middleton et atitis are well established.Progressive deal.1971).Inaddition, cholesterolisredis- struction of the pancreas continues even after tributed among the various intestinal lymph the individual stops drinking. lipoproteins. If alcohol is injected rather than Surprisingly, chronic alcohol administration drunk, the redistribution does not occur. This to dogsstimulatespancreaticsecretion, suggests that alcohol acts on the small in- whereas alcohol's acute effectis inhibitory testine mucosal enzymes in altering the syn- (Brooks and Thomas 1953). This excitatory thesis and transport of cholesterol. Interest- effect can be abolished by atropine (a drug ingly,chronicalcoholfeedingtoanimals that blocks some nervous system activities) abolishes or inhibits these acute effects of and does not occur in previously vagotomized alcohol on Intestinal lipid 4r,,lsport(Baraona (cutting the nerves connecting the brain to the et al. 1975; Rodgers and0,:',rteri 1975). Thus, stomach)dogs. Again,theneurochemical

47 71 mechanism acting on alcoholic animals is op- Metabolism of Alcohol posite to that seen in nonalcoholic animals. The reason why chronic alcoholism reverses this acute effect of alcohol on the pancreas Is Alcohol is not effectively stored in tissues, not known. and little less than 10 percent of an ingested Regardless of the specific mechanism in- dose can be eliminated through the kidneys, volved, chronic alcohol consumption results In lungs, and skin. For practical purposes, one the secretion of a juice more concentrated in can assume that the body rids itself of alcohol protein. Protein precipitates are rich in cal- only by oxidizing Itin the liver, the organ cium carbonate and are identical to the small containing the bulk of the enzymes required pancreatic stonesfound Inhumans with for alcohol oxidation. The liver's complexity chronic pancreatitis (Nakamura et al. 1972). In and unique role in alcohol oxidation contribute both dogs and humans, these "plugs" of pre- to the many deleterious effects of alcohol cipitated protein obstruct the ducts, blocking within the liver. Unlike other major sources of secretion. Acetaldehyde is a highly labile and calories, alcohol can' at be stored either in the reactive substance that readily forms adducts liver or in other ti sues; it must therefore be with proteins. If sufficient amounts of acet- metabolized immeoiately in preference to all aldehyde are present in the pancreas, it may other fuels. contributetothe formationofpancreatic Threeliverenzyme systemshavebeen stones which obstruct the ducts. shown to promote the oxidation of alcohol to The fine structural changes that occur in acetaldehyde. They are, in descending order of the pancreas after alcohol ingestion are sim- importance:alcoholdehydrogenase(ADH), ilar to those found in liver cells (Dar le et al. microsomal ethanol-oxidizing system (MEOS), 1970), and the changes in early human chronic and catalase. The acetaldehyde produced is pancreatitis appear to be similar to those ob- itself toxic, so a second step is subsequently served in animals chronically treated with the required to convert it to a final nontoxic sub- hormones gastrin or chulecystokinin. stance, acetate. A relatively recent finding is that a specific The major pathway for alcohol metabolism genetically controlled cell surface antigen (a involves ADH. Although an increase in ADH substance that activates the immune system) activity above that seen normally may not has an increased prevalence in individuals with necessarily increase the rate of alcohol oxi- chronic pancreatitis due to alcoholism. This dation, reductions in ADH activity do diminish suggests a possible genetic mechanism pre- alcohol metabolism (Bosron and Li 1980). Thus, disposing alcoholics to pancreatitis (Fauchet low protein diets, which 'reduce ADH levels, et al. 1979). slow the metabolism of alcohol both in rats Anassociationbetweenalcoholismand and in humans (Pekkanen etal.1978). Con- cancer of the pancreas has been hypothesized. sistent with this observation, prolonged fasting Burch and Ansari (1968) were the first to make reduces the metabolism of alcohol (Bode and such a suggestion, based on a retrospective Thiele 1975). Moreover, the sex steroid tes- study in which 75 percent of the patients with tosterone inhibits ADH activity while estra- pancreatic cancer also had a history of mod- diol, an estrogen, enhances it (Rachamin et al. eratetoheavyalcoholintake.Additional 1980). support for this thesis was provided by the As noted above, other systems in addition to report that the risk of pancreatic cancer was ADH can oxidize alcohol. Thus, In animal ex- twice as great in males who consumed alcohol periments, as much as 30 percent of the total daily as it was in nondrinkers (Lieber 1977). chronically administered alcohol may be oxidized by a non-ADH enzyme pathway in which MEOS plays the major role (Matsuzaki et al. Alcohol and the Liver 1981). However, the contribution of this system to alcohol elimination In humans has not Until recently, it was unclear whether liver been quantitated. The issue in humans is com- disease associated with alcohol consumption plicated by the presence of many forms of was a direct effect of the alcohol or of the ADH, including one form, thew ADH, which malnutritionthatoftenaccompaniesalco- has an activity profile similar to MEOS (Bos- holism.Thelandmarkwork,primarilyof ronetal. 1979). Nonetheless,following Lieber (1981) andhiscolleagues,has now chronic alcohol consumption, the MEOS sys- established that alcohol is directly toxic to the temissignificantlyincreasedinactivity liver. (Lieber and DeCarli 1968).

48 72 In humans, alcohol consumption accelerates relatively high concentrations of alcohol in- blood alcohol clearance, particularly athigh hibit the uptake of amino acids (Krebs et al. alcoholconcentrations.This observationis 1973). consistentwiththemetabolicactivityof Patients with cirrhosis frequently have an MEOS (Salaspuro and Lieber 1978) but is also increased plasma levelofaromatic amino consistent with the activity of i ADH. MEOS acids (Ono etal.1978). These amino acids activity generates only heat, while ADHoxi- convert to amines within thegastrointestinal dation can produce storable forms of energy. tract and can adversely affect the central This may account for the observation that nervous system by acting asfalseneuro- alcohol produces a greater Increase In oxygen transmitters.Inthis regard, Faraj and co- consumption in alcoholics than in normal in- workers (1976,1979) found a statistically sig- dividuals, and also for the lesser growth In nificantcorrelation betweenthelevelof animals that are fed alcohol as compared to plasma tyramine (an amino acid product) and their controls (Piro la and Lieber 1972). Such the degree of hepatic encephalopathy(liver- energy wasting couldexplain, at least in part, caused brain damage). theweightlossexperienced when alcohol The level of alpha amino N-butyric acid calories are substituted for a balanced diet (AANB) in the blood is increased after chronic (Lieber et al. 1965). alcohol consumption, which has led to sug- Alcohol oxidation always produces acetal- gestions that it may be of use as a biochemical dehyde which, in turn, Is metabolized to ace- marker or indicator of alcoholism (Shaw et al. tate. It is generally accepted that morethan 1976). However, the plasma level of AANB different factors pre- 90 pertnt of the acetaldehyde formed as a may reflect at least two consequence of alcohol oxidationis oxidized sent in chronic alcoholicindividuals: Chronic by aldehyde dehydrogenase (ALDH) to acetate alcohol consumption tends to increasethe immediately within the liver. level of AANB, while dietary proteindefi- The principal cellular site of acetaldehyde ciency tends to decrease it.Itis therefore factors if metabolismlieswithinthemitochondria, necessary to control for nutritional which are found in the cytoplasm of cells. one is to use the level ofAANB in plasma as a Moreover, the major portion of acetaldehyde biochemical marker of chronic alcohol con- oxidationwithinthemitochondriaoccurs sumption (Shaw and Lieber 1978). where ALDH is located. Alcoholics with cirrhosis and malnutrition Acetaldehyde,likeitsprecursoralcohol, have depressed hepatic levels of carnitine, an adversely affects many tissues. It appears to amino acid needed for oxidation of fattyacids interferewith vitamin B6 metabolism and (Rudman et al. 1977). Possibly this is due to an promotes the vitamin's degradation(Veltch et impaired ability of such patients to synthesize (an amino al.1975). Acetaldehyde has been shown to it. The blood level of free proline impair the synthesis of proteins in theheart acid) is higher in some patients with cirrhosis and can inhibit protein secretion by liver cells compared with controls (Rojkind andDeLeon (Schreiber et al.1972,1974; Sorrell et al. 1970) and appears to be proportional to the 1983). Finally, acetaldehyde can depress the collagen (the structural protein that accumu- capacity of the liver to oxidize fattyacids lates In cirrhosis) content of the livers of such (Cederbaum et al.1975). The alcoholic may individuals (Kershenobich et al. 1970). therefore be a victim of a vicious cycle; high Increased levels of acetaldehyde have been acetaldehyde levels and chronic alcohol con- noted in patients with alcohol-induced liver sumptionimpairtheliver'smitochondrial disease, and acetaldehyde, but not alcohol, has function, which decreases acetaldehyde me- been shown to interfere with protein synthesis tabolism, which accelerates the accumulation (Schreiber et al.1972,1974; Sorrell etal. of acetaldehyde, all leading to liverdamage. 1983). Consistent with this finding is the observation that alcohol does not inhibit protein Amino Acid and Protein Metabolism synthesis by those liver cells that do not oxidize alcohol to form acetaldehyde (Morland et Alcohol disrupts amino acid (the building al. 1979). A similar lack of an inhibitoryeffect blocks of proteins) metabolism in the liver, occurs in a variety of nonhepatictissues in which leads to their excessive accumulation which the ADH activity Is absent orless than (Krebs et al. 1973). Amino acid abnormalities that present in the liver(Perin and Sessa in the b1, 3d appear in patientswith alcoholic 1975). Thus, the inhibitory effects of alcohol dependent, at least in hepatitis,cirrhosis,andliverinsufficiency on protein synthesis are (Rosen et al. 1977). In an isolated rat liver, part, on alcohol metabolism toacetaldehyde. 73 49 Fatty Acid Metabolism by the liver and contributeto the mild hyperglycemia. Fatty infiltration of the liver after alcohol consumption is the mostcommon hepatic ab- Other Metabolic Effects normality associated with alcohol abuse. The infiltration Is due to an increased accumula- Chronic alcohol ingestion leadsto prolif- tion of triglycerides inresponse to alcohol. eration of liver microsomes, fineintracellular The origin of the triglyceridesdepends upon structures that are responsible for detoxifying the pattern of alcohol consumption (doseand many drugs. Therefore, it is not surprising that duration) and the lipid content of the diet. an enhanced metabolism of drugs iscommon in With acute ingestion ofa large dose of alco- alcoholics. For example, the metabolism hol, the excess hepatic triglycerides of are de- meprobamate, pentobarbital, antipyrine,tol- rived from peripheral fatstores,while after butamide. warfarin, and diphenylhydantoin chronic alcohol ingestion, the is excess of tri- enhanced after heavy alcohol Intake andcan glycerides is the result of fat synthesisby the persist for up to 3 weeks after alcohol intake liver itself. has been discontinued (Mezey 1979). The replacement of dietarytriglycerides Chronic drinking is associated witha raised containing long chain fatty acids withfat metabolic rate, which Is characterizedby in- consisting of medium chain triglyceridesre- creased oxygen consumption, inefficientuse of duces the propensity of alcohol to inducea calories, increased heat output, and weight fatty liver (Lieber and DeCarli 1966).Appar- loss (Piro la and Lieber 1972). This hypermeta- ently the greater propensity of mediumchain bolic state has been hypothesizedto result, at triglycerides to undergo oxidationaccounts for least in part, from increasedenzyme activity this phenomenon (Lieber 1967). Protein defi- within the liver (Israel et al.1973). The in- ciency may also contributeto an alcohol- creased rate of oxygen consumption induced fatty can be liverin some circumstances; markedly depressed by surgically removingthe however, even with adequate protein inthe thyroid and can be abolished by treatment diet, alcohol may cause the developmentof with propylthiouracil (PTU), fatty liver. a thyroid inhibitor It would appear that the main (Orrego et al. 1979). These observationssug- factors leading to the development ofalco- gest that PTU may be of potential therapeutic holic fatty liver are as follows: Alcoholre- value in alcoholic patients with liver disease. places fatty acids as the preferred fuelfor Indeed, in a recent study, PTUwas reported to mitochondria. The metabolicconsequence is exert a beneficial short-term effecton both that more lipid (fatty acid) Is synthesized and the magnitude and the rate of improvementin less is burned. In addition, alcoholat high patients with alcoholic hepatitis (Orregoet al. concentrations inhibits the transport of newly 1979). Moreover, the therapeutic valueof PTU synthesized lipids out of the liver cell. Thenet was found to be greatest in those patients with effect is accumulation of fatty acids. the most severe liver disease. Thereare, how- A consequence of the hepatic accumulation ever, some conflicting reports. For example, of fatty acid is the excess formation of ke- Halle et al. (1982) performeda double-blind tones (Lefevre et al. 1970). This results in al- controlled trial in patients withsevere acute coholic ketoacidosis (increased levels of ke- alcoholic hepatitis. No beneficialeffects of tones and acids in the blood), which Is usually PTU therapy were observed. The question of associated with a mild hyperglycemia (ele- the therapeutic usefulness of PTU therefore vated blood sugar). Susceptibility to alcoholic remains to be answered. ketoacidosisvaries amongindividuals.The basis for alcoholic ketoacidosis Is still unclear; Pathology however, its development may not be related to the amount of alcohol ingested nor to the There are three specific subtypes ofhepatic levels of alcohol in the blood. Itis possible pathology associated with alcoholuse: alco- that disrupted hormone levelsare involved. holic fatty liver, alcoholic hepatitis,and al- Blood insulin levels are low during theketo- coholic cirrhosis. In its early stages, alcoholic acidosis episode, while those of growth hor- liver disease is characterized byaccumulation mone, epinephrine, glucagon, and cortisol are of excess fat in the liveras a result of the high. Such a hormone pattern could act tomo- mechanisms already described above.Alco- bilize free fatty acids from peripheral adipose holic hepatitis is characterized by the death (fat) tissue to enhance fatty acidmetabolism and inflammation of individual liver cells.This

50 74 more severe formof alcohol-associated he- Alcohol and Muscle Systems patic injury may cause death in10 to 30 percent of the afflictedindividuals. Eventually the entire structural and functionalcapacity Heart Muscle of the liver is impaired, resultingin cirrhosis, irreversible Anassociationbetweenalcoholism and the most severe and presumably for more form of alcohol-induced liver disease. heart disease has been recognized Most patients with alcoholic fattyliver are than 100 years. Until recently, however,heart malnutri- virtually asymptomatic; the variouslaboratory disease was thought to result from and not tests appear nearly normal.Importantly, al- tion, particularly thiamine deficiency, coholic fatty liver is a completelyreversible alcohol itself. Now that thiaminedeficiency contrib- lesion that does not necessarily progressto a has been eliminated as an Important uting factor, heart disease has beendirectly more severe disease. The study of patients with alcoholichepa- linked to alcoholism. a primary titis may lead to an understandingof the nat- Specifically,cardiomyopathy, ural evolution of alcoholic liver diseasecul- disorder of heart muscle, is often foundin in minating as cirrhosis.In some populations, chronic heavy drinkers. It generally appears in Europe and Japan, cirrhosis patients with a long history ofalcohol con- particularly than 10 develops in alcoholics without anapparent sumption, usually somewhat greater ofalcoholichepatitis years in duration. The majorsymptoms of al- intermediatestage shortness of (Karasawa et al. 1980). This observation raises cohol cardiomyopathy are chronic alcohol can pro- breath and signs of congestive failure such as the question as to whether and mote the developmentof cirrhosis without edema, chest pain, fatigue, palpitations, alcoholic hepa- blood-stained sputum. being preceded by a stage of Alcoholic cardiomyopathy does not occur titis. It now appears from bothhuman and animal studies that alcoholic hepatitis maynot suddenly (Demakis et al.1974). It gradually of alcoholic progresses from asubclinical condition char- be necessary for the development findings and cirrhosis (Popper and Lieber 1980). acterized by minimal cardiac According to a new theory, theballoon-like nonspecific electrocardiographicabnormalities hepatitis to overt congestive heartfailure. The severity swelling characteristic of alcoholic related directly to develops as a resultofthe accumulation of the illness appears to be protein, which the duration of alcohol abuse. The prospectfor within the cell of lipid and If the individual normally would have been secretedinto the recovery Is reasonably good, blood. The retention of such proteins presum- ceases to drink, but recoveryIs slow and may effects of al- require 5 to 6 years (Fuster et al.1981). ably results from degenerative the cohol on subcellular structures(microtubules) It is generally believed that damage to activity cell mitochondria of the heartmuscle is the that are important for the secretory alcoholic of the liver (Matsuda et al.1979). Thus, the major mechanism responsiblefor effect of alcohol may be similar tothat of cardlomyopathy(Alexander 1967). Electron proteins and microscopic studies clearly showdegenerative drugs which bind to the cellular to produce lesions similar to those seenin human changes of the mitochondria in response (Denk et chronic drinking (Alexander 1967;Alexander liver cells with prolonged alcohol use structures also al. 1979). et al. 1977b). Other subcellular alcoholmay be abnormal, leading todepression of The severityofthe various mi- associated pathologies of the livercorrelates mitochondrial respiration, liberation of of drinking or tochondrialenzymes,andareductionof poorly with either the duration (Alexander the amount of alcohol consumed. energy-providing ATP in the heart Not all patients with alcoholichepatitis et al. 1977a). hepatitis ap- Incontrast, some epidemiologicalstudies develop cirrhosis, and alcoholic doses pears to occur in29 percent of male and 47 have indicated that alcohol in moderate (Wilkinson et al. may have a health enhancingeffect on the risk percent of female alcoholizs 1980). 1969; Morgan and Sherlock1977;Gavaler for coronary heart disease(Klatsky anti- However, it has also been shownthat at mildly 1982). Since specific histocompv:ibility affects gens (HLA) are morepreve$L lt in patients intoxicating doses alcohol adversely these genetic left ventricular function(Ahmed et al. 1973). with cirrhosis than in controls, of the factors might determine analcoholic's sus- Larger doses actually impair the ability heart muscle to contract. Thus,alcohol de- ceptibility to develop cirrhosis;Goodwin 1971; function at blood Bell and Nordhagen 1980). presses the heart muscle

51 75 concentrations found during alcoholintoxi- essary for muscle contraction, in the cell. cation. Gimeno and coworkers (1962)observed Cardiac arrhythmlas(heartbeat such depression in rats Irregu- at concentrations of larities), such as ventricularfibrillation and alcohol as low as 0.1 percent. Spannand his palpitations, are common in individuals colleagues (1968) found that heart with contrac- alcohol-relateddiseaseand,inparticular, tions ofleftventricular muscles, obtained during alcohol Intoxication (Ettinger from both normal cats and those etal. with chronic 1978; Greenspon et al.1981). Gould and his heart failure, are slowed by alcohol.As the coworkers (1969) have suggested alcohol dose is increased, the heart that sudden muscle death probably caused by cardiacarrhythmlas contractions continue to be slowed.Nakano may be relatively common among and Moore (1972) observed young adults a similar heart who are found, at autopsy,to have large 'fatty muscle velocity/alcohol dose relationshipIn livers, presumably due to alcohol guinea pigs. abuse. It Is likely that these alcohol-inducedcardiac ar- Delgado and his associates (1975)observed rhythmlas are due to the direct effects ofal- that consuming one to two drinksof Scotch cohol upon the heart muscleas well as to the whisky affected the heart In normalsubjects adverse 30 to 90 minutes following effects ofacetaldehyde upon the Ingestion. Simi- conduction system. As littleas 2 ounces of larly, Ahmed et al. (1973) foundthat whisky whisky, consumed by individuals ingested over 2 hours by normal with existing subjects organic heart disease,can suppress the heart's resulted in a reduction of the durationof ability to generate musclecontractions that systole. pump the blood throughout the body (Newman The peripheral circulatory andneurohor- and Valicenti 1971). Moreover, monal effects of alcohol tend another study to obscure the has indicated that alcoholintoxication can unfavorable action of alcoholon the heart. result In a complete heart block (absence Both acetaldehyde and of acetate (metabolites of heartbeat),requiringpacemakertherapy alcohol) have been shownto have direct ef- (Leier et al. 1974). fects on the vascular system resulting in vas- Finally, it appears that patientswith exist- odilatation (dilated blood vessels) (Liangand ing heart disease are sensitive Lowenstein to adverse my- 1978).Acetatealsoincreases ocardial effects of alcoholor acetaldehyde cardiacoutputandleftventricularpeak (Conway 1968; Gould et al. 1971). pumping rate and reduces the resistanceof peripheral blood vessels, all varying withthe Skeletal Muscle alcohol dose (Liang and Lowenstein 1978). Interestingly, alcohol cannot be metabolized Myopathy, the disease of skeletalmuscle, by the heart because alcohol dehydrogenaseis has been associated with alcohol absent abuse for in the heart (Lochner etal.1969). about 120 years. Modernconcepts of alcoholic Acetaldehyde dehydrogenase ispresent, how- myopathy began, however, In 1955 withthe ever, and thus acetaldehyde can be and is studies of Ekbom and his associates(1964), metabolized by cardiac muscle (Forsythet al. who first described a syndrome of 1973). Despite this lack of muscle alcohol metabolism, weakness without evidence of othersigns or Regan and his associates (1969)have shown symptoms In alcoholics. Eventually,a wide that following alcohol administrationto dogs spectrum of alcoholic myopathy has various ions and enzymes usually found come to only be recognized, from the completelyasympto- inside cells are released by heart muscleinto matic to the near fatal (Hed et al. 1962). the blood. This leakage of cellularcontents Subclinical myopathies occur inmore than presumably indicates cellular damage,sug- one-third of alcoholics. Some alcoholicswill gesting that alcohol itselfistoxic to the have a history of musclecramps, weakness, heart. Moreover, Swartz and coworkers (1974) and occasional episodes of darkurine (myo- have reported that calcium uptake andbinding globinurea) which Is thoughtto be due to the in the heart, which is needed for musclecon- presence of myoglobin released by damaged traction, is inhibited by alcohol. Furthermore, muscle tissue (Faris et al. 1967). Williams and his coworkers (1975) have dem- The development of muscleweakness in any onstrated a dose-dependent Inhibition ofthe alcohol-abusing Individual could Implyacute sodium-potassium-ATPase activityofblood alcoholic myopathy. Such Individualsmay° ex- vessel membranes isolated from guinea pig perience a sudden attack of muscle painor a hearts, with both alcohol and acetaldehyde. rapid progression ofa previously diagnosed The enzyme plays a critical role incontrolling chronic myopathy. Such attackscan be fatal. the amounts of sodium andpotassium, nec- Generally, the musclesare exquisitely tender

52 7 6 during attacks, and are centeredin one group diet for several monthswilldeplete body of muscles, although on occasion theeffect stores, and the diet of mostalcoholics con- minimum can be diffuse.Fortunately, if alcohol use is tains significantly less than the daily discontinued, the disease andits symptoms requirement of this vitamin (Wu et al.1975). disappear. Therefore, folic acid deficiency is the primary cause of megaloblastic(abnormal red blood cells) anemia in alcoholics (Sullivan and Her- Smooth Muscle bert 1964; Hines and Cowan1974). Because Alcohol's effects on smooth muscle have folk acid deficiency causes Ineffective pro- with beenrecognizedonlyrecently.Previously, duction of red blood cells, it is associated when alcohol was used as an analgesicfor increased iron turnover in the bloodand a de- muscles occa- layed red blood cell incorporation ofiron. pregnant women, the uterine in- sionallystopped contracting.Thisledre- Therefore, folic acid deficiency leads to searchers to speculate that alcoholdirectly creased Iron absorption and may be responsible inhibited smooth muscle contractions(Chap- for the increased iron stores in somechronic man and Williams1951). This concept was alcoholics. Impaired liver function mayalso challenged, however, when Fuchs and Wagner contribute to these effects. Notonly is folate (1963) reported that alcohol interfered with intake reduced, but in individuals withalco- the release of oxytocin, ahormone responsible holic liver disease, folate may bereleased for uterine contractions, and thatthis inhi- from stores in the liver and lost in the urine, bition of hormone activitywas the major thereforefurtherreducing folate stores factor responsible for the diminisheduterine (Cherrick et al.1965). Thus, folate deficient contractions. However, more recently, several alcoholics may need to be treated withfolic research teams have shown that alcoholin low acid in therapeutic doses much largerthan the concentrations does indeed directlydepress amount needed to simplymaintain normal uterine contractions (Gimeno etal.1971; function. deficiency, Laversen et al. 1973). The symptomsofriboflavin Moreover, Fischer et al. (1965), Winship and which include anemia, underdevelopedbone his associates (1968), Hogan et-al.(1972), and marrow, and abnormalitiesin developing blood Kjellen and Tibbling (1978) have reportedthat cells, are identical to those seen inchronic also alcohol reduces sphincter (a smoothmuscle) drinkers. Thus, riboflavin deficiency may esophagus. Even more contribute to the anemia present In alcoholics. pressure in the lower its recently, Altura and colleagues(1976, 1978) Vitamin B6 is ineffectively converted to (Lumeng have shown that both alcohol andacetaldehyde active coenzyme form in alcoholics consistently enlarge the peripheralblood ves- and Li 1974). The coenzyme deficiency ap- sels, by relaxation of the smooth musclein the pears to cause severalclinical problems In anemia as vessel walls. alcoholics, Including some forms of well as changes in the bone marrow,peripheral neurological disease, convulsions, and worsen- Alcohol and Blood Disorders ing of liver disease (Davis andSmith 1974; Hines 1975). Prolongedproteindeprivationanddefi- Finally, it is possible that alcohol Itself may ciency of B vitamins, particularlyriboflavin, inhibit heme (aconstituent of hemoglobin) pyridoxine, and folic acid, play a rolein re- synthesisinred bloodcells(Moore1974; ducing the formation of new bloodcells. In Ibrahim et al. 1979). animal studies, protein deficiency orthe re- Most alcoholics without iron deficiencyhave moval of even a single essentialamino acid enlarged redbloodcells(macrocytosis),a from the diet can produce anemiawith re- recognizedbutpoorlyunderstooddisorder duced blood formation in the bone marrow, (Binghman 1960). Such blood cell dysmorphol- normal diet ogy may be the resultof a variety of under- which recovers after resuming a defi- (Ghitis et al.1963). Thus, protein deprivation lying mechanisms, including (1) folate important role in the pro- ciency, (2) increased numbers ofImmature red r -)bably plays an of duction of both the anemia and theabnormal blood cells, and (3) increased deposition cholesterol and phospholipids in red cell mem- iron levelsseeninalcoholics,particularly branes, associated with liver disease. those with liver disease. first to The close relationship of folicacid defi- Unger and Johnson (1974) were the been recog- report that, during routinescreening of em- ciency to chronic alcoholism has number of nized for years. Consumption of afolate-poor ployees of an insurance company, a 7 7 53 alcoholics were discovered to have an elevated There is additional evidence of altered im- MCV (mean corpuscular volume,or average munologic activity of white blood cells inal- bloodcellsize)inthe absence ofother coholics. Studies of animals and humans during changes usually associated with alcoholism, periods of alcohol ingestion found that the such as folate deficiency, increased numbers Immunologic response of the skinwas reduced of immature red blood cells,or significant (Gluckman et al. 1977). Also,many patients liver disorder. Since then, many reports have with alcoholic hepatitis havean altered immu- confirmed their observations (Buffet etal. nity to liver antigens (Young et al.1979). 1975; Morin and Porte 1976; Davidson and Furthermore, lymphocytes (one type ofwhite Hamilton 1978; Wright and Ree 1978). An in- blood cell) from patients with alcoholic liver creased MCV has been found in about 90per- disease may attack the patients'own liver cent of alcoholics, which suggests that the cells (Paronetto and Lieber 1976). Insummary, MCV may be useful as a marker for alcoholism these observations suggest that abnormalities (Unger and Johnson 1974; Buffetet al. 1975; of lymphocytic functionoccur in alcoholics Morin and Porte 1976). Furthermore, insev- and that immunologic mechanismsmay ac- eral large population studies, the number of count for some of the liver damage induced by alcoholic drinks taken daily correlated with alcohol even after abstinence (Lue et al. 1979). the MCV (Whitehead et al. 1978; Eschwege et The natural tendency for the blood toco- al. 1978). Even with abstention, littleor no agulate and seal a bleeding wound is disrupted change in the MCV occurs for many weeks; in alcoholics, principallyas a complication of usually 2 to 4 months of abstentionare re- advanced liverdisease. These changes are quired before the MCV returnsto normal similar to those occurring in patients with (Unger and Johnson 1974). other chronic liver diseases. Most often, the Leukopenia(areduced number ofwhite levels of the clotting factors dependenton blood cells) is relatively common in alcoholics vitamin K aredecreased.Moreover,the (Cowan and Hines 1971). Eichnereal. (1972), clotting compounds themselvesmay be ab- for example, observed leukopeni? 8 percent normal in alcoholics (Weinstein and Deykin of their cases. Other studies found 1.6 percent 1978; Conoso et al. 1979). (Eichner 1973) and 8.5 percent (Liu 1973) of subjects with leukopenia. Bone marrow smears obtained from such Alcohol and Kidney Disease individualsconsistentlyshowadecreased number ofcellswithmarkedlydecreased Alcoholics with liver diseasemay have en- numbers of mature granulocytes. The leuko- larged kidneys with increased fat, protein, and penic episodes in alcoholics tend to be tran- water (Van Thiel et al.1977). Seven to 14 sient, lasting 2 to 4 days, and usually followed percent of alcoholics, about 20 times the rate by rapid recovery and an increased number of of nonalcoholics, suffer tissue lossintheir white blood cells. kidneys (Edmondson et al. 1966; Longacre and As long ago as 1938, Pickrell noted in rab- Popky 1968). In one study, 12 of 20 alcoholics bits that white blood cells (which kill intruding suffered kidney tissue loss during their first bacteria) were inhibited from moving into attack of acute kidney infection,with the sites of bacterial infections within the skin lower urinary tract the source in most cases. and lung during alcohol intoxication. He noted These infections occurred in alcoholics with- also that the white blood cells attacked the out cirrhosis, suggesting that alcohol abuse bacteria normally. Similar results have been and not liver disease was thecause. Such a obtained in mice (Louria 1963) and in humans conclusioniswarranted because kidney in- (Brayton et al. 1970). MacGregor and hisas- fection does not accompany other types of sociates (1974; Gluckman et al.1977) have severe liver disease. shown that alcohol inhibits the movement of human white blood cells. Alcohol consumption for as short as 6 to 8 days can result in such Alcohol and Pulmonary Disease inhibition. The mechanism by which alcohol impairs such white blood cell functions re- Chronic obstructive pulmonary diseaseis mains unclear, although It has been suggested common among alcohol-abusingmales,es- that increased intracellular concentrations of pecially smokers (Rankin et al.1969). Other cyclic AMP (adenosine monophosphate) after pulmonary problems such as pneumococcal consuming alcohol may be partly responsible pneumonia are more likely tooccur in alco- for this phenomenon. holics than in the general population.Itis

54 78 possible that poor dentalhealth, combined indirect consequences of alcohol-induced liver with recurrent abnormal respiration(aspira- disease, has gained considerable credence. tion) during intoxication, may be responsible The specific mechanisms by which alcohol for the increased preval nce of bacterial lung adversely affects testicular function are being abscesses in alcoholics. Tuberculosis is a well. - unraveled slowly. Vitamin A is essential for recognized health problemin .malnourished creating sperm, and alcohol may interfere alcoholics, and impaired connections between with vitamin A activation in the testes (Van the arteries and veins in the lungs of alco- Thiel et al. 1974a). Alcohol metabolism may holics, especially those with advanced liver shift the balance between essential enzymes in disease, can cause cyanosis (reduced hemo- the testes as it does in the liver, thereby lim- globin), hyperventilation, and hypoxia. iting the generation of testosterone (Van Thiel and Lester1976a).Similarly,acetaldehyde, either produced in the testes or entering the Alcohol and the Endocrine System testes from the blood as a result ofalcohol metabolism outside the testes, may have deleterious effects upon testicular mitochondria, Gonadal and Adrenal Effects subcellular organelles thatarecriticalfor Low levels of androgens (malehormones) generating steroids (Gavaler et al. 1983). In- are found in alcoholic men.Thus, 70 to 80 deed, the conversion of cholesterol to the percent experience decreasedlibido and/or steroid pregnenolone, a reaction that occurs in impotence (Van Thiel 1980). In addition, 70 to mitochondria, is inhibited when mitochondria 80 percent of such men show both testicular are exposed either to alcohol or toacetalde- atrophy and infertility (Van Thiel and Lester hyde. Several studies have found a reduced 1979a). capacity to produce steroids in the testes ob- Not only do alcoholic men produce fewer tained from alcohol-fed rats (Chiao etal. androgens, but such men also produce excess 1981; Cicero et al. 1980). estrogens, the female hormones. Fifty percent Not only is testicular testosterone produc- of alcoholic men with cirrhosis develop femi- tion inhibited as a result of alcohol exposure, nine pubic hair patterns, and 20 percent de- but recent studies have demonstrated that velop enlarged mammary glands (Van Thieland alcohol interferes with gonadotropin(a sub- Lester 1979a). These signs of chronic alco- stance that stimulates the gonads) binding to holism, unlike the transient impotence com- testicular tissue. Furthermore, chronic monly experienced with an acute alcoholic drinking is associated with a pituitary- bout, persist even in the absence of intoxica- endocrine defect for gonadotropin secretion tion and are due in large measure to alcohol- (Van Thiel et al. 1978c). Alcoholics thus have induced tissue injury. low gonadotropin concentrations in their blood Until recently, liver disease was considered and respond inadequately to stimuli such as to be a primary cause of the sexualdr,f,Inc- luteinizinghormonereleasingfactorthat tion present in alcoholics. During the p1t 10 provoke gonadotropin release (Van Thiel et al. years, however, this concepthas been severely 1978c). Similar inadequate gonadotropin challenged, and a diametrically opposite view responses can be demonstratedinchronic has gained currency (Van Thiel andLester alcohol-fed rats and after acute alcohol ad- 1979a). This recent view is the result of evi- ministration to normal rats (Van Thiel et al. dence showing that sexual dysfunction can be 1979a). The cumulative evidence suggests that present in alcoholic men withessentially nor- chronicdrinking induces gonadal injury mal livers (Van Thiel etal.1974b). Plasma through its direct effects on the gonad, as well levels of testosterone, a male hormone, are as through indirect effects on thehypothala- reduced in men within hours afterdrinking mus (a part of the brain thatintegrates endo- enough alcohol (approximately sevendrinks) to crine activity) and the pituitary gland. produce a hangover (Ylikahri etal.1974). In addition to having reduced gonad per- Many of the features of alcohol-induced sexual formance, alcoholic men also have relatively dysfunction can be produced in experimental high levels of estrogens (Van Thiel and Lester animals with normal livers (Van Thiel etal. 1976b,1979a). As noted earlier, they show 1975a, 1979a). Furthermore, alcohol reduces many of the secondary sexcharacteristics of testosterone levels in mice and rats(Van Thiel women. Such femininization resultsfrom in- and Lester 1979a). Thus, the conceptthat the creases inestrogen-responsive proteins and sexual changes observed in alcoholic men are the hormone neurophysin (Van Thieletal. the result of alcohol per se, rather thanthe 1975b). The increases in the hormone prolactin

55 (associatedwithmilkproduction)seenin reduced blood levels of estradiol andproges- cirrhosis are also probably related to estrogen terone, loss of secondary sex characteristics, (Van Thiel et al.1978d). Because atrophy of andinabilitytoovulate.The biochemical the testes can be produced by estrogen, the mechanisms for such failure are probably the testicular damage observed in alcoholicmen same as those occurring within the testes of with cirrhosis can also be ascribed toexcess the male, as the pathways for generating estrogens.Bloodlevelsof oneestrogen, steroids are the same in the gonads of thetwo estradiol, are either normal or slightlyin- sexes. An alcohol dehydrogenase, seen in the creased in alcoholic men, and indeed,some ovaries of alcoholic women, may contributeto estrogen levels, e.g., estrone, are increased endocrine failure. moderately (Van Thiel et al. 1974b, 1975b; Van In addition to a direct effect on the gonads, Thiel and Lester 1976a, 1979a). This finding of chronic alcoholics, whether male or female, normal or increased estrogen levelsinthe also showed evidence of a defect in thecon- presence of androgen deficiency is paradoxi- trol by the brain over sex hormone secretion cal, since estrogens can be produced only by (Gordon et al. 1979). Thus, despitesevere go- conversion from preformed androgens.The nadal injury,follicle-stimulating hormone presence of normal or moderately increased levels in the female, expected to increase to blood estrogenlevels thus requires further correct gonad failure, are well below levels explanation. expectedforthedegreeofreproductive Preliminary results suggest that increased failure present. estrogens are the result of both the direct effects of alcohol and indirect effects mediated through the development of liver disease. The Hypothalamic-Pituitary-Adrenal Axis Contrary to initial expectations, however, the metabolic clearance rate for estradiol inmen The hypothalamus, deep inside the brain, is with alcoholic cirrhosis has been found to be the master hormone controller. It sends hor- normal, not reduced. Evidence is accumulating mones to the pituitary gland, which in turn to suggestthatadrenaloverproductionof emits other hormones to other glands,in- weak estrogen precursors regularly occurs in cludingthe adrenal gland.This systemis alcoholic men (Southren et al. 1973; Olivo et called the hypothalamus-pituitary-adrenal al. 1975; Gordon et al. 1975; Van Thiel et al. axis.Early studies on animals showed that 1980). Furthermore, signs ofexcess adrenal alcohol changes the activity of the adrenal steroids resembling Cushing's syndrome have cortex (Hion-Jon 1925; Smith 1951; Forbes and been described in such men. These patients Duncan 1951; Czaja and Kalant 1961;Ellis develop loss of peripheral muscle mass, obe- 1966). These changes could be prevented by sity, hypertension, facial redness, increased removing the pituitary gland. A sharp decrease cortical steroid levels in the blood, and loss of in the pituitary hormone ACTH (adrenocor- the normal diurnal variation of the steroid ticotropin hormone) (Noble et al. 1971) caused cortisol in the blood. The mechanism respon- by alcohol suggested that the primary effect sibleforthisoverproduction ofestrogen- of alcohol is at the pituitary level rather than precursors is unknown. at the adrenal gland itself (Ellis 1966). In contrast to the male, the alcoholic fe- In normal humans, intoxicating doses of al- male is not superfeminized but instead shows cohol produce an immediate increase in the severe gonadal failure commonly manifested blood level of the steroid cortisol (Fazekas by reduced or absent menstruation, loss of 1966). The cortisol responseappears to par- secondary sex characteristics such as bast allel the blood alcohol level. This acutere- and pelvic fat accumulation, and infertility. sponse in normal individuals is probably due to Studies of ovaries from alcoholic women who a hypothalamic stress reaction and pituitary died of cirrhosis while still in their reproduc- release of ACTH. tive years (20 to 40 years of age) have shown a In contrast to this acute stress reaction, paucity of developing ovarian follicles and few animal studies found that alcohol Intoxication or no corpora lutea, both of which are neces- and withdrawal are associated with inhibition sary for successful pregnancy (Jung and Russ- of the release of corticotropin releasing factor field1972).Moreover, these findings have (CRF) and impairment of the ACTHstress been reproduced recently in animals (Van Thiel response (Tabakoff et al. 1978). et al. 1978a). Researchers have recently begun to study The failure of the ovaries to produce hor- the effect of endogenous (naturally occurring mones in alcoholic women is manifested by within the nervous system) opiates (enkepha-

56 S lins and endorphins) on the control of pituitary catecholamine secretion in response to alcohol releasing factors. Such opiates appear to in- (Walsh and Truitt 1970). hibit CRF and thereby ACTH release. They therefore might contribute to reduced ACTH The Thyroid release seen during alcohol intoxication and withdrawal (Morley et al. 1980). This hypoth- The most consistent effect of alcohol on the esis is consistent with other observations that function of the thyroid is to moderately de- opiates alter some of alcohol's effects. For crease the hormone thyroxine (T4) levels in example, the opiate antagonist, naloxone, im- the blood and to markedly decrease the hor- proves the psychomotor impairment and demone trilodothyronine (T3) in the blood (Israel pressed level of consciousness induced by al- et al. 1979). It has been suggested that the low cohol (Jeffcoate et al.1979; Jefferys et al. T3 levels after alcohol consumption reflect 1980). injury to the liver and reduced ability of the The urine of patients with cirrhosis, espe- liver to remove iodine from T4 (Orrego et al. cially those with edema, contains increased 1979). Despite the considerable data amounts ofthe steroidaldosterone, which suggesting that alcohol affects the thyroid controls the amount of fluid and salt in the (and its interactions with the hypothalamus body(6ongiovanniandEisenmenger 1951). and pituitary) indirectly via the liver, alcohol Individuals witn cirrhosis are likely to have an can directly cause an increase in the thyroid increased secretion rate and blood levels of uptake of iodine, which is needed to synthesize aldosterone (Coppage et al. 1962). the thyroid's hormones (vadav et al.1970). Chronic liver disease is associated with a Moreover, Wright (1978) and Van Thiel et al. significantly decreased blood flow in the liver, (1979b) have reported a diminished thyroid the site where aldosterone is metabolized. As stimulating hormone (TSH) response to a result, the clearance of aldosterone from the thyrotropin releasing factor (TRH) in body is reduced and the duration of the ac- alcoholics. tivity of the hormone is prolonged (Coppage et al. 1962). It should be noted, however, that the Growth Hormone and Prolactin resultant elevated blood levels of aldosterone in cirrhotic individuals reflect not only a de- Considerable evidence suggests that alcohol creased metabolic clearance but also an in- blocks the release of growth hormone. Early creased secretion rate of the hormone occur- studies of laboratory animals suggested that ring, at least in part, in response to an inalcohol produces degenerative changes in the creased productionof angiotensin,which pituitary (Sanchez-Calvo 1941). More recently, stimulates aldosterone secretion. the acute administration of large doses of al- The state of the hypothalamic-pituitary- cohol to rats has been shown to abolish spon- adrenal axis during alcohol withdrawal has taneous growth hormone secretion (Redmond been studied extensivelyinanimals.After 1980). Alcoholics with cirrhosis, in contrast, alcoholis withdrawn from mice% they are have elevated levels of growth hormone and likely to be hyperactive, with seizures and frequently respond abnormally to stimuli of increased corticosteroids in the blood (Gold- growth hormone (Van Thiel et al. 1978b). stein 1972). Chronic alcoholics also experience Two studies (Torro et al. 1973; Earll et al. increased corticosteroid levels during alcohol 1976) have reported that a single dose of al- withdrawal (Stokes 1973). cohol had no effect on prolactin (a hormone Interestingly, the pituitary reserve of ACTH associated with milk-stimulation as well as in alcoholics experiencing withdrawal is fre- other functions). However, Loosen and Prange quently reduced (Wright et al.1975). Alco- (1977) reported reduced prolactin levels, but holics who abstain from drinking often show with minimally impaired prolactin responses to persistent abnormalities of the hypothalamic- TRH duringalcoholwithdrawal. Jungand ..pituitary-adrenal axis (Oxenkrug 1978). Russfield (1972) reported an increased prev- In addition to altering steroid hormone re- alence of prolactin-secreting cells in the pi- lease by the adrenal gland, alcohol stimulates tuitaries of male and female patients who died the secretion of catecholamines, e.g.,epi- of alcoholic liver disease. Ylikahri et al. (1976) nephrine and norepinephrine, and increases the noted increased prolactin responses to TRH In adrenal content of catecholamine synthesizing alcoholics, a finding confirmed by Van Thiel enzymes (Pohorecky1974).Studiesinrats and his coworkers (1978a, b, c, d). Van Thiel have suggested that acetaldehyde is princi- and his associates (1978a, b, c, d) also reported pally responsible for these observed changes in that elevated prolactin levels occur incir-

57 81 rhosis, and that cirrhotics have reducedpro- most likely due to an alcohol-induced decrease lactln responses to TRH. Incontrast, individ- In blood magnesium levels (Estepet al. 1969). uals with fatty liver have reduced prolactin Magnesium is well known to be importantin levels and exaggerated prolactin responsesto the regulation of parathormone secretionand TRH. Preliminary studies In therat also sug- In the mediation of the hormone'speripheral gest that alcohol increases prolactin levels in action (Rasmussen 1974). Both malabsorption the blood (Gordon and Southren 1977). of calcium and a primary dietary deficiencyof vitamin D probably are responsible,at least In Vasopressinand Oxytocin part, for the hypocalcemia in individuals with advanced alcoholic cirrhosis. Finally, Williams Alcohol produces diuresis, whichseems to and his coworkers (1978) recently havere- occur because the hormone vasopressin, the ported that alcohol resultsIn an Increased body's antidiuretic hormone, is Inhibited. In- level of the hormone calcitonin, whichmay deed, several groups have found reducedvas- play a role in developing hypocalcemia. opressln levels after acute alcohol adminis- It is of some interest that a decreased den- tration (Linkola et al. 1977; Helderman et al. sity of tibial bone has been reported inrats 1978). Little orno tolerance to the diuretic chronically fed alcohol(Saville and Lieber effects of alcohol or its inhibition ofvaso- 1965). Alcoholic patients do havea decreased pressin release has been observed In alcoholics bone mass and anincreasedincidenceof (Marquis et al. 1975). Alcohol's suppressionof fractures (Nilsson1970).Finally, low phos- vasopressin release appears to originate in the phate in the blood, which also iscommon In hypothalamus. Thus, stimuli applied directlyto alcoholics, may contribute to the development the hypothalamus can override the diuretic of the metabolic bone diseaseseen in alco- effects of alcohol. Alcohol may, however, in- holics (Knochel 1977). hibit the electrically evoked discharges of the hypothalamus (Raiha 1960). The Endocrine Pancreas More recently, studies showed thatvaso- pressin was suppressed while blood alcohol Several studies have shown that alcohol in- levels were increasing. After the maximum creases insulin secretion in response to glucose blood alcohol levels were attained, thevaso- (Singh and Patel 1976; Shahet al. 1977). In- pressin levels increased (Marquis et al. 1975). te. estingly, alcohol increases the insulinre- On the basis of bioassay data, alcohol would sponse to other compounds that stimulatese- appear to inhibit the release of the hormone cretion as well as to glucose (Kuhl andAnder- oxytocin,whichistheprincipaluterine- son 1974). contracting and lactation-stimulating hormone Glucose intolerance is common in individ- ofthepituitary gland (Wagner and Fuchs uals with alcoholic liver disease, particularly 1968). No data, however,are available on the those with portal hypertension (Phillips and actual blood levels of oxytocin during alcohol Safrit 1971; Kreisberg et al. 1972). Insulin and administration and withdrawal. especially glucagon (a hormone that ultimately increases blood glucose) levelsare increased in Parathormone such individuals (Marco etal.1973).Itis thought that the glucose intolerance Insuch Alcohol causes hypocalcemia (reduced blood individuals is due primarily to raised levels of calcium) in both dogs and rats (Penget al. glucagonin the blood.However, abnormal 1972). Parathormone, the parathyroid hormone glucose tolerance can occur in alcoholics due that controls blood calcium levels, doesnot to chronic pancreatitis as well ato advanced reverse this hypocalcemic effect of alcohol liver disease. (Peng and Gitelman 1974). The fall incalcium The syndrome of fasting alcoholic hypogly- may be related to the shift of calcium ions out cemia (low blood sugar) develops within6 to of the blood (Peng et al. 1972). Some studies in 36 hours after ingestion of alcoholby a pre- normal volunteers and in alcoholics havesug- viously malnourished or fasting individual.No gested that alcohol produces an increased uri- age group appears to be exempt from this type nary excretion of both calcium and magne- of alcohol- Induced reaction, but children and sium (Kalbfleisch etal.1963; Jones etal. women seem to be particularly susceptible. 1969). Alcohol has been shownto reduce the Several studies have reported thatalcohol is transport of :ium in the duodenum (Krawitt capable of producingsevere and conceivably 1975). The defect in calcium stability foundin fatalhypoglycemiainsusceptiblesubjects alcoholics withhypocalcemia,however,is (Marks and Medd 1964; Arky andFrienkel

58 1966). In addition to children, athletes are at hypotheses have been generated,inclue'ng: particular risk for the development of severe alcohol acting as a solvent to increase the hypoglycemia following the combination of entry of carcinogens into cells (McCoy and alcohol ingestion, fasting, or exercise (Arky et Wynder 1979); alcohol-induced enzyme al. 1968). changes leading to the conversion of procar- cinogens(noncarcinogenic substances)into active carcinogens (Seitz et al. 1981a,b; Garro Alcohol and Cancer etal.1981);and repeated alcohol-induced cellular damage promoting cancer in the liver Evidence for the strong associations be- (Lieber 1969). tween chronic alcohol consumption and can- cersofthemouth,pharynx,larynx,and esophagus has existed for many years (Lieber Summary et al. 1979). In addition to the cancers of the upper respiratory and alimentary tracts, more Chronic alcohol consumption leads to ubi- recent studies indicate that alcohol may play a quitous toxic effects in the body, with medical role in cancers of the liver, pancreas, stom- consequences ranging from slight functional ach, large intestine, rectum, breast, and ma- impairment to life-threatening disease states. lignant melanoma (Williams and Horm 1977; The most common site of injury is the liver, Rosenberg et al. 1982; Tuyns 1978). the organ most responsible forridding the There are no supporting data from animal body of alcohol. ,studies to clearly show that alcohol by itself is In the early stages of alcoholic liver disease, carcinogenic. This issue Is further clouded by the liver becomes fatty, a condition that may the fact that, either by accident or as a result progress to hepatitis. After an extended period of the production process, carcinogenic ma- of chronic drinking, the liver structure may be terials were formerly found in various alco- affected,followed bya breakdowninits holicbeverages.Thesesubstancesinclude functional capacity. The result Is cirrhosisan nitrosamines, polycyclic hydrocarbons,fusel often fatal disease. oils, and asbestos fibers (McGlashan etal. Because the liver Is so essential for metab- 1968; Wehman and Plantholt1974; Spiegel- olism and detoxification, many organs and holder et al. 1979). body systems may be adversely affected in- While the basis for the relationship between directly by alcoholic liver disease. Excessive alcohol and cancer is unknown, It is estimated alcohol also may directly injure the gastro- that alcohol by itself, or In combination with intestinaltract, muscles, and pancreas. As substances such as tobacco, is associated with alcohol and its metabolites travel through the 3 percent of the carer deaths in the United body in the blood stream, they may affect the States (Rothman 198); Doll and Peto 1981). major body systems, including the cardiovas- The interaction between alcohol consump- cular system, the nervous system, and the en- tion and tobaccoisparticularly strikingIn docrine system. Furthermore, thereisevi- terms of cancers of the mouth, pharynx, and dence of a strong association between chronic larynx, where the total risk is increased in a alcohol use and cancer of the stomach, large synergistic manner (Rothman and Keller 1972; intestine, pancreas, and liver. Tuyns 1978; McCoy and Wynder 1979; Schot- Many of alcohol's deleterious consequences tenfeld 1979). As an example, one study In- are the resuIl of effects on the endocrine dicated that alcohol consumption and heavy system hormones. For example, fewer andro- smoking produced up to a fifteenf old increase gens are produced in alcoholic men, often in the risk of oral cancer, compared with the leading to a femininization of their appear- chances ofpeople who neitherdrank nor ance, decreased libido, and infertility. Alco- smoked. Heavy smoking alone increased the holic women are affected also, frequently with risk by only twofold to threefold (Lemon et al. ovarian dysfunction. Alone, and in conjunction 1964; Lyon et al. 1976; Phillips 1980). with dietary deficiencies frequently associated Despite the absence of a known mechanism with alcoholism, alcohol abuse can produce of action, it is clear that heavy alcohol con- nutrition-related deficits in the body. These sumption is a risk factor for the development deficits result In altered protein metabolism of cancer. To account for this action, several and vitamin-related disorders such as anemia.

83 59 References

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66 R. Contamination of beer with trace quantities nal of Laboratory and Clinical Medicine 101: of N-nitrosodimethylamine. Food and Cosmetics 21-33, 1983b. Toxicology 17:29-31, 1979. Van Thiel, D.H., and Lester, R. Alchoholism: Its Sporn, M.B.; Dunlop,N.M.: Newton, D.L.; and effect on hypothalamic-pituitary-gonadal func- Smith,J.M. Prevention of chemical carcino- tion. Gastroenterology 71:318-327, 1976a. genesis by vitamin A and its synthetic analogs Van Thiel, D.H., and Lester, R. Sex and alcohol: A (retinoids).Federation Proceedings 35(6):1 332- second peek (editorial). New England Journal of 1338, 1976. Medicine 295:835-836, 1976b. Stokes, P.E. Adrenocortical activity in alcoholics VariErel7 D.H., and Lester, R. The effect of during chronic drinking.InSeixas, F.A., and chronic alcohol abuse on sexual function. Clinics Eggleston, S., eds. Alcoholism and the Central inEndocrinologyandMetabolism 8 :499 -510, Nervous System. 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67 91 releasinghormone-inducedthyroid-stimulating cancer sites with tobacco and alcohol consump- hormone secretion in chronic alcoholic men with tion and socioeconomic status of patients: In- liver disease. Alchoholism: Clinical and Experi- terview study from the Third National Cancer mental Research 3 :302 -308, 1979b. Survey. Journal of the National CancerIn_stitute Van Thiel, D.H.; Gava ler, J.S.; Slone, .F.L.; Cobb, 58:525-547, 1977. C.F.; Smith, W.I.; Klaus, M.B.; and Lester, R. Is Winship, D.H.; Caflisch, C.R.; Zboralske, F.F.; and feminization in alcoholic men due in part to Hogan, W.J. Deterioration of esophageal per- portal hypertension: A rat model. Gastroenter- istalsisin patients with alcoholic neuropathy. ology 78:81-91, 1980. Gastroenterology 55:173-178, 1968. Veitch, R.L.; Lumeng, L.; and Li, T.-K. Vitamin Winsor, A.L., and Strongin, E.I. The effect of al- 136 metabolism in chronic alcohol abuses The cohol on the rate of parotid secretion. Journal of effect of ethanol oxidation on hepatic pyridoxal Experimental Psychologx 16:589-597, 1933. 5'-phosphate metabolism.JournalofClinical Wright, J.; Merry, J.; Fry, D.; and Marks, V. Pitu- Investigation 5511026-1032, 1975. itary function in chronic alcoholism. In: Gross, Verdy, M., and Caron, D. Ethanol et absorption du M.M., ed. Alcohol Intoxication and Withdrawal. calcium chez l'humain (Ethanol and calcium IL Advances in Experimental Medicine and Bio- absorption in man]. Biologie et Gastroenterologie logy, Vol. 59, 1975. pp. 253-255. 6:157-160, 1973. Wright, J.W. Endocrine effects ofalcohol.In: Wagner, G., and Fuchs, A.-R. Effects of ethanol on Marks, V., and Wright, H., eds. Metabolic Effects uterine activity during suckling in post-partum of Alcohol. Clinics in Endocrinology and Metab- women. Acta Endocrinologica 58:133-141, 1968. olism, Vol. 7., No. 2, 1978. pp. 351-367. Walsh, M.J., and Truitt, E.B. Acetaldehyde media- Wright, S.G., and Ree, G.H. Blood in the alcohol tioninthemechanismofethanol-induced stream (letter). Lancet 1:49, 1978. changes in norepinephrine metabolism. Molecular Wynder, E.L. Toward he prevention of laryngeal Pharmacology 6:416-424, 1970. cancer. Laryngoscope 85:1190-1196,1975.. Wang, 1, and Pierson, R.N. Distribution of zinc in Wynder, E.L., and Chan, P.C. The possible role of skeletal muscle and liver tissue in normal and riboflavin deficiency in epithelial neoplasia. II. dietary controlledalcoholicrats.Journalof Effect on skin tumor development. Cancer 26: Laboratory and Clinical Medicine 85:50-58, 975. 1221-1224, 1970. Wehman, H.J., and Plantholt, B.A. Asbestos fibrils Yadav, H.S.; Chaudhuri, B.N.; and Mukherjee, S.K. in beverages. I. Gin. Bulletin of Environmental Effect ofethylalcohol onthyroidaliodide Contamination and Toxicolo 1 h267-272, 1974. trapping and renal clearance of1311 label in Weinstein, M.J., andDeykin,151gy. Quantitative ab- rats. Indian Journal of Medical Research 58: normality of an alpha-chain molecular weight 1421-1427, 1970. form in *he fibrinogen of cirrhotic patients. Ylikahri, R.H.; Huttunen, M.O.; and Harkonen, M. British Journal of Haematology 40:617-630, 1978. Effect of alcohol on anterior-pituitary secretion Whitehead,T.P.;Clarke,C.A.; andWhitfield, of trophic hormones. Lancet 1:1353, 1976. A.G.W. Biochemical and haematological markers Ylikahri, R.; Huttunen, M.; Harkonen, M.; Seuder- of alcohol intake. Lanzet 11978-981, 1978. ling, U.; Onikki, S.; Karonen, S.-L.; and Adler- Wilkinson, P.; Santamaria, J.N.; and Rankin, J.G. creutz, H. Low plasma testosterone values in Epidemiology of alcoholic cirrhosis. Australian men during hangover. Journal of Steroid Bio- Annals of Medicine 18:222-226, 1969. chemistry 51655-658, 1974. Williams, G.A.; Bowser, E.N.; Hargis, GA.; Kuk- Young, G.P.; Dudley, F.J.; and Van-der-Weyden, reja, S.C.; Shah, J.H.; Vora, N.M.; and Hender- M.B. Suppressive effect of alcoholic liver disease son, W.J. Effect of ethanol on parathyroid hor- sera on lymphocyte transformation.Gut20: mone and calcitonin secretion in man. Proceed- 833-839, 1979. iniis of the Society for Experimental Bio1;1117.VW Zeus, J. Histologische Untersuchungen and dlstalen Medicine 159:187-191, 1978. Oesophagus zur Pathogenese der Oesophagitis Williams, J.W.; Tada, M.; Katz, A.M.; and Rubin, E. unter besonderer Beruecksichtiwing der Bezie- Effects of ethmol and acetaldehyde on the (Na+ hung zum Sodbrennen (Histological research on + K +)- activated adenosine triphosphatase activ- the distal esophagus and pathogenesis of esoph- ity of cardiac plasma membranes. Biochemical agitis, with special consideration ofItsrela- Pharmacology 24:27-32, 1975. tionshiptoheartburn].DissertationErlangen. Williams, R.R., and Horm, J.W. Association of 1970. Chapter V The Effects of Alcohol on Pregnancy Outcome

Clinicalreports and experimental studies used in this chapter, is more inclusive and publishedin the past10 years leave little contains, in addition, pregnancy complications doubt tha: prenatal alcohol exposure poses a and outcomes such as small-for-gestation-age threat to the health of the unborn child. This weight. These factors usually place the infant threat ranges from miscarriage and newborn at higher risk for an adverse health occur- death, to a cluster of abnormalities called rence, but are not in their own right anomalies. fetal alcohol syndrome (FAS), to subtle behavioral disturbances such as hyperactivity, which may occur in the absence of observable Historical Perspective physical abnormalities. This chapter represents a selective review and status report on current knowledge con- Although even during ancient times alcohol cerning the effects of alcohol on pregnancy may have been considered a pregnancy risk, by outcome. It is not intended to be exhaustive. A the 1700s a link between alcohol and birth number of recent more detailed reviews have defects was strongly suspected. In1759, for dealt with a full range of issues involving al- example, the London College ofPhysicians cohol-relatedpregnancycomplicationsand petitioned the British Parliament to reinstate birth defects (see, for example, Rosett and taxes on gin so that it would be less available Weiner 1981; Rosett et al. 1981; Sokol 1981, and, therefore, would constitute less of a risk 1982; Abel 1982a; Randall 1982). In addition, to pregnant women and their infants (Warner overviews of fetal alcohol research are con- and Rosett 1975). Despite reinstatement of tained in the Third and Fourth Special Reports these taxes, a steady outpouring of warnings to the U.S. Congress on Alcohol and Health about drinking during pregnancy continued, (USDHEW 1978; USDHHS 1981). indicating that the problem did not disappear The present survey examines current find- after the law was changed. ings about alcohol and pregnancy and needs for In 1899, a report appeared in England which future research. The first section begins with documented in a novel way many of the ad- a brief historical introduction. This Is followed verse effectsofalcoholduringpregnancy by an examination of data documenting alco- (Sullivan 1899). Six hundred offspring of 120 hol as a teratogen (a substance that can cause alcoholic women in a Liverpool jail were com- birth defects). Some specific alcohol-related pared with offspring born to 28 nondrinking pregnancy complications and birth defects are female relatives of these women. Infant mor- then examined, with particular emphasis on tality and stillbirth rates for the alcoholic? new information about brain damage and be- children were 2-1/2 times higher than the havioral disorders. The need for further in- rates among offspringofthe comparison formation about time of exposure, patterns of group. Even more dramatic was the finding drinking, type of beverage, determination of that many of those alcoholic women who pre- dose/responserelations and thresholds, and viously had infants with severe and often fatal host susceptibility are discussed in conjunction complications gave birth to healthy children with ways of improving pregnancy outcomes when forced to become abstinent because of by preventing alcohol-related birth defects. imprisonment. The obvious inference drawn by It should be noted that this chapter uses, the author was that alcohol is toxic to the where appropriate, the terms alcohol-related fetus. birth effect- as well as alcohol-related birth Although several relevant studies pointing defects. Birth defects include entitles such as to fetal damage from prenatal alcohol expo- organ anomalies. The term birth effects, as sure were performed during the early 20th

69 9 century, interestinalcohol and pregnancy Evidence of central nervous system ab- notably decreased during Prohibition, and only normality,including,forexample, ab- sporadic reports can be found in the world normal neonatal behavior, mental retard- literature from the succeeding 50 years (Sokol ation,orother evidence of abnormal 1982;Abelinpress).Modernrecognition neurobehavioral development awaited the publication of two key papers in 1973 by Jones, Smith, and their colleagues. None of these features alone is specifically These investigators reported that 11 children characteristic of fetal exposure to alcohol. In of chronically alcoholic mothers were growth- fact, many other nonspecific abnormalities are retarded and had craniofacial and cardiac de- seen in conjunction with FAS, as well as in fects, as well as developmental delay (Jones isolation,which makesdiagnosisdifficult. and Smith 1973; Jones et al. 1973). Perhaps, in These include eye and ear defects; heart mur- retrospect, the major contribution of these murs, which are often associated with septal papers was the coining of the term fetal al- defects (openings between the chambers of the cohol syndrome, which refocused interest on heart); genitourinary anomalies, such as un- important scientific and public policy ques- descended testicles; hemangiomas (a type of tions. These reports gave particular impetus birthmark); fingerprint and palmar crease ab- because they appeared during a period of in- normalities;and other anomalies, suchas creased public and professional concern with hernias. Any of these abnormalities may be maternal/fetal/infant health.Ifalcohol con- seen individually,evenwithoutmaternal sumption represented an important and po- drinking. However, when these conditions are tentiallyavoidable pregnancyrisk,perhaps seen in conjunction with a pattern of abnor- pregnancy outcomes could be improved when malities consistent with FAS, the diagnosis of the risk had been recognized. FAS may be made. Alcohol-related birth effects are complications of pregnancy,risk associated pregnancy outcomes(e.g.,small- for-gestation-age weight), and birth defects Fetal Alcohol Syndrome and that can be attributed to alcohol use after Alcohol-Related Birth Effects statistical analysis has corrected for the contribution of other possible factors. Numerous cases of fetal alcohol syndrome from all over the world have now been de- Prevalence scribed in the scientific literature, e.g., from Australia,Belgium,Brazil,Canada,Chile, The reported prevalenceof FAS varies Czechoslovakia, France, Germany, Hungary, widely and no firm national data are as yet Ireland,Italy,Japan,SouthAfrica,Spain, available. Depending on the location and the Sweden, Switzerland, and the United States population under study, the overall prevalence (Abel in press). Because standardized criteria has varied from 0.4 per 1,000 in Cleveland were not used for many of the diagnoses, the (Sokol et al. 1980) to 2.1 per 1,000 in Boston Fetal Alcohol Study Group of the Research (Rosett etal.1983).InSeattle, where the Society on Alcoholism proposed specific cri- syndrome was first identified, one study in- teriain1980 (Rosett1980). These criteria dicated a prevalence of 1.3 per 1,000 (Hanson require that at least one feature from each of etal.1978).Estimates from Europe have the following three categories be present for a ranged from 1.6 per 1,000 ir, Sweden (Olegard diagnosis of fetal alcohol syndrome: et al. 1979) to 2.9 per 1,000 in France (De- haene et al. 1977). It appears then that, cal- Growth retardation before and/or after culated on the basis of total number of births, birth the overall prevalence of FAS is in the range of 1 to 3 per 1,000. A pattern of abnormal features ofthe Estimates of the frequency of the full fetal face and head, including small head cir- alcohol syndrome, calculated on the basis of cumference, small eyes, or evidence of occurrence only among women who have been retarded formation of the midfacial area, identifiedasproblemdrinkersoralcohol including a flattenedbridge and short abusers, are somewhat more consistent and length of the nose, and flattening of the higher than the above figtees, ranging from 23 vertical groove between the nose and to 29 per 1,000 (Hanson et al. 1978; Sokol et mouth, i.e., the philtrum al. 1980; Rosett et al. 1983). Further, as might

A 709 beexpected,alcohol-relatedbirtheffects alcohol's damaging effects. This may partially have been reported considerably more fre- explain why only one of two women who con- quently among alcohol abusers. However, the sume the same amount of alcohol may give estimates vary widely, ranging from 78 per birth to a child with FAS. 1,000 to 690 per 1,000 (Ouellette et al. 1977; Observational :tudies involving many pa- Hanson et al.1978; Sokol et al.1980). This tients rather than b...gle cases, however, can wide range may be attributed to the differing be more difficult to interpret. Recent detailed criteria used for inclusion in this diagnostic critical reviews of such studies (Neugut 1981; category. Thus, although only a limited pro- Sokol1980b)haveidentifiedtwogeneral portion of the offspring may have enough ab- problem areas, the first involving the issue of normalities to be diagnosed as FAS, some ef- bias.Inmany published casereportsand fects possibly attributable to alcohol appear to studies,thecliniciandiagnosingalcohol- occur in relatively high proportions of infants related birth defects may have been aware of bornto women who drinkheavilyduring maternal alcohol abuse, leading to the possi- pregnancy. bility that some of the observed associations In general, about 65 to 70 percent of de- may have been affected by such knowledge. velopmental defects have been noted to be of However, even when infants have been exam- unknown origin (Wilson 1973). Sokol (1981) has ined without knowledge of maternal alcohol calculated that about 5 percent of all con- history, as in the large prospective observa- genital anomalies may be attributable to pre- tional studies funded by the National Institute natal alcohol exposure, suggesting that alcohol on Alcohol Abuse and Alcoholism (NIAAA), may account for a significant proportion of alcohol-related pregnancy complications and previously unexplained anomalies and that it birth effects, including lowered birth weight should be considered a major contributor to and congenitalabnormalities, have been abnormal fetal development. In terms of men- identified (Ouellette et al. 1977; Kuzma and tal retardation, which may be considered the Sokol 1982). most serious and damaging ofallalcohol- A second major problem in human fetal al- related birth defects, Clarren and Smith (1978) cohol studies is called "confounding." Alcohol have stated that maternal alcohol abuse during is but one of a multitude of possible pregnancy pregnancy "appears to be the most frequent risks(cofactors)which includematernal known teratogenic cause of mental retardation characteristics, medical disorders, pregnancy in the Western World." complications, abuse of substances other than The high prevalence of alcohol-related birth alcohol, and exposure to environmental con- defects is worth noting not only because of its taminants.Inobservationalstudydesigns, impact ontheaffectedindividualand on complex statistical techniques are used to try society, but also because ofitssignificant to control and adjust for as many factors as economic impact. While difficult to evaluate possible to support the inference that any ob- precisely, one study has estimated a lifetime served effect is attributable to alcohol. Many cost of $155 million for those born in a given pregnancy risks remain unknown, however, and year with FAS and alcohol-related birth de- these statistical techniques are limited, mak- fe,-..ts in New York State alone (Russell 1980). ingit almost impossible to adjust for confounding completely. While human studies can Problems with Human Fetal document associations between alcohol and Alcohol Studies adverse pregnancy outcome, they cannot demonstrate causality convincingly (Sokol 1980b). The experimental administration of alcohol Experimental studies in animals have there- to pregnant women is clearly unethical. Stud- fore proven to be valuable. If rigorously de- ies of alcohol and pregnancy in humans are signed and performed, animal studies allow limited by virtue of the usual constraints as- greatercontrolandgreatercertaintyin sociated with human subjects to clinical ob- inferring a causative role for alcohol as a servation and nonmanipulative designs. Clin- teratogen. ical reports have been of particular importance in special cases, such as in the birth of twins. For example, a case in which one fra- Animal Models ternal twin was more severely affected with FAS than the other (Christoffel and Salaf sky Alcohol - related birth defects comparable to 1975) suggests that genetic factors are sig- those occurring in humans have been reported nificant in determining fetal susceptibility to among mice (Randall and Taylor 1979), rats 0 71 J (Abel1979), beagles(Ellis and Pick1980), both supports the concept of a causative role sheep (Potter etal.1980),miniature swine for alcohol in inducing fetal malformation and (Dexter et al.1980), and monkeys (Altshuler raises questions about the critical periods of and Shippenberg 1981). These studies in ani- exposure for specific effects and the ability of mals have documented direct dose/response fetal tissues to recover from exposure to toxic effects of alcohol on perinatal mortality, in- levels of alcohol edrly in pregnancy. fant weight, and soft tissue malformation and have shown that these effects cannot be attributed to other factors, such as undernu- Specific Adverse Pregnancy Outcomes trition, often associated with alcohol abuse in humans. For example, Randall and her col- Exposure to intoxicating levels of alcohol leagues(1981),using astudydesignthat over prolonged periodsis clearly associated equatesthenutritionalintakeofalcohol- with a range of specific adverse fetal out- exposed and control animals, clearly demon- comes. Some of these outcomes have been strated in mice that restricted caloric intake described in detail in the Third and Fourth could not account for the teratogenic effects SpecialReportstotheU37Congresson observed. However, nutritional factors,e.g., Alcohol and Health (USDHEW 1978; USDHHS low protein intake, can interact with alcohol 1981) and therefore will be reviewed only exposure, leading to higher blood alcohol lev- briefly. els and more severe alcohol-related birth defects, as suggested by the work of Wiener and Spontaneous Abortion her colleagues (1981). These findings indicate that nutritional factors alone did not account The risk for spontaneous abortion (miscar- for the observed deficits. The alcohol present riage or early pregnancy loss) is increased ap- in the body rather than nutritional factors is proximately twofoldinpregnancies compli- the teratogen. cated by maternal drinking, although perhaps Other compelling evidence for a direct ef- only among the heaviest or most frequent fect of alcohol as a teratogen comes from in drinking 3 to 5 percent of women (Harlap and vitro (literally in glass) studies of embryonic Shiono 1980; Kline et al.1980; Sokol 1980a; tissue. In these experiments, rat embryos have Sokol et al. 1980). Pregnant monkeys also tend been directly exposed to alcohol (Brown et al. to abort early in pregnancy following alcohol 1979).Compared withunexposedcontrols, exposure (Altshuler and Shippenberg 1981), as embryos exposed to 0.15 or 0.3 grams of al- do rodents, as indicated by an increased rate cohol per 100 ml of culture medium (an in- ofresorption,theanalogofspontaneous toxicating dose) had decreased crown-rump abortion in humans (Chernoff 1977; Randall et and head lengths and decreasedtotalcell al. 1981). With respect to later pregnancy loss, counts, as well as retarded development, after i.e., the stillbirth rate, the data are less clear. only 24 hours of exposure. The rat embryo at A statisticallysignificantincreaseinthe this stage cannot metabolize alcohol to its stillbirth rate was detected in an initial study primary metabolite, acetaldehyde; thus, this from France for women consuming three or study strongly supports a causative role for more drinks per day (Kaminski et al. 1978), but alcohol as an agent directly toxic to the fetus not in a subsequent study by this group (Ka- but does not rule out the possibility that acet- minski et al.1981). P lso, no increase in the aldehyde also may be a teratogen (Popov et al. stillbirth rate was noted in a large study from 1981). the Cleveland area (Sokol et al. 198G). Studies Additional support for a direct effect of in animals are likewise equivocal with respect alcohol in inducing aberrant fetal development to alcohol and stillbirths (Ellis and Pick 1980; is provided by a notable study performed in Abel et al. 1981b). mice. Sulik and her colleagues (1981) administered early in pregnancy two large closely Physical Congenital Anomalies spaced doses of alcohol on a single day, such as might occur in binge drinking. They were Virtuallyallof the congenital anomalies able to produce abnormal facial features in reported to be alcohol-related birth defects in the mol1se fetus that appear remarkably sim- humans have now been duplicated in animals ilar to those observed in human FAS. However, prenatally exposed to alcohol, although prob- certain methodological issues raise questions ably only when blood alcohol levels exceeded as to the immediate applicabilityofsuch 0.1 percent--the legal level of intoxication in findings to humans. Nonetheless,this study most States (Randall 1982). Acute intragastric

7296 administration (directly into thestomach) of Intrauterine growthretardation. - -Incon- alcohol to mice on one day of pregnancydid trast to the data involving prematurity,the not result in a significant increasein birth evidence linking in utero alcohol exposure and defects, compared with two nutritional control decreased fetal growth is very strong. For groups (Lochry et al.1982). Thus, it appears example, in their study of more than 12,000 that duration as well as level of exposure are pregnancies, Sokol and his colleagues(1980) importantdeterminantsofalcohol-related found that with alcohol abuse birth weight was physical birth defects. decreased by about 190 grams, in the absence of any effect on pregnancy duration.Similarly, in another group of approximately 5,000 wom- Lowered Birth Weight en in a different part ofthe country, Kuzma Lowered birth weight is the most reliably and Sokol (1982) detected about a100-gram observed effect attributable to in utero alco- decrement in birth weight, limited to the most Little hol exposure in humans and animals.Based on frequently drinking 3 percent of women. a review of more than300 reported cases of (1977) noted astatisticallysignificant de- FAS, the average birth weight of such children crease in infant birthweight of 91 grams for was 2,000 grams(Abel 1982b), compared with women reporting averagealcohol use of 1 in the ounce (twodrinks) per day for the prepreg- the median birth weight for all infants decrement for UnitedStatesof more than3,300grams nancy period, and a 160-gram (NCHS 1980). Further, decreased birthweight late pregnancy consumption at that level. has been observed even in theabsence of full Prenatal growth retardation associated with ob- FAS (Ouellette et al. 1977; Sokol et al.1980). maternal alcohol consumption has been These findings are of concern becauselowered served in numerous animal studies(Ellis and birth weight is widely recognized asbeing as- Pick 1980; Lee and Leichter 1980). The extent sociated with significant increases inrisk for of this retardation appears to bedose-depend- fetal and infant mortality and long-termab- ent with exposure during thethird trimester normalitiesinneurologicdevelopment and having a more severe effect on birth weight intelligence. Lowered birth weight maybe the than did exposure earlier in gestation(Abel 1979; Lochry et al.1982). The decrease in result of preterm delivery (prematurity) or single intrauterine growth retardation, or both. birth weight can be seen even after a administration of alcohol shortly before term Preterm delivery.--Effects ofalcoholon (Greizerstein and Abel 1979; Lochry et al. 1982). These observations are consistent with pregnancydurationareunclear.Alcohol- related prematurity was not identifiedin one studies in humans that indicate thatdrinking (Sokol continued through the third trimester is as- study of more than 12,000 pregnancies (Little et al.1980). Two more recent studies, how- sociated with decreased infant weight delivery may result 1977; Rosett et al. 1978). ever, suggest that preterm help from prenatalalcohol exposure.Berkowitz Studies in animals are also beginning to (1981), in a study of 175 mothers of preterm identify mechanisms by which alcohol may infants, found decrease fetal growth. For example, animal infants and 313 mothers of term ef- that alcohol consumption prior tothe third embryos provide evidence for the direct with fects of alcohol and acetaldehyde onfetal trimester of pregnancy was associated 1981). preterm delivery. Furthermore,in a more de- growth (Brown et al. 1979; Popov et al. Berkowitz Inaddition, alcohol exposure may lead to tailed analysis of the same data, hy- and her coworkers (1982)found that heavier chronic fetal hypoxia (Abel 1982b), or to alcohol consumption (an averageof two or poglycemia, i.e., low blood glucose. Decreased day) during pregnancy was fetalnutritionresulting from hypoglycemia more drinks every levels could associated with an approximatelythreefold induced by high blood alcohol in- contribute to fetal growth retardation(Tanaka increase in risk for preterm delivery; no that alcohol creased risk was identified forlighter drinking. et al. 1982). Other studies suggest Hospital may affect fetal cell growthby interfering In a recent study from Boston City the of1,690 births, maternal drinkingpriorto with the passage of amino acids across pregnancy was found to beassociated with placenta (Henderson et al,1981). With inade- 1982). It is quate transport of amino acids tothe fetus, shortened gestation (Hingson et al. inhib- interesting to note that pretermdelivery does protein synthesis and growth would be incorporationof not occur in pregnantanimals that are given ited.Moreover, decreased delayed amino acids into protein inalcohol-exposed alcohol--in fact, par*.irition may be (Henderson et (Bond 1982). fetuses has also been reported

73 97 al. 1979, 1980). Although alcohol-related de- mental retardation (Streissguthet al. 1978a), creased absorption of zinc has also beensug- and when the same individualswere retested, gested as a contributor to growth retardation, the IQ scores did not change (Streissguthet al. the evidence on this i,ssueis contradictory 1978b). Similar resultswere obtained in the (e.g., Samson and Diaz 1981; Flynnet al. 1981; study from Sweden in which childrenwith Ghishan et al. 1982). physical signs of FASwere found to have an Based on these results, ItIs reasonable to average IQ below 70 (Olegard et al. 1979). conclude that alcohol is associated with low- Two studies of mental and motordevelop- ered birth weight, related possiblyto both ment identified infants exposed in uteroto shorter gestation and decreased intrauterine alcohol and investigated those who didnot growth. Diminished prenatal growth is dose- exhibit full FAS. Streissguth and hercowork- related and may be moresevere when alcohol ers (1980) administered an Infant development is consumed in the third trimester. test to a group of infants at theage of 8 months.Theyrecordedsignificanttrends Abnormal Neurobehavioral and toward lower scoreson mental and motor tests Neural Development relatedtoincreased maternalalcoholuse during pregnancy. In surviving fetuses, the mostsevere alco- Golden and her colleagues (1982) hol-related birth defects evaluated are those Involving neurobehavioral developmentin 12 infants the central nervous system. Congenital anom- with physical alcohol-related birth defectsand alies, even those that are verysevere, e.g., a history of maternal alcohol abuse and heart defects, com- are oftenrepairable.Brain pared them with 12 normal infants. Thesetwo damage, however, is permanent and irrevers- groups of infants were examined ata mean ible. Alcohol-relatedanatomical,electro- age of1 year without knowledge of thepre- physiological, and biochemical abnormalities natal drinking -history. Both the mental in the brain have and now been Identified and may motor scores were 20 points lower in theal- underlie the observed behavioral deficits. cohol group, a notable difference. Further- more, thealcoholgroup hadsignificantly Behavioral development.--The adverse ef- higher frequencies of postnatal growthre- fects of alcohol on behavioral development tardation and microcephaly, i.e., abnormally may be divided into three main categories: small heads. Although itwas not possible in abnormal neonatal behavior,as reflectedin this study to adjust for the confoundingef- sleep problems and state regulation disorders; fects of maternal smoking, therewas strong childhood hyperactivity; and mental retarda- evidence that the abnormal neurobehavioral tion, as indicated by lowered IQscores (Abel development of the infantswas attributable to 1981a). alcohol alone or in combination withcigarette Infants born to heavy drinkersor alcoholics smoking. have been found to bemore restless during Landesman-Dwyer and her coworkers (1981) sleep and not to sleep as muchas other studied 272 offspring of women without alco- children (Rosett et al. 1979). Abnormalelec- hol problems and found thatat age 4, the troencephalographic (EEG)activityduring children with greater in utero alcoholexposure sleep has been noted foras long as 6 weeks generally were less attentive and lesscom- after birth in some of these children. pliant with parental commands. Morerecently, Hyperactivity in children with FAS has been Streissguth and her colleagues (1983b), after noted in several clinical case studies (Abel observing 4-year-olds, foundthat maternal 1981a). It has also been notedin 15 children alcohol use duringpregnancy is significantly who had physical abnormalities consistent with related to decreased attention andlonger re- FAS, but whose IQ scores were within normal action time. They suggested that alcoholuse limits. All 15 of these children eventuallyre- by pregnant womencan have long-term be- ceived recommendation for special education havioral effects in children. services because of their restlessness, short As with physical anomalies, attention spans, and distractibility (Shaywitz some studies in animals duplicate many of the behavioralab- et al. 1980). normalities noted in humans with fetal alcohol Lowered IQ scores In conjunction with heavy exposure. For example, hyperactivity has been prenatal alcohol exposure have been noted in noted consistently in rats prenatally other countries. In the United States, exposed the av- to alcohol (Bond and DiGiusto1976;Abel erage IQ scores for a group of patients with 1982c). Learning difficulties have also FAS was found to be 65, reflecting moderate been identifiedinanimals prenatally exposedto

74 9 alcohol (Bond and DiGiusto 1978; Riley et al. s'fied as problem drinkers (Clark and Midanik 1979a, b; Abel 1979). Riley and his coworkers 1982). During the peak reproductive age range (1979a, b) have proposed that many of the ab- of 18-34, an estimated 5 percent of American normal behavioral effects related to prenatal women consume an average of2or more alcohol exposure suggest an underlying prob- drinks per day or 14 or more drinks per week lem in response inhibition. The magnitude of (Clark and Midanik 1982). Estimates of the this effect appears to be dose-related(Lochry proportion of women who drink at least this and Riley 1980). On balance, the behavioral amount during pregnancy vary widely, ranging abnormalities found in animals are similar to from a low of 0.5 percent in parts of Cali- those In children with fetal alcohol syndrome. fornia (Harlap and Shiono 1980) to a high of 16 percent In Buffalo (Russell and Bigler1979), Neuraldevelopment.--Neuroanatomicand and a median of 2 percent (Abel in press). Be- biochemical abnormalities probablyunderlie cause alcohol readily crosses theplacenta, alcohol-related abnormal neurobehavioral de- yielding levels of alcohol in the fetus almost velopment; these areas are currently under identical to those in the mother, it is reason- study. Microcephaly, an important component able to conclude that a significant number of in the diagnosis of FAS, indicates an overall unborn children in the United States are ex- decrease in brain growth. Moreover, anatomic posed to the equivalent of two drinks a day. abnormalities have been observed in brains of children born to alcoholic women as studied at Drinking Patterns in Pregnancy autopsy, as well as in animals prenatally exposed to alcohol. These include hydrocephalus The amount and timing of alcohol consump- (increasedfluiddistendingcavitiesInthe tion that put the fetus at risk are still un- brain), absence of the corpus collosum (the known. Scientists have considerable difficulty bundle of fibers connecting the two sides of in addressing this issue because of problems in the brain), and abnormal growth patterns of obtaining reliable drinking histories and in nerve and other brain cells(Clarren etal. definingabusivedrinkinganddependence. 1978;Pelf feretal.1979; Rasmussen and Furthermore, drinking patterns often change Christensen 1980). during pregnancy. Subtle changes in brain structure have been Essentially all reported studies of drinking noted in animals following prenatal alcohol during pregnancy have relied on self-reports of exposure. West et al. (1981)found that rats patients.The inherentlimitationsofself- exposed to alcohol throughout gestationhad reports suggest that the alcohol intakein- abnormally distributed nerve fibersinthe formation obtained must be understoodin hippocampus (deepinsidethebrain),and broad terms, rather than in precise measure- Barnes and Walker (1981) identified a decrease ments. The amount of alcohol actually imbibed in the cell content of rats' hippocampus. In in a drink might vary from 1 to 8 ounces, de- addition, Davies and Smith (1981) identified a pending on the individual giving the history considerable decrease in the extent of the and the method by which the history is ob- neural dendrites (parts of the nerve cell that tained (Rosett et al. 1983). A detailed recall receive signals) of the hippocampus in mice. of drinking behavior is likely to be inexact, Taken together, these anatomic abnormalities particularlyfortheheavyordependent in the hippocampus may be the structural basis drinker who may be unable or unwilling to re- for some of the behavioral abnormalities ob- call specifically how much she drank. Self- served in humans and animals, as this part of reportsofdrinkingduringpregnancyare the brain is involved in learning/memory per- therefore of limited value. This in turn seri- formance and in inhibitory control of behavior. ously limits the credibility of estimates relating a given number of drinks per day to a particular risk to the fetus. Moreover, itis Alcohol Use, Abuse, and Dependence likely that actual alcohol intake is underre- and Pregnancy ported by the abusive drinker, the individual most likely to be at risk for giving birth to a child with alcohol-related birth defects (Sokol Drinking in Women et al.1981). This could lead investigators to Approximately 60 percent of adult Ameri- overestimate the risk to the fetus of what can women drink alcoholicbeverages; 40 per- might appear to be "two drinks a day." cent are abstinent. An estimated6 percent of Allinvestigators studying drinking during adult women in this country have beenclas- pregnancy have been faced with the problems

75 9 of obtaining reliable drinking histories and potential determinants of infant birth weight have used a multitude of definitions of prob- adjusted for gestational age and foundno lem drinking, abusive drinking, heavy drinking, significanteffect ofpaternalalcohol con- and alcohol dependence. For example, studies sumption. Similarly, Randall and her cowork- by Rosett etal.(1981),Streissguth etal. ers (1982) were unable to detect any effects of (1981), and Kuzma and Kissinger (1981)all chronic paternal alcohol consumption on fetal useddifferentcriteria.Suchvariancesin growth and development in mice, in terms of definition increase the difficulty of making the number ofimplantation sites,prenatal comparisons across studies. mortality, fetal weight, sex ratio, or the fre- The stage of pregnancyis an important quency ofsofttissuemalformation.These considerationinassessing women's drinking findings were confirmed by Bennett etal. habits because women tend to decrease the (1982).Somestudiesreportingpaternally amount they drink as pregnancy progresses, an mediated alcohol effects in conjunction with observationfirstreported byLittleetal. alcohol have had such methodologic flaws as (1976) and subsequently corroborated by others lack of nutritional controls. (e.g., Rosett et al.1978; Sokol et al.1981; Weiner et al. 1983) and by the National Center Knowledge and Attitudes for Health Statistics neonatality surveyas discussed in chapter 1 of this report. Fried and Public education efforts concerningrisks his coworkers (1980) in a study of 217 Cana- associated with alcohol use during pregnancy dian women found that prior to pregnancy 18 have been actively pursued since the mid- percent of women were heavy (0.85 ounces per 1970s. Broad coverage in the media has been day) social drinkers, but that during the first obtained for publichealthadvisories from trimester this proportion was reduced by two- NIAA A,the American Medical Association, thirds. The proportion of women who were and the March of Dimes on a national level, as drinking heavily continued to decrease during well as for an advisory from the Surgeon Gen- the last two trimesters of pregnancy. In the eral (FDA 1981). Public education has also Cleveland study (Sokol et al. 1981), the heav- been attempted by many State governments. ier drinking group also was found to decrease Most A nericans have been exposed to such Its alcohol intake significantly as gestation public health messages, and 90 percent of the progressed. These are encouraging findings, respondentsin a recent survey knew that inasmuch as decreases in drinking would be drinking during pregnancy might be harmful. expected to minimizebirthdefects.They However, three-quarters ofthe respondents point up the problem, however, of attempting who thought abstinenceisunnecessary be- to summarize a woman's drinking throughout lieved that an average of more than three pregnancy with a single number, e.g., "two drinks per day was safe (Little et al. 1981). drinks a day." These findings suggest that current public education/prevention programs may not be fully Paternal Drinking adequateinpermeatingthepubliccon- sciousness. Women who drink heavily tend to be married Although knowledge of potential adverse to men who drink heavily (Gomberg 1975). This effects of alcohol on pregnancy outcome has suggests that some of the abnormalities de- changed, and public attitudes have shifted scribed as alcohol-related birth defects might over the past 10 years, the question remains: be relatedto paternal drinking.Long-term Has the drinking behavior of women during consumption by men of large amounts of al- pregnancy changed? The purpose of a recent cohol is known to be associated with impo- study was to compare drinking patterns during tence, reduced sperm motility and ultimately pregnancy in the same population in Seattle loss of sperm, and abnormalitiesin sperm overa 6-yearinterval(Streissguthetal. structure (Lester and Van Thiel 1977). Thus, 1983a). Samples of pregnantwomer were in- fertilization with defective sperm is possible, terviewed in 1974-75 and in 198041. Although which might result in fetal anomalies. Some theproportionofwomendrinkingduring investigators have argued that the male parent pregnancy was found to have decreased during could contribute to alcohol-related birth de- the 6-year interval, the proportion of women fects (Anderson etal.1981); however, no drinking at least an ounce of absolute alcohol convincing evidence exists of such paternally (two drinks) each day was relativelyconstant. mediated anomalies related to alcohol. Re- Because precisely this limited proportion of cently, Kuzma and Sokol (1982) examined 44 the population Incurs the highest risk for al-

76 Oti cohol-relatedbirthdefects,thesefindings Heavy drinking in late pregnancy leads to an suggest cause for concern. increar ;A frequency of congenital anomalies (Rosett et al. 1978; Rosett and Weiner 1981). Although organogenesis, the development of Conclusions the organs of the embryo, may be completed Although studies of drinking during preg- during very early pregnancy, nerve cells, for nancy depend uponself-report and the reli- example, continue to make new connections ability and precision of such data are limited, through pregnancy. Heavy drinking could im- it appears that drinking during pregnancy is pair the growth of these connections. The re- not uncommon. Many women who drinkeither sults of animal studies suggest that after toxic decrease their drinking naturally or become substances are withdrawn, the fetus may com- abstinent during pregnancy. Public education pensate for earlier impairments withaccel- efforts may well reinforce this change in be- erated growth and repair before development havior. However, persistently heavydrinking is completed (Snow and Tam 1979; Andersand during pregnancy remains a problem for some Persaud 1980). Further basic science studies in women despite public educationefforts. animals and clinical research in humans regarding critical periods of exposure and the capacity of the unborn offspring for compen- Implications of Current Knowledge satory growth and repair are needed, because the results of such studies might be usefulin Frontiers counseling patients whose fetuses have been The preceding sections have summarized the exposed to significant levels of alcohol during current status of information concerningrisks early pregnancy. for alcohol-related dangers to pregnancyand Beverage source (wine, beer, whisky, etc.) birth defects. Progress in scientific evaluation mayaffectinfantsdifferentially.Animal of these risks has clearly been very rapid over studies have been few and inconclusive(Abel the past decade. However, it is equallyclear 1981b; Abel et al.1981b). Nonetheless, pos- that many questions remain. siblerelationships between beverage source and pregnancy outcome have been reported (Kaminski et al. 1978; Kuzma and Sokol 1982; Need for Further Research Berkowitz et al. 1982). Timing, pattern, and beverage source.-- Be- cause a reliable biochemicalindicator for al- Moderate drinking.--Moderate drinking may cohol intake is not available, clinicalinves- increase the riskfor lowered birth weight tigators must depend on patient reports.How- (Little1977), abnormal neurobehavioral de- ever, as previously noted,human drinking is velopment (Streissguth et al. 1980), and spon- difficult to represent numerically in a single taneous abortion (Harlap andShinno1980; (and simple) measure of alcohol use;volume, Kline et al.1980). However, others (Rosett frequency, and beverage source of alcohol 1980;Sokol1980b,1982) have questioned intake must be considered. Also, other poten- whether the women manifestingthesein- tial determinants of pregnancy outcome, e.g., creased pregnancy risks are in fact moderate other substance use, medical/obstetricfac- drinkers. They note that the women with al- should be taken cohol-related pregnancy risk constitute only tors, and socioeconomic status 10 percent) of into account. the heaviest drinking (5 to Improved measures of alcohol intake would pregnant women. As research continues to heighten understanding of the stages of preg- expand knowledge, the answers to this impor- nancy when drinking is mostdangerous to the tant clinical question will emerge. fetus. Different alcohol-related birth defects might result from drinking during different Susceptibility.--Different species and dif- critical periods, e.g., either early or latein ferent strains within a species of animal may pregnancy. Sulik and hercolleagues (1981) differ in their susceptibility to alcohol-related suggest that heavy alcoholconsumption early birth defects. Also, differences amonganimals in pregnancy might contribute tosuch birth in the same exposed litter are commonlyob- defects as abnormalities in the face and cen- served. As noted earlier, human fraternal tral nervous system. Studies of therelation- twins may not be equally affected by alcohol ship between early pregnancydrinking, par- exposure (Christoffel andSalafsky 1975). Such ticularly binge drinking, and physical congen- findings suggest the possibility of differential ital anomalies in the human could be valuable. susceptibility on a genetic basis. Interactions

77 of alcohol consumption with otherpregnancy physicians, nurses, and other healthcare pro- risks, such as poor nutrition, other substance viders may afford a rational and cost-effec- use, or medical Illnesses, may also altersus- tive approach to prevention of alcohol-related ceptibility. Information about interactingrisks birth defects. If these individualscan be edu- would help in designing more focused and po- cated to take an active role in influencingthe tentially more effective prevention strategies. drinking habits of their patients,it may be A profile of patients particularlyat risk for possible to decrease theoccurrence of alco- the adverse effects of in utero alcoholexpo- hol-relatedbirthdefects and improve the suialso would aid the practitioner ingiving probability of successful pregnancies. direct patient care. Prevention and Treatment Summary Problems.Althoughmajorprogress has bee-A-7. over the past decade In under- Heavy drinking duringpregnancy adversely standing the risks of alcohol use duringpreg- affects organic and behavioral fetaldevelop- nancy, much remains unknown. Methodsare ment and increases the risks of miscarriage. being developed to identify and treat pregnant When consumed In large amounts, alcoholcan women with alcohol problems (Rosett et al. result in fetal alcohol syndrome.It appears 1981; Sokol et al. 1981). Educationprograms that the overall prevalence of FASis in the aimed at professionals may modify attitudes range of 1 to 3 cases per 1,000 births. Alcohol- and clinical behavior (Weiner etal.1982; related birth defectsoccur more frequently Littleetal.1983). Professional education, than FAS. based on firm scientific evidence concerning Alcohol can induce abnormal fetaldevel- risks for alcohol-related birth defects, effec- opment that varies in intensity, dependingon tive methods of detection of abusive drinking, dose, genetic susceptibility, nutritionalstatus, and treatment methods for abusivedrinking and other as yet unknown factors.Heavy ma- and alcohol dependence,appearstobe a ternal drinking may affect the fetalnervous promising avenue for the prevention of alco- system, which may result in abnormal neonatal hol-related birth defects and other anomalies. behavior, childhood hyperactivity, andmental retardation. Current statements and recommendations.-- Alcohol probably affects allorgan systems Basedoncurrentlyavailableinformation, of the fetus, but many questions remainas to some broad statements with prevention and the mechanisms and their potential reversi- treatment implicaticas appear to be warrant- bility. Many variables, suchas the amount of ed. Extensive public education effortshave alcohol and the time duringpregnancy of alerted women tothe dangers and fewer consumption, may influence thenature and American women appear to be drinking during degree of adverse effects. Studies in animals pregnancy. However, the frequency of heavy suggest that,athigh alcohollevels,birth or abusive drinking may not have decreased. It anomalies are directly related to theamount can be stated with some certainty that those of alcohol exposure. pregnant women mho are the heaviest (most Public education efforts concerningrisks frequent) drinke.4 (about 5-10 percent)are associated with alcohol use have been actively exposing tiror unborn children to a significant pursued over recent years. These education risk. If these women abstain or significantly efforts have encompassed mediamessages, decrease their drinking during pregnancy, the public health advisories, andprograms at the evidence from both animal and human studies State level. Most Americans havebeen ex- suggests that they can have healthier babies. posed to public health messages; however,the Effective prevention strategies for alcohol- impact on heavier drinking inpregnancy has related birth defects, including FAS, remain been less than desired. One study found that elusive. More information is needed about al- while the proportion ofwomen who drank cohol abuse and dependence inyoung women, during pregnancy decreasedover the past 6 so that more focused approaches to prevention years, the proportion of women drinking at can be developed. Professional education of least two drinks a day had not changed.

102 78 Referent**

Bond, N.W., and DiGiusto, E.L. Effects of prenatal Abel, E.L. Prenatal effect of alcohol on adult alcohol consumption on open-field behaviour and learning in rats. Pharmacology, Biochemistry and alcohol preference in rats. psychopharmacckly Behavior 10:239-243, 1979. Abel, E.L. Behavioral teratology of alcohol. ?Ix- (Berlin) 46:163-165, 1976. chological Bulletin 90:564-51, 1981a. Bond, N.W., and DiGiusto, E.L. Avoidance condi- Abel, E.L. Prenatal effects of beverage alcohol tioning and Hebb-Williams maze performance in on fetal growth. Progress inBiochemical Phar- rats treated prenatally with alcohol. Psycho- macology 18:111-114, 1981b. pharmacology (Berlin) 58:69-71, 1978. Abel, E.L. Alcohol and Reproductions A Milo; Brown, N.A.; Goulding, E.H.; and Fabro, S. Ethanol mtyl . Westport, Conn.: Greenwood Press, 1982a. embryotoxicity: Direct effects on mammalian Abel,LL. Consumption of alcohol during preg- embryos in vitro. Science 206: 573-575, 1979. nancy: A review of effects on growthand de- Cahalan, D.; Cisin, LH.; and Crossley, H.M. Amer- velopment of offspring. Human Biology 54:421- icanDrinking Practices: A National Study of 453, 1982b. DrirkinBehavior and Attitude. Monograph No. Abel, E.L. In utero alcohol exposure and develop- ew runsw ck, N.J.:utgers Center of Al- mental delay of response inhibition. Alcoholism: cohol Studies, 1969. Clinical and Experimental Research 6:369-376, Chernoff, C.F. The fetal alcohol syndrome in mice: 1982c. An animal model. Teratology 15:223- 229, 1977. Abel, E.L. Marijuan.Tobaccod Alcohol Effects Christoffel, K.K., and Salaisky, I.Fetal alcohol in Repro.t. z.P-1aR'atmc, syndrome in dizygotic twins. Journal of Pediat- in press. rics 87:963-967, 1975. Abel, E.L.; Dintcheff, B.A.; and Bush, R. Behav- Clark, W., and Midanik, L. Alcohol use and alcohol ioral teratology of alcoholic beverages compared problems among U.S. adults. Results of the 1979 to ethanol. Neurobehavioral Toxicologyand Ter- national survey. Ins National Institute on Alcohol atoloity 3:339-342, 1981a. Abuse and Alcoholism. Alcohol Consumption and Abel, E.L.; Dintcheff, B.A.; and Bush, R. Effects of Related Problems. Alcohol and Health Mono- beer, wine, whiskey and ethanol on pregnant rats graph No.1. DHHS Pub. No. (ADM)82-1190. andtheiroffspring._Teratology23:217-222, Washington, D.C.: Supt. of Docs., U.S. Govt. 1981b. Print. Off., 1982. pp. 3-52. Altshuler, H.L., and Shippenberg, T.S. A subhuman Clarren, S.K., and Smith, D.W. The fetal alcohol primate model for fetal alcohol syndrome re- syndrome: A review of the world literature.New search.NeurobehavioralToxicolo and Tera- England Journal of Medicine 298:1063-1067, 1978. tology 3:121 -126,981. Clarren, s.K.; Alvord, E.G.; Sumi, S.M.; Streiss- Anders, K., and Persaud, T.V.N. Compensatory guth, A.P.; and Smith, D.W. Brain malformations embryonic development in the rat following ma- related to prenatal exposure to ethanol. Journal ternal treatment with ethanol. Anatomischer of Pediatrics 92864-67, 1978. Anzeiger: 148:375-383, 1980. Da7a71517and Smith, D.E. Effects of peri- Anderson,R.A.; Furby,J.E.; Oswald, C.; and natallyadministered ethanol on hippocampal Zaneveld,L.J.D.Teratologicalevaluationof development(abstract).Alcoholism: Clinical mouse fetuses after paternal alcoholingestion. and Experimental Research 5:147, 1981. Neurobehavioral Toxicology and Teratology3: Dehaene, P.; Samaille-Villette, C.; Samaille, P.; 117-120, 1981. Crepin, G.; Walbaum, R.; Deroubaix, P.; and Barnes, D.E., and Walker, D.W. Prenatal ethanol Blanc-Garin,A.P.Le syndrome d'alcoolisme exposure permanently reduces thenumber of foetal dans le nord de la France. [The fetal pyramidal neurons in rat hippocampus. Develop- alcohol syndrome in the north of France.) Revue mental Brain Research 1:333-340, 1981. de l'Alcoolisme (Paris) 23: 145-158, 1977. Bennett,A.L.;Sorette,M.P.; and Greenwood, Dexter, J.D.; Tumbleson, M.E.; Decker, ID.; and M.R.C. Effect of chronic paternal ethanol con- Middleton, C.C. Fetal alcohol syndrome in Sin- sumption on 19-day rat fetuses. Federation Pro- clair(S-I; miniature swine. Alcoholism: Clinical ceedings 41:710, 1982. and Experimental Research 4:146-151, 1980. Berkowitz, G.S. An epidemiologic study of preterm Ellis, P.v., and Pick, J.R. An animal model of the delivery. American Journal of Epidemiology 113: fetal alcohol syndrome In beagles. Alcoholism: 81-92, 1981. Clinical and Experimental Research 4:123-134, Berkowitz,G.S.; Holford, T.R.; and Berkowitz, 1980. R.L. Effects of cigarette smoking, alcohol, cof- Flynn, A.; Miller, S.I.; Martier, S.S.; Golden, N.L.; fee and tea consumption on pretermdelivery. Sokol, R.3.; and Del Villano, B.C. Zinc status of Early Human Development 7:239- 250, 1982. pregnant alcoholic women: Adeterminant of Bond, R.W. Prenatal exposure to ethanol: Associ- fetal outcome. Lancet 1:572- 575, 1981. ation between Increased gestational length and Food and Drug AdmInistration. Surgeon General's offspring mortality. Neurobehavioral Toxicology Advisory on Alcohol and Pregnancy. FDA Drug and Teratology 4:501-503, 1982. Bulletin 11:9-10, 1981.

79 1 11 Fried, P.A.; Watkinson, B.;Grant, A.; and Knights, Kline, 1; Shrout,P.; Stein,Z.; Susser, M.; and R.M. Changing patterns of soft drug use prior to Warburton, D. Drinking duringpregnancy and and during pregnancy: A prospective study. Drug spontaneous abortion. Lancet 2:176-180, 1980. and Alcohol Dependence6:323-343, 1980. Ghishan, F.K.; Patwardhan, Kuzma, 1W., and Kissinger, D.C. Patterns ofal- R.; and Green, H.L. cohol and cigarette use in pregnancy. Neurobe- Fetal alcohol syndrome: Inhibition ofplacental havioral Toxicology and Teratology 3:211-221, zinc transport as a potential mechanismfor fetal 1981. growth retardation in the rat. Journal ofLabo- Kuzma, J.W., and Sokol, R.J. Maternal drinking ratory and Clinical Medicine 100:45-52, 1982. behavior and decreased intrauterine growth. Al- Golden, N.L.; Sokol, R.I1 Kufinert,B.R.; and Bot- coholism:Clinical and Experimental Research toms, S.F. Maternal alcoholuse and infant de- 6:396-402, 1982. velopment. Pediatrics 70: 931-934, 1982. Landesman-Dwyer, S.; Ragozin, A.S.; and Little, Gomberg, E.S. Alcoholism and Women: State of R.E. Behavioral correlates of prenatalalcohol Knowledge Today. New York: NationalCouncil exposure: A four-year followup study. Neurobe- on Alcoholism, 1975. 12 pp. havioral Toxicology and Teratology 3:187-193, Greizerstein, H.B., and Abel, E.L.Acute effects of 1981. ethanol on fetal body composition and 'electro- Lee, M., and Leichter, J. Effect of littersize on lyte content in the rat. Bulletin ofthe Psycho- the physical growth and maturation of the off- nomic Society, 14:355-356, 1979. spring of rats given alcohol during gestation. Hanson, 1W.; Streissguth, A.P.;and Smith, D.W. Growth 441327-335, 1980. The effects of moderate alcoholconsumption Lester, 7., and Van Thiel, D.H. Gonadalfunction in during pregnancy on fetal growthand morpho- chronic alcoholic men. In: Gross, M. M., ed. Al- genesis. Journal of Pediatrics 92:457-460,1978. coholIntoxication and Withdrawal. Ma. Bio- Harlap, S., and Shiono, P.H. Alcohol, smoking and logical Aspects of Ethanol. Advances inExperi- incidence of spontaneous abortionsin the first mental Medicine and Biology 85a:399-414, 1977. and second trimester. Lancet 2:173-176, 1980. Little, R.E. Moderate alcohol use duringpregrancy Henderson, G.I.; Hoyump7,77M., Jr.;McClain, C.; and decreased infant birth weight. American and Schenker, S. The effects ofchronic and Journal of Public Health 67:1154-1156, 1977. acute alcohol administrationon fetal develop- Little,R.E.;Schultz,F.A.; ment in the rat. Alcoholism: andMandell,W. Clinical and Ex- Drinking during pregnancy. Journal of Studieson perimental Research 3:99-106, 1979. Alcohol 37:375-379, 1976. Henderson, G.I.; Hoyumpa, A.M., Jr.;Rothschild, Grathwohl, H.L.; Streissguth, A.P.; M.A.; and Schenker, S.Effect of ethanol and and McIntyre, C. Public awareness and knowl- ethanol-induced hypothermiaon proteinsyn- edge about the risks of drinking duringpregnancy thesis in pregnant and fetalrats. Alcoholism: in Multnomah County, Oregon. American Journal Clinical and Experimental Research4:165-177, of Public Health 71:312- 314, 1981. 1980. Little,R.E.;Streissguth,A.P.; Guzinski, G.M.; Henderson,G.I.;Turner,D.;Patwardhan, R.V.; Frathwohl, H.L.; Blumhagen, 1M.; and McIntyre, Lumeng, L.; Hoyumpa, A.M.; and Schenker,S. C.E. Change in obstetrician advice followinga Inhibition of placental valine uptakeafter acute two-year community educational programon andchronicmaternalethanolconsumption. alcohol use and pregnancy. American Journal of JournalofPharmacolo and Ex erimental Obstetrics and Gynecology 146:23-28, 1983. erapeutics 216:465-472, 19 . Lochry, E.A., and Riley, E.P. Retention of passive Hingson, R.; Alpert, 11; Day,N.; Dooling,E.; avoidance and T-maze escape in rats exposedto Kayne, H.; Morelock, S.; Oppenheimer,E.; and alcohol prenatally. Neurobehavioral Toxicology Zuckerman, B. Effects of maternaldrinking and and Teratology 2: 107-115, 1980. marijuana use on fetal growth anddevelopment. Lochry, E.A.; Randall, C.L.; Goldsmith, A.A.;and Pediatrics 70:539-546, 1982. Sutker, P.B. Effects of acute alcoholexposure Jones, K.L., and Smith, D.W. Recognitionof the during selected days of gestation in C3H mice. fetal alcohol syndrome in early infancy.Lancet Neurobehavioral Toxicology and Teratology 41 21999-1001, 1973. 15-19, 1982. - Jones, K.L; Smith,D.W.;Ulleland,C.N.;and National Center for HealthStatistics.Monthly Streissguth,A.P. Pattern of malformationin Vital Statistics Report: Annual Summary for the offspring of chronic alcoholicmothers. Lancet United States, 1979. Hyattsville, Md.: theCen- 1:1267-1271, 1973. ter, 1980. Kaminski, M.; Rumeau-Rouquette, C.; and Neugut, R.H.Epidemiologicalappraisalofthe Schwartz, D. Alcohol consumptionin pregnant literature on the fetal alcohol syndrome in women and the outcome of hu- pregnancy. Alcohol- mans.EarlyHuman Development5:411-429, ism: Clinical and ExperimentalResearch 2 :155- 1981. 163, 1978. Olegard, Ft.; Sabel, K.-G.; Aronsson, M.; Sandin,B.; Kaminski, M.; Franc, M.; Lebouvier, M.;du Mazau- Johansm, P.R.; Carlsson, C.; Kyllerman,M.; brun, C.; and Rumeau-Rouquette, C.Moderate Iversen, K.; and Hrbek, A. Effects on the child of alcoholuse and pregnancy outcome.Neuro- alcohol abuse during pregnancy: Retrospective behavioral Toxicology and Teratology3:173-181, and orospective studies. Acta Paediatrica Scan- 1981. dinavica (Supplement No. 275):112-121, 1979. 80104 Weiner,L.; and N.P.; and Rosett, H.L.; Ouellette, E.M.; Ouellette, E.M.; Rosett, H.L.; Rosman, during offspring of ma- Owens,E.Therapy of heavy drinking Weiner, L. Adverse effects on pregnancy. AmericanJournal of Obstetrics and ternalalcoholabuse during pregnancy.New 297:528-530, 1977. Gynecology 51:41-46, 1978. England Journal of Medicine Rosett, H.L.; Weiner, L.; Lee,A.; Zuckerman, B.; Peiffer, J.; Majewski, F-.;Fischbach, H.; Bierich, embryo- cnd feto- Dooling, E. and Oppenheimer,E. Patterns of IR.; and Volk, B. Alcohol alcohol consumption andfetal development. Ob- pathy: Neuropathologyofthree children and 539-546, 1983. Neurological Science stetrics and Gynecology 61: three fetuses. Journal of Rosett, H.L.; Snyder, P.;Sander, L.W.; Lee, A.; 41:125- 137, 1979. Cook, P.; Weiner, L.; andGould, J. Effects of Popov, V.B.; Vaisman, B.L.;Puchkov, V.E.; and regulations. effect of ethanol maternal drinking on neonate state lgnat'eva, T.V. Embryotoxic Developmental Medicine andChild Neurolocy and products of itsbiotransformation in post- Byull Exsp Biol 21:464-473, 197.i. implanted rat embryo culture. Russell, M. The impactof alcohol-related birth Med 92(12): 725-728, 1981. State. Neurobe- M.T.; and Hetzel, defects (ARBD) on New York Potter, BO.; Belling, G.B.; Mano, havioral Toxicology 2:277-283,1980. B.S. Experimental productionof growth retar- for to al- Russell,M.,andBigler,L.R.Screening dation in the sheep fetus after exposure problemsin an outpatient Australia 2:191-193, alcohol-related cohol. Medical Journal of obstetric-gynecologic clinic.Amer:-..in Journal 1980. of Obstetrics andGynecology 11.577:12, 1979. Randall, C.L. Alcohol as a teratogenin animals. In: Altered development of Abuse and Alco- Samson, H.H., and Diaz, J. National Institute on Alcohol brain by neonatal ethanol exposure:Zinc levels holism. Biomedical Processesand Consequences Alcoholism: Clinical and Health Monograph during and after exposure. of Alcohol Use. Alcohol and Experimental Research51563-569, 1981. No. 2. DHHS Pub.No.(ADM)82-1191. Washing- and Shaywitz, B.A. Docs., U.S. Govt. Print.Off., Shaywitz, S.E.; Cohen, D.3.; ton, D.C.: Supt. of Behavior and learning difficultiesin children of 1982. pp. 291-307. normal intelligence born toalcoholic mothers. Randall, C.L., and Taylor, W.J.Prenatal ethanol Teratogenic effects. Tera- Journal of Pediatrics 96:978-982, 1980. exposure in mice: Snow, M.H.L., and Tam,P.P.L.Is compensatory tology 19:305-312, 1979. factor in mouse tera- W.J.; andWalker, D.W. growth a complicating Randall, C.L.; Taylor, tology? Nature 279:555-557,1979. Ethanol-induced malformationsin mice. Alco- R.3.77aol-in-pregnancy: Clinical research Clinical andExperimentalResearch Sokol, holism: problems. NeurobehavioralToxicology and Ter- 1:219-224, 1977. T.A.;Lochry,E.A.; and atology 2:157-165, 1980a. Randall, C.L.; Burling, Sokol,R.J.Alcohol and spontaneousabortion Sutker, P.B. The effect ofpaternal alcohol con- 2:1079, 1980b. in mice. Drug and (letter to the editor). 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Sokol, R.J.; Miller, S.I.; and tion A, Pathology 88:285-289, the alcohol abusingobstetric/gynecologic pa- Riley, E.P.; Lochry, E.A.;and Shapiro, N.R. Lack In: National Insti- prenatally exposed tient: A practical approach. of response inhibition in rats Abuse and Alcoholism.Pre- Psychopharmacology 62:47-52,1979a. tute on Alcohol to alcohol. FetalAlcoholEffects:A Practical Lochry,E.A.;Shapiro,N.R.;and venting Riley,E.P.; Guide for Ob/Gyn Physiciansand Nurses. DHHS Baldwin, J. Response perseverationin rats ex- Washington, D.C.: Supt. Pharmacology, Bio- 'Pub. No (ADM ')81 - 1163. posed to alcohol prenatally. of Docs., U.S. Govt. Print.Off., 1981. pp. 5-20. chemistry and Behavior 10:255-259,1979b. perspective on the fetal Streissguth, A.P.; Herman,C.S.; and Smith, D.W. Rosett, H.L. A clinical Intelligence, behavior anddysmorphogenesis in alcohol syndrome (editorial).Alcoholism:Clin- A report on 20 ical and ExperimentalResearch 4:119-1%. 1980. the fetal alcohol syndromes patients.JournalofPediatrics92:363-367, Rosett,H.L.,andWeiner,L.Identify ingand 1978a. treating pregnant patients atrisk from alcohol. C.S.; and Smith, D.W. Journal 125:149- Streissguth, A.P.; Herman, Canadian Medical Association Stability ofintelligence in the fetalalcohol 1317,1781. Alcoholism: Edelin, K.C. Strate- syndrome: A preliminaryreport. Rosett, H.L.; Weiner, L.; and Research 2:165-170, gies for prevention of fetalalcohol effects. Ob- Clinical and Experimental 1978b. stetrics and Gynecology 5711-7,1981. 105 81 Streissguth, A.P.;Barr, H.M.; Martin, D.C.; and Alcohol a:1d Health. DeLuca, Herman, C.S. Effects of maternal 3.R., ed. DHHS alcohol, nic- Pub. No. (a1M)81-1080.Washington, D.C.: Supt. otine and caffeineuse during pregnancy on in- of Docs., U.S. Govt. Print. fant mental and motor development Off., 1981. at 8 months. U.S. Department of Health,Education, and Wel- Alcoholism: Clinical andExperimental Research fare. Third Special Reportto the U.S. Congress WI5K04, 1980. on Alcohol and Health. Noble, E.P., Streissguth, &P.; Martin, D.C.; ed. DHEW Martin, 3.C.; and purrZTADM)79-83/.Washington, D.C.: Supt. Barr, H.M. The Seattle longitudinalprospective of Docs., Govt. Print. Off. 1978. study on alcohol and pregnancy. Neurobehavioral Warner, 12.H., and RosettRosett,H.L. Toxicolo and Teratolo The effects of 3:223-233, 1981. drinking on offspring:Anhistorical survey of the Stre ssgut h, ..; ar y, B.L.; Barr, H.M.; Smith, American and IR.; and Martin, D.C. Britishliterature.Journalof Comparison of drinking Studies on Alcohol 36:1395-1420,1973. and smoking patterns duringpregnancy over a Weiner, L.; Rosett, H.L.; six -year interval. American Journal and Edelin, K.C. Behav- of Obstet- ioral evaluation of fetalalcohol education for rics and Gynecology 145s 716-724,1983. physicians.Alcoholism:Clinical andExperi- Streissguth, A.A.; Martin,D.C.; Barr, H.M.; Sand- mental Research 6:230-233, man, B.A.; Kirchner, G.L.; and 1982. Darby, B.L. Weiner, L.; Rosett, H.L.;Edelin, K.C.; Alpert, 3.3.; Infra- uterine alcoholexposure and attentional and Zuckerman, B. decrements In4-year-old children Alcohol consumption by (abstract). pregnant women. Obstetricsand Gynecology Alcoholism:lolisnaglnical and ExperimentalResearch 61:6-12, 1983. 7:122, 1983. West, J.R.; Hodges, C.A.;and Black, A.C., Jr. Sulik, K.K.; Johnston,M.C.; and Webb, M.A. Fetal Prenatal exposure to ethanol alcohol syndrome: Embryogenesis alters the organi- on a mouse zation of hippocampalmossy fibers in rats. Sci- model. Science 214:936-938, 1981. ence 211:957-939, 1981. Sullivan, W.C. A noteon the influence of maternal Wiener, S.G.; Shoemaker,W.3.; Koda, L.Y.: and inel3riety on the offspring. Journal ofMental Bloom, F.E. Interaction ofethanol and nutrition Science 45:489- 503, 1899. during gestation: Influenceon maternal and off- Tanaka, H.; Suzuki, N.; andArima, M. Hypogly- spring development In therat. Journal of Phar- cemia in the fetal alcohol syndromein the rat. macology and ExperimentalTherapeutics 2161 Brain and Develoement 4:97-103,1982. 372-379, 1981. U.S. Department of Health andHuman Services. Wilson, J.G. Environmentand Birth Defects. New Fourth Special Report to the U.S. Congresson York: Academic Press, 1973.303 pp.

82 Chapter VI

Adverse Social Consequencesof Alcohol Useand Alcoholism States and the leading cause of deathin the Heavy drinking and chronic alcoholism con- (Ross 1982). tribute to a variety of social problems.In ad- 1- to 35-year-old age group reports,simulated dition to accidents involving variousmodes of After analyzing case transportation, accidents occur in thehome, driving conditions, andepidemiologic data, unequivo- at work, and during recreationalactivities. researchers have consistently and of work cally concluded that alcoholcontributes sig- Alcohol use also contributes to loss The higher the productivity, homicide, suicide, andassaultive nificantly to traffic accidents. Gallup survey, amount of alcohol consumed,the greater the behaviors. In a 1982 national and that one-third of persons interviewedsaid alcohol likelihood that an accident will occur families (Gallup the accident will be serious orfatal. had caused problems in their In a report to the National Institute onAl- 1982). (NIAAA), Camer- Research on the contributionof heavy alcohol Abuse and Alcoholism social on (1977) cited 23studies showing that at least cohol consumption and alcoholism to accidents had problems varies in quality.Although the causal one-third of the drivers in fatal nonexistent, the blood alcohol concentrations(BACs) exceeding link is sometimes weak or equals that in best evidence available stronglysuggests that .10 percent. This effect roughly much more likely a 155-pound manwho consumed at least five many of these problems are within an hour. estimates to arise among alcoholics orheavy drinkers or six drinks or more Moreover, the po- place the annual number ofdeaths in traffic than among other persons. driver had been tential for some of these problemsto occur accidents in which at least one drinking at 16,000 to 30,000(Roizen 1982). may be heightened by evenmoderate con- killed in sumption (Moore and Gerstein1981, pp. 44- Between 20 and 40 percent of people these drinking-driving accidents were persons 45). Since moderate drinkers outnumberheavy other than the drunk driver(Reed 1981). moderatedrinkingmayactually drinkers, Borkenstein and colleagues(1974)inter- contribute substantially tosocial problems. drinking and Because most individuals do notbelieve they viewed Indiana drivers about their drinking-related tested their blood alcohol contents.Regardless personallywillexperience drivers reported has been difficult tosensitize the of the frequency with which problems, ; BACsIncreasedcrash public to social problems causedby moderate drinking,elevated probabilities.Studies comparingdriversin drinking. fatal accidents with drivers notinvolved In accidents in similar locations atsimilar times Alcohol and Accidents sugg'st that drivers withBACs above .10 percent are 3 to 15 times morelikely than nondrinking drivers to be involved in afatal Traffic Accidents crash (Cameron 1977). For youngdrivers, in Traffic accidents across the countryre- particular, the risk of a fatal crashincreases (USDOT 1983). sharply with increasing BAC levels(Perrin et sulted in 49,268 deaths in 1981 1981). For further Nearly 150,000 persons are permanentlydis- al. 1971; Wagenaar et al. discussion of this topic, see tables4 and 5 in abled each year in automobileaccidents, and injuries that re- chapter 1 of this volume. 1.8 million persons sustain Because of the high risk offatal accident strict their activities for atleast 1 full day Council 1982). involvement after heavy drinking, therisks after a crash (National Safety drinking are During the past decade, morethan 450,000 posed by driving after moderate constituted the fifth sometimes overlooked. According tostudies In traffic accident fatalities (McCarron and Haddon 1962) leading overall cause of death inthe United New York City

83 and Vermont (Perrine et al. 1971),even drivers volved in only a small fractionof fatal acci- with BACs of .05 percentto .099 percent are dents. Sterling-Smith (1976) reportedthat of 1.25 to 3.25 tiroesmore likely to be involved drivers known to be responsible infatal accidents than nondrinking for fatal a..:- drivers. cidents in the early 1970s inMassachusetts, According to the U.S.Department of Trans- only 4 percent had portation (Fell 1982), while 50 a previous DWI arrest, percent of fa- about one-tenth of those in thestudy with a tally injured drivers had BACsabove .10 per- BAC above .05 percent. The cent, 12 percent had elevated BACs implication is between thatevenhighlysuccessfulrehabilitation .01 percent and .10percent. Reed (1981) has programs aimed at the arrested drunk driver estimated that if all drivers inthis country in may influence only a small minority of drunk 1977 were only exposed to the risk if drivers drivers. If the percentage of drunkdrivers who who do not drive after drinking,there would are arrested increases, however, these have been 24 percent fewer suc- accidental deaths cessful rehabilitation percentages may (11,700deathsprevented) and156,000to increase. 300,000 fewer injuries. Despite widespreadawareness of itsrisk, Alcohol contributes to trafficaccidents by drunk drivingoccursrelatively affecting cognitive and behavioral frequently. function, Researchers have estimated thatat any given often in multipleways in the same accident. Alcohol in th time 2 to 3 percent of the drivingpopulation blood at levels above .10per- are legally intoxicated, and that the cent is knov.to (1) lower divided attention percentage doubles at night or on weekends, thehours performance, (2) reduce dynamicvisual ac- during which accidentsare most frequent tivity, (3) reduce adaptationto brightness and glare (Damkot et al. 1977; Haddonand Blumenthal resistancerecovery,and(4)reduce 1981). As manyas 20 percent of nighttime ability to see flickering lights,e.g., turn sig- drivers randomly stopped have been nals (Perrine 1974). Some found to researchers believe have measurable BACs (Damkotet al. 1977). alcohol also interferes with thebrain's ability Statewide random samplesurveys of nearly to process large quantities of information at 1,000 adults in Massachusetts in1981indi- one time (Moskowitz 1974). Still otherscite cated that 29 percent of driversreport driving the sedating, fear reducing,and disinhibitory after drinki' effects of alcohol it least four times in the prior on aggressiveness or self- month, and percent report driving after six destructiveness.Cognitiveeffectssuchas or more drinks at least four times short-term memory loss a month. or learning deficits Males, persons whoare unmarried, and those may also contribute to accidents (Barry 1974). under age 25 most often reported Those willing to drive after driving after heavy drinking, of drinking heavily (Hingsonet al. 1982a, 1983). course, may generally engage in high risk- At least threereasons explain why people taking behavior andmay be impulsive and drive afterdrinking.First, a considerable careless (Jones and Juscelyn 1978).This may number of people who drink do place them .at increased risk for not know the highway ac- level of drinking that makes individualslegally cidents regardless of their drinkingbehavior. too intoxicated to drive. The 1981 Massachu- Most researchers concur thatchronic heavy setts survey indicated that 10 percent of drinkers or alcoholics the are more likely than respondents who drive didnot know the level light drinkers or nondrinkersto be involved in of legal intoxication, and 17percent felt that traffic accidents (Fell 1982).Estimates vary a person can drink six or more drinks without widely, however, on the proportionof acci- being legally too drunk to drive. Second, dents involving each category, largely even because though the relative risk of accidentinvolve- of variable criteria for diagnosingalcoholics. ment for persons who drive under the Klatsky et al. (1981) compared influ- 2,015 Kaiser ence is much higher than for nondrinkers,the Permanente plan members who averagedsix or probability of an accident duringa trip when more drinks daily with 6,045 light drinkers and the driver is under the influenceis still quite nondrinkers matched byage, sex, race, ciga- low, only about 2 per 1,000 trips (Ross 1982). retteuse,andcity.Those who reported The risk of arrest is roughly drinking more than six dri. ks daily comparable, after were three which the drunk driver would stiPstand only a times more likely than the. ,st of the sample to die in a traffic accident during 50-50 chance of being punished(Jones and the sub- Joscelyn1978; Ross 1982).Finally,driving sequent 10 years. after drinking has long been Although persons with considered so- a previous driving- cially acceptable behavior. Whilepolitical and while-intoxicated (DWI) arrestrun a higher social pressures have prompted accident risk than other drivers, they 34 States to are in- change their drunk driving laws duringthe past 1. 0 84 2 years (Volpe 1982), it is not clearwhether Occupational Accidents thiswillsubstantiallyalter public compla- for cency about drunk drivingand the frequency Work-related accidents were responsible of its occurrence. 13,000 fatalities in 1980, and 80,000 persons were permanently disabled,partially or totally Pedestrian Accidents (National Safety Council 1982). National survey data suggest thatyearly 25 percent of At least 8,000 pedestrians are killedand workers sustain some sort of injury on thejob 100,000 injured each year by motor vehicles. (Quinn and Shepard 1974). About 35 percentof Research indicates measurable BACs among the work-related fatal accidents are repre- fatally injured pedestrians ranging from 35 to sented in the traffic accident statisticsal- 74 percent (Blomberg et al.1979). ready cited. Only two studies compared fatally injured Accidents on the job are not as extensively pedestrians with noninjured pedestrians who researched as traffic accidents; less isknown passed the same spot at a similar time ofday about their occurrence and contributory fac- and day of week (Haddon et al. 1961;Blomberg tors (including alcohol). Bakerand associates et al. 1979). In the more recent and more ex- (1982) indicated that in 1978, 148Maryland tensive study (Blomberg et al.1979), between workers died in job-related accidents.Blood BAC alcohol concentration levels were obtained on July 1972 and March 1976, postmortem BACs could results were obtained on all 86fatally injured 79 percent of those from whom pedestrians taken to a New Orleanshospital. technically have been obtained. About 11 fatalities and All 180 injured pedestrians taken tothe same percent of both motor vehicle hospital between March 1975 and March1976 fatalities from other causes had BACsabove were also tested.Pedestrians who passed the .08 percent. In contrast, according to a na- of the accidents tional survey of workers (Quinn andShepard same site within 30 minutes popula- on the same day ofthe week and year were 1974), only 2 percent of the workilig control tion can be expected to drink on the job on any also stopped; 1,208 of 1,469 eligible jobs and respondents were given blood alcohol testsand given day. Although the types of worker characteristics In a nationalsample interviewed. in Thirty-six percent of the injured pedestrians may systematicallydifferfromthose had BACs over .10 percent, as did45 percent Maryland, these data suggest that people who much of the pedestrians who died. Only13 percent have fatal accidents on the job were of controls had BACs at that level.Compared more likely than tetheremployees to drink at with age- and sex-matchednondrinkers, the work. risk of accident involvement forpedestrians Giventhewell-establishedrelationships was two times higherwith BACs above .10 between blood alcohol levels and poor coor- for those with dination, faulty judgment, and lengthened re- percent and five times higher alcohol often BACs above .20 percent. The relativerisk rose action time, it is plausible that rapidly as the blood alcohol concentrationin- contributes to accidents at work. Of course, of work. creased beyond .20 percent. the risk may well vary with the type Driver error was less frequently the cause Some data also suggest that alcoholics are when the pedestrian had been drinking.Alco- more likely than other workers toexperience hol-involved accidents were more frequent work-related accidents, but the resultshave aged 20 to 49 and not been consistent. Shain(1982) studied one among male pedestrians and tended to cluster on weekends and atnight. firm located in the eastern United States found that alcoholics are two to threetimes more likely than otheremployees to be in- Airplane Accidents volved in work accidents, but alcoholism was Alcohol is also a factor in aviation accidents not adequately defined in thisstudy. Trice Transportation Safety Board (1965) compared 72 alcoholic employees with (U.S.National be- 1979). In 678 fatal plane crashes nationwideIn "normal" employees and found no relation in 30 tween alcoholism and accidentinvolvement 1979, alcohol impairment was identified fol- pilots, most of whom had BACsabove .10 during the 5 years preceding and 1 year percent. Because the proportionof pilots who lowing diagnosis. of flight Additional research is needed on alcohol use fly after drinking and the proportion In- time under the influence are notknown, how- and alcoholism as they affect accident aviation accidents at volvement at work. Research priorityshould ever, the relative risk of to various drinking levels is yet unclear. be given to (1) national or regional surveys 109 85 determine the prevalence ofon-the-job In a review of the available literature, Win- drinking and the incidence of accidents after gard and Room (1977) identified onlya half drinking, (2) systematic BAC testingon all dozen U.S. reports. since 1950on alcohol and occupational fatalities, and (3)case control fatalitiesfromfalls,drowning,andfire- studies comparing alcoholuse by employees related injuries. Since studies showeda con- involved In occupational accidents with that of siderable variation in the proportion of fatal employees who work at similar jobs butwere accident victims in whom alcoholwas present, not involved in accidents. it Is not clear whether alcohol ismore likely Valid data may be difficultto obtain be- to be Involved in certain types of accidents. cause of legal questions concerning financial Haberman and Baden (1978), ina report on responsibility for defective products as well as 121 falling, fire, and drowning deaths inNew worker compensation when the workerhad York City between 1974 and 1975, indicated been drinking prior to the accident. Further- that 43 percent of such victims hadblood al- more, other characteristics that contribute to cohol concentrations above .10 percent. That drinking on the job (job boredom, stress)could proportion actually exceeded the proportionof independently relate to accident involvement. motor vehicle and pedestrian accidents In- volving blood alcohol at that level duringthe Home and Recreational Accidents same time period. Only about half the accidents in each of those categories duringthat Nationwide, in 1980, 22,800persons died and time period were available for study. Yet, another 90,000 were permanently injuredin even if all the omitted accidents did not in- home accidents.Falls accounted for about volve alcohol, 20 to 25 percent of the falls, one-third of home accident deaths, and burns burns, and drownings would still have occurred or Injuries resulting directly from firescom- to persons with BACs above .10 percent. In prised another 20 percent. Outside the home, contrast, on any given day onecan expect only 21,000 persons died and 60,000were perma- 3 percent of the population ina large urban nently injured in non-motor-vehicle accidents area to consume the equivalent of five or such as falls, drownings, and otherrecrea- more drinks, the amount needed to achieve tional a accidents. From1970 to1980,the BAC of .10 percent (Hingson et al.1981). sharpestdeclinesinfatal accidentrates- - However, the proportion of persons In similar about 25 percent--wererecordedinthese social and demographic groupsas those in ac- groupings (National Safety Council 1982). cidents who consume that much hasnot been The role of alcohol Is less well understood in determined. home and nontransportation accidents than in Alcohol'scontributionto traffic accidents may accidents because on-the-scenein- vary by type of accident. In some, suchas vestigations are less frequently conducted and falls, alcohol may reducesensory motor co- most studies are undertaken In hospitalemer- ordination.In drownings, alcohol maycon- gency clinics. Moreover, because these acci- tribute by increasing the risk-taking behaviors dents encompass a wider variety ofcircum- of swimmers or boatersor by reducing coor- stances, identifying specific causes for each dination so that capsizing ismore likely. Once accident type is more difficult. Since different the person is in the water, alcoholmay hasten researchers use different taxonomies, itis a loss of body heat (Stanley and Siegal 1981). difficult to combine the results into effective Alcohol may prompt smokers to fall asleepand generalizations. risk cigarette fires (Levine and Radford 1977). The few studies available suggest that al- Some studies compare death rates fromac- cohol may contribute tosome of these acci- cidents of alcoholics or heavy drinkers with dents. Wechsler et al. (1969) compared home those of the rest of the population. When accidentadmissionswith emergency room Brenner (1967), Nicholls et al.(1974), and admissions for other reasons,e.g., circulatory Schmidt and de Lint (1972) compared alcoholic or digestive disorders. Twenty-two percent of samples with matched age- and sex-specific 620 patients in home accidents hadpositive populations, they found a 5 to 13 timesgreater BACs compared with 9 percent of nonaccident riskof dying from falls among alcoholics. patients.Eleven percent had bloodalcohol Schmidt and de Lint also reporteda tenfold concentration levels above .05 percentcom- increase in death rates in firesamong alco- pared with 3 percent of nonaccident patients. holics. Social class and possible livingenvi- The relationship was statistically significant ronment differences between the groups were even after adjusting for age, sex, and socio- not, however, controlled In these studies. In economic status of persons in eachgroup. the study of 2,015 Kaiser Permanente Health Plan members (Klatsky etal.1981), heavy These findings have prompted some re- drinkers were 2.7 times as likely as theoverall searchers to hypothesize a direct causal re- sample to diein an accident (other than lationship between heavy alcohol consumption trafficaccident) during the subsequent10 or alcoholism andmurder. Numerous theories years. Specific comparisons onthe types of attempt to explain how alcohol maybe di- accident were not made and none ofthese rectlyrelatedtoviolent crime (Pernanen studies examined alcohol consumption Imme- 1981). To cite a few: diately prior to the accident. Of course, using alcohol or being alcoholicis Alcohol may reduce inhibition and re- only one of many factors that contribute to lease violent impulses. such accidents, andits presence does not necessarily imply a causal role. Researchis Alcohol may alter neurotransmitter ac- needed to assess when alcohol may have an tivity. independent effect beyond other factors such as age, architecture, poverty, poorhousing, Chronic excessive alcohol use may lead and smoking. The national fire surveydoes not to temporal lobe dysfunction,which in query fire witnesses and victimsabout alcohol, turn may contribute to violentbehavior. even though drinkers aremuch more likely than nondrinkers to smoke and smoking is well Still other argue that alcohol use contributes known to relate to the incidenceoffires to violence only in the presenceof such con- (FEMA 1982). Case control studies that com- ditions as hypoglycemia, produced by poor pare persons infallswith persons passing nutrition among chronic heavy drinkers, or similar locations at similar times ofday who persistent lack of REM (rapid eyemovement) do not fall would help establish therelative sleep activity as a result of prolonged drink- risk for intoxicated persons. ing.Either ofthese factors may produce heightened irritability among drinkers. However plausible these theories may be, no Alcohol and Crime studies to date provide clear evidencethat alcoholis an independent causal factorin murder.AccordingtoCollins(1981),"the Homicide number of scientists arguing for direct and In 1980, there were 22,516 murdersin the simple relations between the presence of al- United States or 9.8 per 100,000inhabitants. cohol and crime has decreased as the com- The rate per 100,000 inhabitants rose1.1 per- plexity of logic and sophistication of designs Edgerton cent since 1976 (USDO31981). hasIncreased."Mac Andrew and It has long been recognized thatalcohol is (1973), using cross-cultural analyses, suggest frequently present in both perpetratorsand that behavior while intoxicated maydepend victims. Wolfgang's landmark study(1958) in more on what is consideredsocially acceptable Philadelphia indicated that either the victim while intoxicated than on disinhibitory effects. or the offender orboth had been drinking in Several researchers have also noted that nearly two-thirds of the slayings hestudied, some variables simultaneouslycontribute to been con- both alcohol use or alcoholism and crime, and in 44 percent, both parties had relation suming alcohol. possiblymaking the alcohol-crime Roizen and Schneberk (1977) identified11 coincidental rather than causal. For example, studies that reported a range ofalcohol in- heavy drinking is more apt to occur in marital volvement in from 28 to 85 percentof ar- situations in which neither partner is satisfied rested offenders. Greenberg's review(1981) of or happy(Hingson et al.1931). While such 28 studies indicated that a majorityof victims situations may also be more likely to result in or offenders or bothdrank prior to the crime. murder, it is difficult to say whether alcohol Reports of involvement varied somewhatby and/or the underlying unhappiness contributed type of study. Studies of police reportsand to such murders. arrested populations identified alcoholin 66 Similarly, Wolfgang (1967)has cautioned percent of cases, whereas 9prison studies that drinking is a part of the mores of low- identified its involvement in44 percent of income young males, the group Involvedin cases. In 4 of 5 studiesreviewed by Greenberg most murders. But tension and frustration may (1981), at least 20 percent of theIndividuals also be more common among this subgroup, who committed murder also had analcoholism which in turn prompts some to commit murder Also, alcohol use and vio- problem. as well as to drink.

87 11 1 lence are both more likelyto be found in set- (Collins1981; Menuck and Volneskos 1981). tings(e.g.,bars) where low-incomeyoung According to Blum (1981), "Under males congregate. It no circum- is difficult to establish stanceswillalcoholbea solecauseof whether alcohol contributesto violence, or violence." whether it at timeseven helps avert violence In sum, alcoholuse is part of the lifestyle of and murder by relievingtension andfrus- low-income young males, those tration. most apt to commit or be involved in murder.Even if Few studies in thisarea attempt to control drinking may have disinhibitory for these possibly confounding effects or factors. Of 35 long-term effects on mental functioningthat studieson crimereviewedbyGreenberg in turn contribute to violence, it is (1981), only 5 controlled unrealistic for age, sex, and to cite alcohol as the majorcause of the race, factors related not only to the incidence frustration and anger in this population of murder but also to drinking. that also contribute to high murderrates.Nor, Othermethodologiclimitationsofthe however, is it realistic to dismiss alcohol existing research as on this topic have been dis- irrelevant,Alcohol may alterperceptions, cussed by Roizen and Schneberk (1977).Dis- cognitive performance, moods, emotions, tinctions are seldom drawn between and presence responsecapabilitiesandpreferences.The of alcohol and actual intoxication,and length frequent association of alcohol of time since alcohol ingestion among mur- is rarely indi- derers and their victims suggests itis more cated. Data are collectedat different points than coincidental. inthejudicial process:arrest,court, and Itis reasonable to expect thatalcohol is prison. The limited data availablesuggest that more likely to contribute in some types of murderers who had been drinking and are murders than in others,e.g., quarrels among caught are more likely to be convictedand family members, friends, and hence overrepresented in acquaintances prison populations that escalate Into murder. Alcoholisless (Greenberg 1981). In all studiesof murder, the likely to be involved in premeditated definition of the crime itself murders may be blurry; in which the perpetrator makescareful plans for example, manslaughter andhomicide may to avoid detection. At this point, because of be combined. inherent difficulties in studying murderand The presence of alcohol in the victimis not limitations in available research aboutalcohol clearly and adequately understood.The few and murder, one can conclude only studies of victims suggest that they that alco- were hol may be one of numerous factors thatat frequently drinking. It is possible thatdrinking times may independently contributeto some victims who had been drinking eitherlacked types of murder. adequate judgment to avoid antagonizingthe offender or were unable to modifythe offender's anger insome way (Braucht et al. Rape 1980).Itisalso possiblethatintoxication rendered victims less able than soberpersons In 1980, there were 36.4 forciblerapes re- to defend themselves or to avoid an attack. ported per 100,000 persons in thepopulation, In studies of homicide and alcoholism,the or 82,088 rapes (USDOJ 1981). This rate has presence of alcohol at the scene and time of steadily increased 38 percent from the crime is seldom identified. 1976 to Moreover, al- 1980 in part because of changingpublic and coholics are more likely to havecourt records law enforcement attitudes, such as DWI offenses, thepush from loitering,etc., and women's groups to encourage victimsto report hence to be known by police. This has prompt- rapes, and the general increaseinviolent ed some researchers to ask:Are alcoholic crime in the United States. criminals more likely toget caught? (Roizen Rape is an extremely difficult crimeto in- and Schneberk 1977). vestigate (Rabkin1979). Local legal codes, It should be kept in mind thatthe majority police of criminal offenders enforcement,and publicattitudes are not alcoholics and toward rapists and victimsvary greatly by the majority of alcoholicsnever commit seri- region, resultingin different reporting and ous crimes (Collins 1981). Even explanations recording rates. Low reporting andconviction that identify alcohol as a potential contributor rates limit inferences about the character- to violence cite other contributorsas well, istics of rapists. In general, e.g.,hereditary studies of rape factors,braindysfunction, draw from interviews and otherdata collected availability of guns, media violence,and nu- from apprehendedrapists, who may differ merous other social and psychological factors from undetected rapists.

88 112 still In a study of violent crime inWestern Can- crime. Thus, the role of alcohol in rapes is ada (Gerson and Preston 1979), 60 percentof poorly understood. the rapes in a 12-month period were considered to be alcohol related; either the victim or Other Crime the defendant had been drinking,and the crime involved violation of an alcoholstatute The relationship of alcohol to other crime Is or occurred in a licensedalcohol establish- even less clear. Data onthe characteristics of ment. Groth (1979) found that 50 percentof a perpetrators should be considered withmuch murder offend- group of men who raped oldervictims reported greater caution than those of being high on alcohol or on alcohol and drugs. ers since a lowerproportion reach the atten- Rada and his colleagues (1978), In a study of tion of the police. 382 rapists in a State mental institution,found Fewer studies have been undertaken on al- that 81 percent of the alcoholics and25 per- cohol involvement in other crimesthan in cent of the nonalcoholics drankbefore the murder. Table 1 indicates the relativealcohol assault. In another population, 53 percentof involvement for these crimes in contrast to Comparedwith mentallydisturbedsexoffendersreported murder(Greenberg 1981). drinking heavily (Rada et al.1978). In con- murder, the proportion of thesecrimes with Be- trast, in a general urban population36 percent alcohol involvement appears to be lower. of males can be expected to drink on anygiven cause, with the exceptionof aggravated as- day (Hir %son et al. 1981). A moreappropriate sault, most of these crimes are premeditated comparison would match nonrapistswith rap- and carried out with the intentof avoiding ists on other social and economiccharacter- arrest, itis unlikely that alcohol will be as istics to see whether theirdrinking levels strong a potential contributor asin crimes of differ. passion and violence. Few studies have examined therelated question of frequency of alcoholism among Alcohol and the Family rapists. Rada et al. (1978) found that33 percent of 77 rapists had a historyof alcoholism. Twenty-seven percent of 82 rapists in another Separation and Divorce group of subjects(Barnard et al.1979) were 1977inthe identifiedas alcoholics.The proportionof The annual divorce rate in is much United States among women over the ageof alcoholics in the general population have been lower. 15 was 21 per 1,000. These rates These studies suggest that people who com- climbing steadily since 1967(USDHHS 1980). mit rape are disproportionatelylikely to have Evidence suggests that the rate of separation been drinking or to be alcoholics.However, and divorce among alcoholics andtheir spouses population the reasons for this alcohol-rapeconnection is seven times that of the general understood. Wilson (1981) re- (Paolino and McCrady 1977). Forty percentof are not well in majortheories.Disinhibition family court problems involve alcoholism viewedtwo Seilhamer 1982), and it Is theory suggests that alcohol releasesother- some way (Jacob and wise well-controlled sexual or aggressivebe- estimated that 33 percent (Jacoband Sell- based on hamer 1982) to 40 percent (USDHEW1975) of haviors. An alternative explanation marital social learning principles suggeststhat be- intact alcoholic couples have poor havior after consuming alcohol Isdetermined relationships. effects of alcohol Alcohol is, clearly associated with disrupted by past learning about the family on actions and by personalexpectations about family functioning, but the marital and the consequences of a certain courseof ac- problems may precede the alcoholism, may tion. A sociallearning model ofalcohol- occur solely as aresult of the alcoholic's associated rape might suggest thatalcohol drinking and behavior changes, or may be part consumption is seen as a way todisavow re- of a complex interaction betweenpreexisting weaknesses of the family or of individualsin sponsibility for actions and thereby avoid ex- family ternal punishment, socialdisapproval, or in- the family and the drinking of one ternal guilt for attempting rape. member. In conclusion, It appearsthat alcohol consumption and rape may be associated,but this Family Violence Some rapists link may have been overstated. and may actually pleaddrunkenness or alcoholism The abuse of children by their parents, as a way to avoid legalresponsibility for the the abuse of spouses by their marital partners,

89 113 Table 1. Alcohol involvement incriminal events, by type of crime

Percentage of crime victims or offenders in Frequency of studies whom alcohol was present during criminal SexualAggravated Auto Forgery/ eventa Homicide offenses assault RobberyBurglary Larceny theft bad checks

0 -10 2 1

11 - 20 4 1 1 1 aft 21 -30 2 2 31 -40 2 1 2

41 -50 2 3 1 1 1 1

51 -60 4 1 1 1 1 2 61 -70 4 1 3 2 1 1 71 - 80 2 1 81 -90

91 - 100 1 1 1

=Node OYMIND Total studiesb 28 9 8 5 6 5 3 3

a These percentages reflect the presence of alcohol,as defined in a variety of ways, immediately prior to or during the crime. The number upon which the percentagesare based are therefore either total cases (victims) or total offenders. In studies in which drinking on the part of both victims and offendersis reported, the percentage of victims only is reportedin this table. b This table is based on the findings of 35 studies. The grand total does not addto 35 because some studies include data on only one type of crime, while others include twoor more types of crime and therefore appear in more than one column. Sources Greenberg 1981. have received increasing attention in the me- sampled individualsintreatment. Such in- dia and in the professional literature.Self-help dividuals represent only that fractionof the groups for parents who abuse their children abusing population who have admitted (e.g., they Parents Anonymous) and sheltersfor have problems, or whose abuse hasbecome battered women have proliferatedthroughout severe enough to come to the attention of the country. outside authorities, who requiredthat they The study of family violence,however, is an undergo treatment. extremely sensitive, emotionally laden,and Finally, many attributions ofviolence are difficult pursuit. The definitions ofabuse vary based on retrospective reports ofthe abuser, widely, and incidents of abuseare markedly the victim, or a third party. Recallmay be unreported. Research In thisarea Is hampered faulty,making attributionofviolenceto by the traditional sanctity of thefamily and drinking or drunkennesssuspect. One party the blurred lines between acceptablefamily may place primary emphasis on drinking that behavior and abuse. another would see as Immaterial,or alcohol Most studies that have attemptedto un- use may be presented as an excuse for violent derstand causes for family violence,or the behavior. Aarens et al. (1977) notedin one links between violence and alcoholuse, have study of domestic violence thatthe corn- plainant stated that the abusive party was drinking problem rather than accept other drinking or drunk much more often than was reasons for the abuse(Aarens etal.1977; noted by the police. Finally, alcohol consump- Hilberman 1980). Estimates of actual alcohol tion may be irrelevant or coincidental or may consumption at the time of abuse vary from 29 have created or contributed to a conflict that to 71percent, although virtuallyallthese culminated in violence. figures are based on victim recall and were not verified by objective means such asBAC Child abuse.--This discussion does not con- analyses. sider child neglect or failure to provide nec- Several theories have tried to explain the essary food, shelter, or medical carebut in- role of alcohol in spouse abuse. Gel les and stead focuses on willful commitment of injury Straus (1979) have suggested that alcohol is to the abused person. A national survey con- used as an excuse for violence because, when ducted in 1965 revealed that 2 to 4 percent of drunk, a person may deny responsibility for his the adults surveyed personally knew families or her actions. Denial ofresponsibility for in which child abuse had occurred in the pre- actions when drinking is common in American vious year (Gil 1970). Three literature reviews society (Richardson and Campbell1980). So- concerningdrinking,alcoholism,andchild cial learning theorists (Wilson 1981) suggest abuse (Aarens et al. 1977; Hamilton and Col- that people learr, to expect to behave more lins 1981; Orme and Rimmer 1981) Identified aggressively when drinking and therefore do only three studies that determined thefre- so, even if the alcohol itselfdoes not have a quency of drinking duringactual episodes of direct disinhibitory effect on their behavior. child abuse. Two of these note that 12 percent These two models are in direct contrast to of abusers were drinking at the time (Gil 1970; disinhibition theory, which suggests that al- Thomson et al. 1971), while only 3 to 6 percent cohol directly disinhibits people so thatthey were drinking in the thirdstudy (Scott 1973). express their real, underlyingaggressive im- When considering the frequency of alcohol pulses. A fourth model suggests an interactive problems or alcoholism in child abuse cases, relationshipbetween drinking and violence reports range from "no association" to38 (Genes 1972;Pernanen 1976). Arguments percent of abusers' having alcoholproblems. about a husband's drinking may escalate into The most frequently reported figures are that arguments about many areas of maritalprob- between 11 and 17 percent of abuse cases in- lems. The alcohol may diminish the drinker's volve alcoholism. ability to reason and to control his behavior, Overall,the currentlyavailable evidence resulting in a growing conflict that may cul- does not indicate a strong association between minate in violence. drinking or alcoholism and child abuse. As Orme and Rimmer (1981) concluded, "When Child Functioning in AlcoholicFamilies estimates of alcoholism and alcohol problems in the general population were available, the The complexity of individual, family, and prevalence appeared to be almost Identical to social factors that interact in a child's de- that in child abusers" (p.284). velopment makes itdifficult to attribute a child'sparticularproblemsorpersonality Spouse abuse.--Figures on spouse abuse tend solely to a parent's alcoholism. The study of to focus almost exclusively on theabuse of children of alcoholics is further complicated women by their husbands orlovers. During by the methodologies usually employed.Chil- 1978,6,6 percent of murder victims were dren In treatment often form the basis of re- women killed by eithertheir husbands or their search samples, but theyreflectonlythe lovers (USDO3 1981). Hamilton andCollins' fraction whose problems are serious enough to (1981) review of 15 studies suggested that 17 come to the attention of treatmentagencies to 35 percent of divorces involve violence. and who are able to find such agencies. Chil- Hamilton and Collins (1981) reported that dren whose parents are In alcoholism treat- moststudies citealcoholismorexcessive ment are another common yet notfully rep- drinking In 45 to 60 percent of spouse abuse. resentative sample, as many people with seri- Most of these reports of alcohol problems ous drinking problems never reachtreatment come from the femalevictims of the abuse. (Hingson et al.1981, 1982b). Attempting to These women may exaggerate or overestimate gain access to children and their families who the seriousness of their partners'drinking or are not connected to the treatment orsocial may prefer to believe their mateshave a services system, however,raisesdiagnostic and ethical issues. When askedabout parents'

91 1.1Fi drinking, for example, a childmay feel he or persons, remained fairly stable from the 1940s she is betraying the parentor may fear re- to the 1960s and has increased only slightly talia tion andthereforeminimizeparental since then. Suicide among young people 15to drink )g. Even if the situation is accurately 24 years of age has increased dramatically, identified, obtaining parental permissionfor however, by 250 percentamong young women the child to participate ina research study and more than 300 percentamong young men. may be difficult. Ethical questions arise also if There are 100 to 200 suiciaeattempts for such children in the course ofa study become every completed suicide of a high school youth. labeledbyasocialinstitution(e.g.,their The other high-riskpopulation group in- school) as socially deviant by virtue ofbeing cludes white men over 45years of age, who the children of alcoholics. commit 30 percent of all suicides eachyear, Woodside (1982) has reviewed the available even though they represent only 10 percent of data on children of alcoholics. Hyperkinesis the population. Men whoare alone or have has been suggested as oneconsequence of suffered recent losses are at particular risk. parental alcoholism. Although earlystudies Black men are at their highest risk forsuicide suggested that alcoholismwas twice as fre- between the ages of 20 and 34, rather than quent among parents of hyperkinetic children when they are older (Hendin 1982). as among normal controls, more recent data In some situations, alcoholismmay con- fail to support this finding (Morrison1980; tribute to a number of problems thatmay in Stewart et al.1980). Children withat least turn precipitate suicide. Separation and di- one alcoholic parent are more likely to havea vorce rates are high among alcoholics (Paolino childhood history of school problems and anti- et al. 1978). Depression is commonamong al- social behavior than other children (Sher and coholics during prolonged drinking boutsas McCrady in press). Other studies reviewed by well as during some phases of alcoholwith- Woodside (1982) have found lowerself-esteem, drawal, and alcoholism alsocauses numerous more emotional detachment, more anxiety debilitating and life-threatening medical symptoms, more social aggression,or more problems; suicide may becomea response to psychosomatic symptoms (such as headaches any of these problems. or stomach aches) among children of alcoholic Because suicide hasmany causes, however, parents than among control children. Most of it is difficult to discern the contributoryrole these associations have not been replicated, of alcoholism whenitcoexists with other however, and do not explore what mechanism problems. As many as 25 percent of female may lead to the childhood problems or what alcoholics, for example, have diagnosablede- protects some children from such problems. pression (Schuckit and Morrissey 1979). If such Summaries of unstructuredor semistruc- a patient commits suicide, it is impossible to tured interviews with children of alcoholics determinetowhat thesuicideshouldbe (Cork 1969) suggest that thesechildren feel ascribed--depression or alcoholism. rejected by their parents, guiltyor somehow Individuals use alcohol in an attempt tocope responsible for the parent's alcoholism,re- with life problems. A person facinga divorce, sentful of the alcoholic parent, and inconstant the death of a parent, or a serious illnessmay fear. However, most of these studies focuson drink and,infact, may develop a serious the casualties of alcoholism--the children in drinking problem. If thisperson commits sui- trouble. One notable exception soughtto un- cide, is the suicide a result of the alcohol derstand what factors spare certain children abuse or of the original life problem? (Wolin et al. 1980). They found thatalcoholic A number of problems with researchmeth- families thatmaintained somepredictable ods further muddy the waters. Socialpressures structures, particularly around the observance often lead to underreporting of suicide,and of 4amily rituals (at meals, holidays, etc.), family members may be reluctanttoac- were less likely to produce alcoholic offspring knowledge the alcoholism ofa deceased rel- than families with disrupted family rituals. ative, thus obscuring the suicide-alcoholism association. Diagnosing alcoholism based only Alcohol and Suicide on survivors' reports is also difficult, especially when attempting to distinguishbetween alcoholism and other psychological disorders. About 27,000 Americans commit suicide Blood alcohol levels are not alwaysdetermined each year (Hendin 1982), but 10 timesas many when someone dies. Finally, theassessment of persons make unsuccessful suicide attempts. intent of a death is sometimes problematic. The overall rate of suicide, at 12.5per 100,000

92 11t For example, a person who dies from combined that persons who consume more than six drinks drug and alcohol ingestion may have planned a day as a group were twice as likely todie his or her death, or may have been unaware of from suicide over a 10-year followup period the way the substances could potentiate each than age- and sex-matched light drinkers and other. Likewise, a person who dies in a single- abstainers. It was not indicated whether these car accident after drinking might have de- people were drinking at the time, but suicidal liberately caused the accident or may have actions are more likely to be damaging when simply lost control of the vehicle. people have been drinking; combinations of Keeping in mind these research limitations, alcohol with other drugs often have greater theFourth Special Report (USDHHS 1981) lethal potential (Eckardt et al. 1981). cited studies- indicating between 15 and 64 percent of suicide attempters and up to 80 percent of suicides had been drinking at the Economic Costs of Alcohol Abuse time of the attempt. The wide range of percentages makes it difficult to assess whether Alcohol and Work Productivity drinkingis in fact causally linked with attempts. A review of violent deaths inthe Foregone work productivityiswidely ac- Cleveland area (Ford et al. 1979) found alcohol cepted to be an important component of the present in 25 percent of suicide victims. Of costs of alcohol abuse. The proliferation of course, determining whether drinking is inde- occupationally based alcoholism programs may pendently associated with suicide would re- In part be attributed to increased employer quire identifying populations of similar soci- awac ?mess of excessive alcohol use and com- oeconomic status, age, race, and sex as those promised job performance. No one has been who commit suicide. It is particularly impor- able to precisely identify the worker produc- tant to compare populations with similar so- tivity costs of alcohol abuse; the majority of ciodemographic characteristics,assuicides studies have examined simple measures such occur disproportionately among the young and as absenteeism. among older single males. The presence of A study of alcohol problems in seven rail- alcohol in the blood stream of a suicide at- road companies examined absenteeism as well tempter at the time of the act provides in- as several empirical measures of lost produc- sufficient data to conclude that alcohol is in- tivity. Problem drinkers had almost twice the dependently related to the attempt. Evidence absenteeism of other workers and cost the is available that alcoholism or a history of company an estimated $3.1 million, assuming drinking problems is more common among sui- 5.2 extra days of absence per year for the cide attempters. Roizen (1982) indicates that 8,670 employees for whom adequate attend- most studies reported that more than 10 per- ance records were available and based on an centofattempters andcompleters had average employee salary of $18,000 (Mannello drinking problems. 1979). Aarens et al. (1977) provide stronger data, Cost-benefit studies of occupational alco- comparing the proportion of problem drinkers holism programs generally support the claim or alcoholics in a random sample surveywith that productivity losses attributable to alco- Beck and associates' (1975) sample of suicide holic employees can be reduced. These studies attempters in two large metropolitan hospi- generally focus on absenteeism rates among a tals. The survey data were standardized by treated group of alcoholic workers before and age, sex, and marital status to matchthe sui- after an intervention.For example, Wood cide population. These data Indicatedthat (1980) suggested that an occupational alco- suicide attempters were four to six times holism program sponsored by New York Tele- more likely than the generalpopulation to phone Company saved the firm $1.5 million, report being problem drinkers or alcoholics. assuming that untreated alcoholics would have Several studies have also shown that, as a bten absent 60 days a year (and also that they group, alcoholics are more likely overthe would have incurred $2,000 in extra treatment course of their lifetimes to commit suicide. costs). Jones (1977) attributed to Kennecott Reviewing reports from 1935 to 1970, Miles Copper Company's alcoholism program a 52- (1977) estimated that 15 percent of alcoholics percent Improvement In attendance, on aver- ultimately complete suicide. Another review age, among the150 men who spent 12.7 suggests that 6 to 12 percent of alcoholics months in treatment. Saxe et al. (1983) have commit suicide, compared with 1 percent of recently reviewed similar studies of programs the population. Klatsky et al. (1981) reported in the Philadelphia fire and police forces

93 11'7 (Jones and Vischi 1979), General Motors, and vices, drugs and sundries, and other outlays the U.S. Air Force (Orvis et al. 1981). All the involved In the diagnosis, treatment, contin- studies indicate that reduced absences and uing care, rehabilitation, and terminal care for cost-effectiveness are associated with those alcohol-related illness and trauma. "Indirect programs. core costs" (estimated for 1977 at $36.8 bil- These studies focus primarily on absentee- lion) reflect the losses of productivityasso- ism andillnesscosts(notproductivityor ciated with alcohol-related morbidity ($26.1 working days), and they lack adequate controls billion) and mortality ($10.7 billion). Table 2 that would suggest causal inferences. They specifies the components of direct and in- explore only identifiedalcoholic employees direct core costs. and leave unresolved the crucial question of "Other related costs," $6.2 billion, include how these employees would have fared in the costs associated with motor vehicle crashes absence oftreatment. Whet' .er problem and fires and a proportionate share of soci- drinking causes substandard job performance ety's expenditures for administering the sys- or, conversely, substandard, unproductive, and tems of criminal justice, social welfare, fire hence unrewarded job performance contributes protection, and highway safety. Also counted to problem drinking remains unanswered. De- areproductivityforegonebyfamilyand velopment of more precise estimates con- friendsofalcoholics,productivitylostby cerning the amount of work productivity lost 83,700 individuals in prisons in 1977 for crimes because of drinking and the proportion that caused by alcohol abuse, and losses associated can be regained if employees with problems with automobile accidents experienced by in- are identified and offered assistance: should be dividuals other than crash victims. Table 3 a research priority in the 1980s. summarizes the breakdown of these other related costs. Estimating the Costs of Alcohol Abuse Cruze et al. (1981) specified that when data are limited or unavailable, their estimates Given the numerous social problems asso- tend to err on the conservative side. When ciated with or caused by alcohol abuse,some causal relations are imperfectly demonstrated attempts have been made toquantifyits between alcohol abuse and associated eco- economic costs to society. Two major esti- nomic costs, on the other hand, their estimation procedures have been used. The popu- mates tend to overstate the real costs. The lation-specificapproach (Berryand Boland issue of establishing causality was flagged by 1977; Berry et al. 1977) compared per capita an advisory panel as "one of the most impor- health care costs of alcohol abusers with those tantfactorsincarrying outthisstudy.... of nonabusers and multiplied the difference by Failure to recognize the difference between an estimate ofthe prevalenceofalcohol causality and association will lead to unreal- abuse, yielding a total cost of $42.8 billion in istically high estimates of the cost to society 1975. This approach has been criticized be- of alcohol abuse" (Cruze et al. 1981, p.D-3). cause itfails to make corrections for other The investigators nonetheless contend that, healthrisksmore common amongheavy overall, their estimates "lean strongly in the drinkers. This would tend to inflate the esti- conservative direction" (Cruze etal.1981, mates (Cruze et al. 1981). p.6-1). The alternative approach identifies specific Itis generally recognized that the total events or illnessesassociatedwith alcohol burden on society of alcohol abuse and alco- abuse. For example, in calculating treatment holism is substantially greater if social costs costs, the illness-specific approach includes all are considered. These include the pain and expenditures for illnesses attributable solely suffering of the alcohol abuser's family anda to alcohol abuse and, for illnesses with mul- hostofmedical,psychological,andsocial tiple causes, only those expenditures that can consequences that a full accounting of costs be ascribed to alcoholabuse.This system would ultimately have to include in one wayor would tend to produce a more conservative another. Few studies do more than grant that estimate. these intangible costs would add billions of Using this latter approach on 1977 data, dollars to the overall economic costs to soci- Cruze etal.(1981) estimated the national ety, assuming they could be measured accu- economic costs of alcohol abuse at $49.4 bil- rately In monetary terms (Cruze et al. 1981). lion. "Direct core costs" (an estimated $6.4 Nor has previous research ventured far into billion in1977) are expenditures for hospi- the analysis of the benefits of alcohol con- talization, outpatient care, professional ser- sumption, which from the standpoint of public Table 2. Estimated core costs for alcohol policy could be considered relevant.Apart abuse, 1977 from the personal pleasures that prompt so (in $ millions) many people to drink in the first place, the alcoholic beverage industry does make a sub- stantialcontributionto the economy. The Total core costs Willi Distilled Spirits Council of the United States, Inc., an associatin, of producers, Importers, Direct 372 and other yrepresentatives,reports Treatment 7,637 that the industry paid $15.7 billion In 1981 in Alcohol-abuse-specific illness taxes and other fees to Federal, State, and specialty setting 707 local governments and employed 826,000 peo- Alcohol-abuse-specific illness ple In 400,000 firms (DISCUS 1982). Addi- --general setting 2,001 tionally, as Gerstein (1981) points out, sales of Alcohol-abuse-related illness alcoholic beverages provide not only con- categories 1,711 tributions to government revenues and jobs in Gastrointestinal tract 220 the economy, but also an Important profit Liver disease 181 margin for many businesses. Nervous system 6 The question for our society seems to be not Heart 17 whether the benefits outweigh the costs, but Endocrine system 608 rather what can be done to reduce the con- Nutritional deficiency 108 siderable expense of alcohol abuse In terms of Cancer 171 human lives, illness, and suffering. Mental disorder 293 Infectious disease 107 Summary Alcohol-abuse-related trauma 1,217 Support 735 Research 28 In 1977, the last year for which there are Training and education 225 reliable estimates, alcohol cost the Nation Construction 193 approximately $50 billion- -about $26 billion in Health insurance administration 289 lost employment and productivity, $17 billion in health care, and $7 billion in property loss Indirect $36,789 and crime. Although the costs are almost Mortality 10 715 certainly much higher now after 5 years of Direct primary causes--alcohol 2,617 Inflation and sharply Increased health care psychosis, alcoholism, costs, alcohol's Impact transcends monetary alcoholic cirrhosis of liver, loss. In many fatalities, alcohol is an accessory alcohol poisoning before the fact. Direct secondary causes--cirrhosis 1,063 Traffic accidents, especially those involving of liver-other, malignant primary alcohol, continue to be a major problem in our liver neoplasms, other malignant society. According to one estimate,ifno neoplasms of gastrointestinal drivers drank in 1977, almost 12,000 deaths tract, pancreatitis, respiratory and perhaps 300,000 injuries would have been tuberculosis, other associated prevented. Drivers who drink in excess of the diseases legal Intoxication level are 3 to 15 times as Indirect causes--motor vehicle 7,035 likely as nondrinking drivers to be involved in crashes, falls, fires, other a fatal crash. Even moderate drinking atlegal accidents, homicides, suicides levels can Increase the likelihood of fatal ac- Morbidity 26,074 cidents.Furthermore, pedestrianskill:din Lost productivity 23,593 traffic accidents are 3 times more likely to be Males 20,178 Intoxicated than noninjured pedestrians. Females 3,415 Although accidents In the home and workplace have not been as extensively researched Lost employment ..wwwww2,481 Trauma 545 as traffic accidents, evidence Isample and Residential treatment 328 growing that alcohol contributes significantly Long-term disability 1,608 to their Incidence and severity. People who drink on the job are much more likely than their coworkers to have fatal accidents at Source: Cruze et al. 1981. work. Results Indicate that alcoholics and

95 119 Table 3. Estimated other related costs liable data are difficult to collect. Suicides for alcohol abuse, 1917 are higher among alcoholics, but drinking may (in $ millions) be a result of depression or other problems that in turn lead to suicide. More carefully designed studiesare required atgaingsaaatziluta 11,212 to establish unequivocally the potential adverse consequences ofalcohol.Meanwhile, Direct $ 4,441 there is clear reason for concern about the so- Motor vehicle crashes 1,782 cial effects of excessive alcohol consumption. Crime _11685 Public criminal justice system 1 479 References Law enforcement -313 Legal and adjudication 139 Corrections 1,027 Private criminal justicesystem 191 Aarens, M.; Cameron, T.; Roizen, 1; Roizen, R.; Law enforcement 184 Room, R.; Schneberk, D.; and Wingard, D. Alco- Legal and adjudication 7 hol, Casualties and Crime. Alcohol, Casualties Corrections - and Crime Project Final Report. Report No. C- Property loss/damage 18. Berkeley: Social Research Group, University 15 of California, 1977. 709 pp. Social welfare programs 142 Baker, S.P.; Samkoff, IS.; Fisher, R.S.; and Van Fire losses 319 Buren, C.B. Fatal occupational injuries. Journal Fire protection 482 ofthe American MedicalAssociation2ti8T6 T Highway safety 31 692-697, 1982. Barnard, G.W.,; Holzer, C.; and Vera, H. Compari- Indirect $ 1,772 son of alcoholics and nonalcoholics charged with Crime careers - rape. Bulletin of the American Academy of Psychiatry and the Law 7:432- 440, 1979. Incarceration 1 418 Homicide Barry, H. Motivational and cognitive effects of 274 alcohol.In:National Highway Traffic Safety Felonious assault 120 Administration.Alcohol,Drugs, andDriving, Robbery 46 Perrine, M.W., ed. Report No. DOT HS-801 096. Burglary 49 Washington, D.C.: NHTSA,1974. pp. 71-105. Drug laws 0 NTIS No. PB-232-111. Driving under the influence 287 Beck, A.T.; Kovacs, M.; and Weissman, A. Hope- Liquor laws 158 lessness and suicidalbehavior: An overview. Public drunkenness 461 Journal of the American Medical Association Other 234(10:114g-1149, 1975. 21 Berry, R.E., Jr., and Boland, J.P. The Economic Motor vehicle crashes 354 Cost of Alcohol Abuse. New York: The Free Press, 1977. 200 pp. Berry, R.E., Jr.; Boland, 3.P.; Smart, C.N.; and Source: Cruze et al. 1981. Kanak, J.R. The Economic Cost ofAlcohol Abuse 1975. Rockville, Md.: National Institute heavy drinkers tend to be involved in fatal on Alcohol Abuse and Alcoholism, 1977. 222 pp. falls, drownings, and fires. NTIS No. P3- 278 -606. More alcoholics and heavy drinkers than Blomberg, R.D.; Preusser, D.F.; Hale, A.; and Ul- mer, R.G. A Comparison of Alcohol Involvement abstainers are involved in homicides, as both in Pedestrians and Pedestrian casualties. Report victims and offenders. The alcohol association No. DOT HS-805 249. Washington, D.C.: National is somewhat weaker for other crimes such as Highway Traffic Safety Administration,1979. rape, theft, robbery, and assault. While there NTIS No. PB80-166275. are some statistical links between alcohol and Blum, R.H. Violence, alcohol and setting: An un- crime, factors other than alcohol may explain explored nexus. Ins Collins, II, Jr., ed. Drinking the relationship. and CrimesPerspectives on the Relationships Heavy drinking seems to affect family sta- Between Alcohol Consumption and Criminal Be- bility profoundly. In families with at leastone havior. New York: Guilford Press, 1981. pp. 110- alcoholic spouse, the rate of separation and 142. Borkenstein, R.F.; Crowther, R.F.; Shumate, R.P.; divorceisseven times that of the general Ziel, W.B.; and Zylman, R. The role of the population. Although some researchers have drinking driver in traffic accidents (The Grand speculated that the incidence of child abuse Rapids study). Blutalkohol 11(Supplement1):1- and spouse abuse may be alcohol-related,re- 1t2,--)9Z4. 14"w

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York State Division of Alcoholism and Alcohol Fourth Special Report to the U.S. Congress on Abuse, 1982. 50 pp. Alcohol and Health. DeLuca, 3.R., ed. DHHS Chapter VII Treatment: Emerging Trends in Research and Practice

During the past decade, several issues sur- classify a sick person as having a disease. The rounding the treatment of alcoholism have importance of diagnostic criteria derives from been subject to controversy. Does the unitary their usefulness in making clinical decisions, disease concept permit reliable diagnosis for estimating disease prevalence, understanding the purposes of early detection and treatment etiology, and planning treatment. While the planning? Is treatment effective and, ifso, diagnosis of alcoholism may seem straight- can the costs of treatment be contained? Are forward to the concerned layperson, Itis in there distinct subgroups of alcoholic persons? fact a complex process. Cantreatmentefficacybeimprovedby Limitations In current diagnostic procedures matching individual patients to specific types were recently reviewed by McIntosh (1982), of treatment? Should abstinence be the sin- who compared data collected in 31 studies of gular goal of treatment or can some problem the prevalence of alcohol-related problems In drinkers engageinnonabusive drinking?If general hospital populations. Variations in the some can, how can these individuals be iden- use of diagnostic criteria, as well as lack of tified? The issues raised by these questions conceptual precision In differentiating alcohol imply much about the theoretical and prac- dependence from related disabilities, have led tical challenges facing the treatment field. to widely differing prevalence estimates of This chapter will focus on the state of the the number of alcoholic patients. In spite of art of alcoholism treatment, giving special the fact that these patients were in hospitals, attention to developments not covered in the most individuals with drinking problems had Fourth Special Report (USDHHS 1981). These neither been diagnosed as such not received developments include innovations In diagnosis, appropriate treatmentfortheiralcohol improved procedures for screening and early problems. intervention, new findings on the costs and The traditional unitary disease concept of benefits of treatment, a continuing debate on alcoholism has been challenged by the obser- the use and viability of controlled drinking vation that there may be multiple patterns of therapies, and emerging models of treatment dysfunctionalalcoholuse,whichresultin efficacy. An encouraging development in re- multiple kinds of disability. A corollary of the cent years has been the enhanced investment unitary disease concept has been the assump- in research and clinical training in the alco- tion that alcoholics could be clearly differ- holism field, and the concomitant emergence entiated from nonalcoholics on the basis of ofa multidisciplinaryresearch community their distinctive disease characteristics. actively involved in the problems of treating Known as the binary classification rule, this alcoholism. As the quality and sophistication assumption has led to the search for universal of clinical research improve, it is likely that and singular criteria applicable to all alco- many ofthe unanswered questions will be holics.This dichotomous approach has not solved. been particularly helpful to programs interested In early Intervention (namely, secondary prevention), nor has It been useful in differ- Recent Advances in Diagnosis entiating prognoses within patient samples in and Nomenclature ways that could clarify important questions about treatment efficacy. An alternative approach (Marlatt1981) characterizes elcohol Diagnosis, the process of identifying and dependence along a continuum of severity, labeling specific disease conditions, uses pre- with no clear demarcation between the be- ciseattributes,ordiagnosticcriteria,to ginning of alcoholism and the end of social

100 124 drinking. An advantage of this approach is that and Fitzgerald 1981; Helzer et al. 1981; Hes- early detection may be improved when levels selbrock et al. 1982). Thus, while the DSM-III of risk have been established. alcohol-related diagnoses contain manyin- An important development in the area of novative features, the usefulness of this ap- diagnosis has been the publication in 1980 of proachforearlyidentification,epidemio- the third edition of the Diagnostic and Sta- logical surveys, and treatment planning re- tistical Manual of Mental Disorders(American mains to be evaluated. Psychiatric Association 1980), "better known as The recent development and successful field DSM-III. As a major revision of the manner in testing of two standardized interview sched- which various disorders, including alcoholism, ules,the Schedule ofAffectiveDisorders are diagnosed and classified,DSM-III intro- (Weissman et al. 1980) and the Diagnostic In- duced several innovations designed to address terview Schedule (Helzer et al.1981), rep- problemsinearlierclassificatorysystems resent a major advance in clinical diagnosis (Spitzer et al.1980). In contrast to previous and psychiatric epidemiology. Both schedules editions of DSM, alcoholism is now included provide objective, standardized procedures for within the separate category of substance use diagnosing alcoholism and other clinical syn- disorders rather than as asubcategory of dromes using DSM-III criteria. As these in- personality disorder. Reflecting a trend struments are used greater frequency to toward increased semantic precision, the term study clinical and population samples, they "alcohol dependence" is used in preference to promiseto advance basic knowledge about the more generic "alcoholism." In addition, a alcoholism and its relationships to psychiatric separate category of "alcohol abuse" isadded syndromes andpersonalitydisorders.Data to permit greater differentiation. As deline- from household surveys using the Diagnostic ated in table1,alcohol dependence isdif- Interview Schedule in three National Institute ferentiated from alcohol abuse by the pres- of Mental Health Epidemiology Catchment ence of tolerance or withdrawal symptoms. Areas suggest that, at some time during their Both diagnoses include a pattern of patho- lives, one in seven adults 18 years of age or logical use or impairment in social or occupa- older met criteria for alcohol abuse or alcohol tional functioning dueto alcohol.Modeled dependence. after diagnostic procedures initially developed A related development in the area of alco- for research purposes (Feighner et al.1972), holism diagnosis is the international program these criteria provide a systematic, stand- ondiagnosisand classificationsponsored ardized approach to diagnostic decisionmaking. jointly by the U.S. Alcohol, Drug Abuse, and DSM-III permits evaluation of the individ- Mental Health Administration (ADAMHA) and uaFTZ6ridition in terms of five independent the World Health Organization (WHO1982). dimensions or axes. Axis I describes the major Th, purpose of this project is to recommend clinicalsyndromes,includingsubstance use improvements in sections of the International disorders, while Axis IIis reserved for con- Classification of Diseases iICD) dealing with comitant personality disorders. AxisIII alcoholism, drug abuse, and mental health. The classifies physical disorders and conditions, a first phase was devoted to a systematic exam- number of which can be coded as alcohol- ination of concepts and nomenclature per- induced, including alcohol intoxication, alcohol taining to alcohol and drug abuse (Edwards et withdrawal, alcohol withdrawal delirium, al- al. 1981). Of particular interest to the alco- cohol hallucinosis, alcohol amnesticdisorder, holism treatment field is the emerging set of and dementia associated with alcoholism.Axis concepts, definitions, and criteria that may IV draws attention to the severity of psycho- well provide the basis for the next revision of social stress (e.g., occupational, interpersonal, ICD. Central to the WHO approach to alco- physical) that may modify the course of the holismis the concept of a dependence syn- current disorder. Finally, Axis Vpermits the drome thatisdistinguished from alcohol- clinician to indicate the patient's highest level related disabilities (Edwards et al. 1976,1981). of adaptive functioning during the past year in As outlined in table 2, the dependence syn- terms of social relations, occupationalfunc- drome is an interrelated cluster of cognitive, tioning, and use of leisure time. behavioral, and physiological symptoms. Preliminary evaluations of DSM-III suggest Alcohol-related disabilities, on the other hand, thatitprovides reliable and valid identifi- consist of those physical, psychological, and cation of alcoholics in clinical settings,but socialdysfunctions that follow directlyor that it may be less useful in detecting alco- indirectly from excessive drinking and holics who are not institutionalized(Mulford dependence.

101 125 Table 1. DSM III criteria for alcohol abuseand alcohol dependence

Diagnostic criteria for alcohol abuse Diagnostic criteria fo0 alcohol dependence

A. Pattern of pathological alcohol use: need A. Pattern of pathological alcoholuse: need fordailyuseof alcoholforadequate fordailyuse ofalcoholforadequate functioning, inability to cut downor stop functioning, inability to cut downor stop drinking, repeated effortsto control or drinking, repeated efforts to controlor reduce excess drinking by "goingon the reduce excess drinking by "goingon the wagon" (periods of temporary abstinence) wagon" (periods of temporary abstinence) or restricting drinking to certain times of or restricting drinking to certain times of theday, binges(remainingintoxicated theday,binges(remainingintoxicated throughout the day for at least 2 days), throughout the day for at least 2 days), occasional consumption ofa fifth of spirits occasional consumption of a fifth of spirits (or its equivalent In wineor beer), amnesic (or Its equivalent In wineor beer), amnesic periods for events occurring while Intox- periods for events occurring while intoxicated (blackouts), continuation of drinking icated (blackouts), continuation of drinking despite a serious physical disorder thatthe despite a serious physical disorder thatthe individual knows is exacerbated by alcohol individual knows Is exacerbated by alcohol use, drinking of nonbeverage alcohol. use, drinking of nonbeverage alcohol. B. Impairmentin social oroccupational B.ImpairmentInsocialoroccupational functioning doe to alcoholuse: violence functioning due to alcoholuse: violence while intoxicated, absence from work, loss while intoxicated, absence from work,loss of job, legal difficulties (e.g.,arrest for of job, legal difficulties (e.g.,arrest for intoxicatedbehavior,trafficaccidents intoxicatedbehavior,trafficaccidents whileintoxicated),argumentsordiffi- whileintoxicated),argumentsordiffi- culties with family or friends because of culties with family or friends because of excessive alcohol use. excessive alcohol use.

Either tolerance or withdrawal:

C. Duration of disturbance of at least 1month. C. Tolerance: need for markedlyincreased amounts of alcohol to achieve the desired effect, or markedly diminished effect with regular use of the same amount.

D. Withdrawal: development of alcoholwith- drawal (e.g., morning "shakes" andmalaise relieved by drinking) after cessation ofor reduction in drinking.

Source: American Psychiatric Association 1980.

According to the WHO dependence model, a phasizing that both dependence andalcohol- complete description of an individual's alco- related disabilities exist in degrees ratherthan hol-related pathology must includestatements in an all-or-none state. concerning the nature and severity of de- In the brief period since itwas first intro- pendence, the kinds and degrees of disability, duced, the dependence syndrome constructhas and the personal and environmental factors receivedconsiderableattentionfromre- that influence the drinking problem. The WHO searchers and clinicians. A number ofin- model departs significantly from DSM-III and struments have been developed to assess its the older binary classification schemes byem- usefulness (Stockwell et al. 1979; Skinner and

102 1 26 Table 2. Constituent elements of the alcohol dependence syndrome

Elements Interpretation/examples

Narrowing of the drinking repertoire The drinking pattern tends to become stere- otyped around a regular schedule of almost continuous daily consumption.

Salience of drink-seeking behavior Drinking is given higher priority than other activities in spite of its negative consequences.

Increased tolerance to alcohol More and more alcohol Is required to produce behavioral, subjective, and metabolic changes; large amounts of alcohol can be tolerated.

Repeated withdrawal symptoms Tremulousness, sweatiness, nausea, etc., appear after short periods of abstinence.

Relief drinking Withdrawal symptoms are relieved or avoided by further drinking, especially in the morning.

Compulsion to drink Subjective awareness of craving for alcohol exists, as well as impaired control over quantity and frequency of intake.

Readdiction liability The syndrome tends to be rapidly reinstated when drinking is recommenced after a period of abstinence.

Source: Adapted from Edwards et al. 1976, 1981.

Allen 1982; Hesselbrock et al. 1983). Research specificity of treatment, an important goal in inboth experimental andclinicalsettings the delivery of treatment services for three suggests that the severity of dependence can essential reasons: (1) economy of cost,(2) correlatepositivelywithattendanceata avoidanceofinappropriateorineffective treatment clinic(Skinner and Allen1982), treatment, and (3) increased efficacy. Sur- cravings for alcohol after a "priming" drink prisingly, outside the area of personality as- (Kaplan et al.1983), and failure to control sessment, little interest has existed until re- drinking following relapse (Orford et al. 1976; cently In differential assessment of the alco- Polich et al. 1981). While further research is holic person. This is due In part to assumptions needed, the dependence syndrome construct about the unitary nature of alcoholism, and in shows considerable promise for early detec- part to the limited methods available to eval- tion, diagnosis, and treatment planning. uate alcoholics. Recent advances in evaluation methodology Differential Assessment (Meyer et al. 1981) have stimulated research in this area, and a number of assessment pro- BothOSM-Ill andthe WHO dependence cedures have been developed. In addition to model reiggirii a general movement toward those already discussed, several investigators differential assessment as evidenced by the (Skinner and Allen 1982) have demonstrated use of multiple criteria to provide a compre- the usefulness of assessing drinking patterns hensive evaluation for treatmentplanning. and alcohol-related problems in an effort to Ideally, specificity of diagnosis should lead to identifyindividualdifferencesrelatedto

103 2 treatment outcome. Other instruments have Psychosocial, Clinical, and been developed recently to providediffer- Combined Assessments entialassessmentofstagesofalcoholism (Mulford1980),clientliabilitiesassociated Because some psychosocial symptoms (e.g., with poor treatment response (Costello and escape drinking,concern about a drinking Baillargeon 1981), severityofaddiction- problem, alcohol-related accidents) may ap- related problems (McLellan et al.1980), and pear relatively early in the alcoholic's drinking stability of the male alcoholic's marital sit- career, their assessment by means of inter- uation (O'Farrell et al. 1981). With the bur- views or self-administered questionnaires has geoning application of computer technology to received increasing attention by researchers individual testing and statistical data analyses, Interestedinscreening and early diagnosis the benefits of differential assessmentmay (Skinner et al. 1981). well become routine in clinical settings. Clearly, the most investigated self-administered diagnostic instrument continues to be theMichiganAlcoholism Screening Test Screening and Early Detection (MAST). Consisting of25 true/falsestate- of Alcoholism ments describing the typical medical, social, and behavioral problems associated with excessive drinking, the MAST has demonstrated Consonant with recent conceptual devel- a considerable degree ofvalidity indistin- opments in the diagnosis of alcoholism, there guishing between known groups of male alco- has been increasing interest in the develop- holics and male nonalcoholics (Brady etal. ment of a simple and accurate screening pro- 1982). Concurrent with validation of the MAST cedure that could facilitate earlyidentifi- has been the development of a variety of cation of alcohol dependence. Clearly, early similarscreeninginstruments(Brownand casefinding can improve the effectiveness of Lyons 1981; Skinner et al.1981). These tests treatment and reduce its costs. Research on are rapid, inexpensive, and relatively accurate earlyidentificationhas progressed on two when used underproperconditions.Their relatively independent planes: (1) the search simplicity,or genderspecificity,however, for biochemical markers for alcoholism and (2) may limit their usefulness for general popu- the elucidation of psychosocial indicators. lation screening, particularly as the obvious intent of the questions leaves them vulnerable todeliberatefalsificationorunconscious Biochemical Markers denial. Recognizing that psychosocialtests have The accumulation of research findings, some limitations when used inisolation,investi- of which have already been noted in previous gators have begun to use clinical, laboratory, chapters of this report, suggests that several and psychosocial tests in combination. The laboratory tests may be useful inthe early results of one study (Skinner et al. 1980) un- detection of alcohol abuse. Serum gamma- derscore the advantages of this approach. Us- glutamyltranspeptidase(GGTP) hasbeen ing the Munich Alcoholism Test, a new In- suggested as an indicator of heavy alcohol strumentthat combines clinicalsigns and consumption among problem drinkers (Reyes symptoms (as identified by the physician) with and Miller 1980). Although its useLdness may self-report information provided by the pa- be affected by concurrentliverpathology, tient, it was found that the two types of in- drug use,and individualdifferences among dicators occurred with relative independence heavy drinkers (Garvin et al.1981), its dis- of each other. Psychosocial problems predom- criminative abilityis enhanced considerably inated in the younger patients, while clinical when interpretedin conjunction with mean signs and symptoms were more frequent in the corpuscular volume (MCV) and othertests older drinkers. (Mayfield and Johnston1980; Chick etal. 1981). That routine blood chemistriesmay be a From Screening to Early Intervention usefuladjunctfordetectingalcoholismis suggested by the results of several studies Developments 'in several countries indicate (Ryback et al.1980, 1982) that have found that concerted efforts are now underway to that the profiles of 25 biochemical tests dif- link new screening technologies to low-cost ferentiatedbetween knownalcoholicsand earlyinterventionstrategies.Buildingon nonalcoholics with a high degree of accuracy. previous research (Edwards et al. 1977), which

104 12 S suggested that one session of advice can be as emphasis away from the sole identification of effective as conventional treatment for some alcohol problems to include any employee alcoholics, a pilot program is currently being problem that adversely affects performance evaluated in Scotland to determine the ef- (Roman 1981). In the more recently developed fectiveness of a brief intervention with prob- employee assistance programs, the role of lem drinkers identified in a general hospital supervisor as diagnostician has been deempha- setting (Chick et al. 1982). Preliminary results sized in favor .of the more traditional roles of of a 1-year followup indicate that a single supervising performance and focusing on un- 35-minutecounselingsessionmayreduce acceptable changes in performance as the drinking and its consequences in a significant basis for intervention and referral. proportionof newly identified problem One recentstudyinvestigated how the drinkers. threat of disciplinary action affects treatment In Sweden, an early intervention program outcome (Freedberg and Johnston 1980). Men was conducted with middle-aged heavy who chose to enter treatment as an alterna- drinkers identified by means of elevated GGTP tive to disciplinary action were compared with values (Kristenson 1982). Individuals randomly others who sought treatment voluntarily. Both assigned to a control group received advice to groups were similar with respect to jobfunc- limit their alcohol consumption. Those as- tioning and drinking behavior after 1year, a signed to an intervention group were repeat- finding that denotes the disciplinary process as edly encouraged to drink less and, In addition, a useful way to engage employees in treat- received feedback about their GGTP levels. ment. Moberg et al. (1982) report followup Compared with the controls, the intervention data on several hundred inpatients from an group showed significantreductionsin ab- abstinence-oriented industrial program. Forty- senteeism, hospitalizations, and mortality up six percent were abstinent 3 months after to 6 years after the initial screening. treatment, while 37 percent were abstinent In France, screening for problem drinking after9months.About 20percentwere and alcohol dependence is conducted routinely drinking moderately at each followup,but inindustry,health care settings,andthe those listed as moderate drinkers at 3 months courts. Individuals identified by means of a had a high relapse rate 9 months after treat- simple clinical exam (the Le Go grid method) ment. Although social support andemployer and biochemical tests (GGTP and MCV) are involvement had a positive influence on out- referred to a nationwide system of more than come, type of referral(voluntary vs. coercive) 130 early intervention clinics. While the ef- made little difference. fectivenessoftheseclinicshasnotbeen Despite increasing interest in the evaluation studied systematically, the program demon- of occupational programs, the relative lack of strates that, from a public health perspective studies in this area, together with limited ac- (Babor et al.1983), early intervention in a cess to the worksite, havemade it difficult to large population is now feasible. assess the overall contributionof these programs to improved job performanceand reduced health care costs. Job-Based Interventions The process by which problem-drinking employees within a work organization are iden- Alcoholism Treatment: Programs tified and engaged in treatment has been the and Therapeutic Approaches subject of much discussion (Googins and Kurtz 1980; Roman 1982). Initially, it was advocated that supervisors and managers be trained to The treatment system that emerged fol- identify impaired job performance, and then to lowing the Second World War is varied, com- confront the employee to determine the nec- plex, and still in the process of development. essarycorrectiveaction.Supervisorshave Many of its programmatic components (e.g., been found to be inconsistent in confronting detoxificaticn facilities, inpatient hospital and their problem-drinking employees (Kurtz et al. residentialprograms,halfwayhouses,and 1980), depending on their own attitudes about outpatient clinics), and the therapeutic ap- alcohol use and abuse and their perceptions of proaches employed in these components, have the union's support for the program(Beyer et only recently begun to receive systematic real.1980). With the impressive expansion of search attention. What is the most appropriate job-based employee assistance programs dur- setting for treatment? What are the most ef- ing the past decade, there has been a shift in ficacious therapeutic approaches? What is the

105 X29 optimal reimbursement policy for medicare, settings. Moreover, while the proponents of medicaid, and private insurance carriers? social setting detoxification contend that it will facilitate referrals to long-termtreat- Detoxification ment, insufficient evidence exists to conclude that this type of referral willoccur more ef- The management of acute alcohol intoxi- ficiently In either social or medical settings. cation and the concomitant alcohol withdrawal What Is clear from the experience ofnon- syndrome Is commonly referred toas detoxi- hospital detoxification programs Is that medi- fication. In the late 1960s, specialized detox- cally oriented inpatient detoxificationmay not ification facilities were developed to address be necessary for the majority of referrals who the needs of the public inebriate; these fa- are not severelydependent and who are cilities expanded rapidly following widespread otherwise In good health (Diesenhaus 1982). adoption by the States of the 1974 Uniform With the Increasing availability of ambulatory Alcoholism and Intoxication Treatment Act and inpatientsocialsettingdetoxification, decriminalizing public Intoxication. At first careful study of the nature and role of detox- these facilities were closely associated with ification In the rehabilitation process would hospital emergency servicesbut in recent seem warranted. The long-range implications years several alternatives to hospital-based of this trend need to be considered. detoxification have emerged. A recentsurvey The high rate of relapseamong detoxified of State Alcoholism Authorities (Den Hartog patients Is another major concern to service 1982) indicated a threefoldincrease in the providers. Although it may be unrealisticto number of States operating or purchasingnon- expect an initial care component toaccom- hospital-based detoxification since 1975. The plish much more than detoxification andre- most controversial of these alternatives has ferral, at present a small proportion of the been "social setting" detoxification, in which public inebriate population utilizesa dispro- the use of drugs such as diazepam and chlor- portionate share of detoxification resources. diazepoxide is avoided in themanagement of Further, these patients often refuserecom- withdrawal in favor of a supportive social mended referrals to intermediatecare facil- climate designed to engage the patient In ities. One study of a predominantly skidrow further treatment. population (Fagan and Mauss 1978) found that Because the different detoxification fewer than one-third accepted theirrecom- methods have not been assessed directly in mended treatment referral after detoxifica- controlled comparisons, little Is known about tion. Another study (Richman and Smart 1981) the relative merits of various approaches in found that the probability of further referral relieving the distress associated with alcohol was lowest In those patients having a history withdrawal, preventing the risks of medical of multiple detoxifications. Two possib.so- complications, and facilitating theprocess of lutions to the problem of "resource absorption" referral to long-term treatment. The need for by detoxification repeaters have beensug- hospital-based, medical detoxification, as well gested. The first is the greater availability bf as the referral to social setting facilities, de- comprehensive services to the skidrow popu- pends on the patient's physical condition,nu- lation; the second is the use of legal coercion tritional status, severity of alcohol depend- to motivate the public inebriate to enter and ence, and overall medical evaluation. remain in treatment (Fagan and Mauss 1978). The growth of social setting detoxification has resulted from Its lower cost, the changing Benefits of Treatment attitudes about theuse ofsedatives and tranquilizers in withdrawal management, and The rapid growth of insurance coverage for evidence indicating that a significant number alcoholism treatment has been predicated in of patients do not experience serious medical part on the assumption that such treatment is complications during withdrawal (Diesenhaus cost-beneficial,i.e., the long-term costs to 1982). A recent review of the publishedlit- both the individual and society will bere- erature in the United States, Canada, and duced. Alcoholics and their families have been Europe (Den Hartog 1982) concluded that de- found to use a disproportionate amount of in- toxification could occur humanely, safely, and patient and outpatient medical services fora efficiently in nonhospital settings. Thesere- wide variety of physical problems relatedto ports need to be substantiated by systematic excessive drinking (Roghmann etal.1981; research, since it is not clear what proportion Putnam 1982a). Reflecting an Increasedcon- of alcoholics require detoxification In hospital cern with the implications of treatment reimbursement policy, a number of new studies inappropriate care and receiving inappropriate have used the improved methods of cost- treatment,sincethealcoholismunderlying effectivenessandcost-benefitanalysisto their illness was often not properly diagnosed. show that cost savings can be accrued over a In a related study of the same HMO (Putnam period of time (Swint and Nelson 1977). The 1982b),alcoholics who received outpatient firstmajor reviewofresearch conducted alcoholismtreatment were compared with during the 1970s (Jones and Vischi 1979) found alcoholics who were identified but refused to surprising consistency across 12 studies. De- accept treatment. An examination ofthe spite some methodological problems,these utilization rates for medical care services studiesindicatedsignificantreductionsin before and after referral to treatment re- medical care use and expenditures related to vealed that both groups showed a higher level various kinds of alcoholism treatment, of service use In the 4-month period prior to amounting to a 40-percent median reduction In referral.Those whoacceptedalcoholism sick days and accident benefits. Additional treatment,however, showedaprogressive studies since that time have confirmed this decrease in use of services during the subse- conclusion (Saxe et al. 1983). quent period, while those who refused treat- Substantiating these findings is a recently ment increased their demand for services ap- conducted study of State employees of Cali- proximately 15 months after the attempted fornia in which 90 families with an alcoholic referral. This increase is related to a high in- member,allenrolledinBlueCross/Blue cidence of problems associated with accidents, Shield, were followed for a period of 5 years. drug overdoses, and violence, and highlights Results indicated that the total medical care the importance of appropriate diagnosis and costsperfamily member decreasedsub- treatment to reduce both the human and the stantially over time once the alcoholic mem- social costs of alcoholism. ber entered treatment (Holder andHallan Finally, a significant non-HMO-based study 1981). (Holder and Hai lan 1981) followed the families These studies have been conducted predom- of 90 State employees in California for a inantly within health maintenance organiza- period of 5 years. Each family had an alcoholic tions (HMOs), primarily because alcoholics are member and all were enrolled in Blue Cross/ relatively easy to track within these compre- Blue Shield. The study indicated that total hensive health programs. A major study of medical care costs per family member de- alcoholism treatment in HMOs recently com- creased substantially over time once the al- pleted by the Group Health Association of coholic family member entered treatment. At America (Plotnick et al. 1982) compared the the end of the study, inpatient costs per per- utilization of four HMO outpatient alcoholic son per month of both the comparisonfamilies treatment programs by alcoholic persons from (N=83) and the alcoholic families (N=90) were 2years beforeentering treatmentto48 similar, and outpatient costs of the compari- months after treatment. The study revealed son families were actuallyhigher. significant reductions in general health care Although many of the studies of alcoholics' use for the alcoholic persons and theirfamily use of health services arelimited in scope, members. In another HMO study (Forsythe et methodology, and populations investigated, the al.1982), treated alcoholics were compared evidence suggests that: (1) alcoholics and their with nonalcoholics over a 4-year period. Al- families initially use more health care services though the cost differential between the two than nonalcoholics; (2) this elevated demand groups was substantial during the entirestudy can be reduced substantially by treatmentfor periods, there was a significant decline in al- alcoholism; and (3) the benefits of alcoholism coholics' demand for services following re- treatment clearly outweigh its costs. ferral to treatment. Focusing on the illnesses that may precip- Treatment Settings itate alcoholics' referral to treatment, Put- nam (1982a) found that alcoholicsmanifested Studies comparing the effectiveness of in- a high number of physical andemotional ill- patient programs with outpatient and day nesses. Problems most likely to be associated hospital treatment are important because of with the alcoholics' hospitalizations entailed the potential for Improved cost-effectiveness psychosocial difficulties such as anxiety, de- and the appeal these approaches may have for pression, and marital discord, as well as ac- alcoholics who reject inpatient or residential cidents, drug overdoses, and violence. In many care. In one study (Longabaugh et al. inpress), cases, the alcoholics were found to beseeking patients participating in a day hospital pro-

1" 1 3 gram (while returning home at night) were In the natural process of identifying alcoholics given the same behavioral treatment program and referring them to treatment (Paulson and that hospitalized inpatients were receiving. At Kaufman 1981; Beckman and Kocel 1982). De- 6-month followup, both groups were compa- spite the increasing variety of programs, set- rable on measures of drinking behavior, need tings, and treatment modalities, many alco- for rehospitalizations, and social and occupa- holics do not have the opportunity to find an tional functioning. The partial hospitalization informal match between their own specific group was superior on measures of psycho- needs and the type of treatment available. logical well-being. Given the lesser cost of This is particularly true of special needs pop- partial hospitalization, the authors conclude ulations, such as women, ethnic minorities, the that this form of treatment is more cost- multidisabled, the elderly, and skid row alco- effective. In another study, comparable find- holics. For these groups, access to treatment ings are reported after 1-year followup of 100 and successful rehabilitation are often imped- patients who were randomly assigned either to ed by cultural barriers, financial constraints, a day clinic or to an inpatient facility offering andprogramdesigncharacteristics.Since a similar treatment program (McLachlan and considerable attention has already been given Stein1982). These results sunrort thecon- to the needs of these groups in the Fourth clusion that the two types of treatment set- Special Report (USDHHS1981)and other ting may be equally effective. sources (Diesenhaus 1982; NIAAA 1982), this Studies comparing the results of Inpatient section will provide a brief update on the is- and outpatient programs have generally not sues common to all special needs populations. shown significant differences in the effects of Because middle-aged white men represent treatment setting (see review by Cole et al. the typical clientele of most treatment fa- 1981). However, it seems likely that day hos- cilities, programs often are not designed with pital and outpatient treatment programs will the needs of other groups inmind. These prove to be substantially less effective for groups may thus be reluctant to seek help be- certain groups of patients, and Spicer et al. cause of a number of structural and group- (1981) caution that conclusions regarding equal specific barriers that restrict access to ap- effectiveness should be limited to clients who propriate facilities. For example, a survey of are appropriate for each type of program. 53 California treatment facilities (Beckman Many studies comparing outpatient with in- and Kocel 1982) suggested that women alco- patient treatment have not controlled for the l'olics were less likely to enter programs possibility that patients choosing outpatient lacking child care services, professional staff, settings are less severely dependent. Inpatient and aftercare programs. However, Institute treatment seems indicated when motivation is experience in providing services for women weak to continue treatment, when patients are reveals that many women do not utilize child psychotic, depressed, or suicidal,and when care services even when provided. Other bar- complicating physical disabilities are present. riers to treatment for some groups are lan- Other factors which may also influence the guage differences and composition of treat- choice of treatment setting include patients' ment staff. Minority staff members represent social stability and the number and severity of only a small proportion of the Nation's alco- their symptoms,, as well as the ability of pro- holism treatment personnel (NIAAA 1980). Yet grams to respond to individual needs (Cole et another barrier may be financial constraints. al.1981; Spicer etal.1981). Researchis Women and minorities tend to be overrep- needed to identify the characteristics of pa- resented in publicly funded facilities and un- tients most likely to benefit from an outpa- derrepresented in private ones (NIAAA 1980). tient program, followed by treatment-match- Without programs' sensitivity to the needs of ing studies to test the validity of the identi- these populations, many individuals may fall to fied patient types. An additional obstacle to seek treatmentuntiltheiralcoholismhas the substitution of residential treatment by reached a severe stage of development. outpatient treatment Is the high rate of client With the growing recognition that utiliza- attrition usually encountered In the outpatient tion rates may be Improved by removing bar- setting. riers to access, greater attention Is now being given to special population groups in the de- Matching Clients with Programs sign of treatment programs. Some facilities seeking to attract Hispanic and Native Amer- Considerable selection takes place on the ican clients are using folk medicine and native part of both the client and the referral agent healing approaches as alternatives or adjuncts 132 108 to traditional medical and psychiatric treat- ology, as firm conclusions about efficacy can ments. Counselors and other treatment staff be made only through systematic comparisons. members are being matched to the sex and ethnic background of their clients. Also, con- Behavior Therapy veniently located, community-based programs, at times staffed and planned in collaboration Behavioral elements most frequently applied with special population groups, are appearing in treatment programs Include social skills and more frequently (NIAAA 1982). assertivenesstraining,contingency manage- What is uncertain, at this time, is the im- ment, deep musclerelaxation,self-control pact the ADM block grant program will have training, and cognitive restructuring (Miller on treatment programs. Of particularinterest and Mastria 1977). Despite their widespread will be the differential rates of service use adoption, these methods have not been subject across States, by both the general population to systematic evaluation with random assign- and special population groups. As these pro- ment of large numbers of patients to various grams become available to special population treatment conditions. groups, research will need to move from pro- Aversion therapy.This approach to treat- gram descriptions to actual evaluation studies ment grew from Pavlovianconditioning in which programs designed for special popu- theory, which predicts that the sight, smell, lation groups are compared with more tradi- and taste of alcohol will acquire aversive tional approaches. properties if repeatedly paired with noxious One exception to the trend to develop ser- stimuli. A thorough review of the research in vices for special population groups and sub- this area (Miller and Hester 1980) concluded types of alcoholic persons has been the small that emetic (nausea producing) aversive con- number of combined programs serving both ditioning can be effective for employed, mar- alcoholics and drug dependent persons. Al- ried, well-motivated alcoholics, but that the though combined treatment for alcoholics and effectiveness of electrical aversion Is doubt- drug abusers has not been widely adopted, the ful. These conclusions are supported by recent feasibility of such programs may have Im- work (Cannon et al. 1981) comparing these two portant implications for the planning of future aversion procedures when used In addition to a treatment services, given the increased tend- standard treatment program. Patients exposed ency for patients to present multiple abuse or to emetic conditioning exhibited significantly addiction patterns at the time of treatment greater improvement after 6 months than pa- (Sokolow et al. 1981). tients exposed to conditioning with electric shock, but the advantage after 1 year was not significant. Therapeutic Approaches Work has also proceeded on covert sensitization, a procedure in which imagined scenes of alcohol ingestion are paired with nausea Several diverse treatments are often de- induced by verbal suggestion. This method may livered within the context of alcoholism ser- overcome some of the practicaldisadvantages vices, depending on the resources and needs of of emetically based aversion therapy. Some clients, as well as the specific training or recent studies have offered support for this orientation of the staff.In many cases, a procedure. One study found that patients re- combination of therapeuticinterventionsis ceivingcovertsensitizationremainedab- provided to all clients, under the assumption stinent longer and demonstrated better psy- that multiple treatments stand a good chance chosocial adjustment than patients In control of meeting at least some of each client's groups (Elkins 1980). In a related study, pa- needs. As the alcoholism treatment system has tientsreceiving covertsensitizationin a grown in size and complexity, evaluating in- standard inpatient treatment program showed dividual therapeutic approaches inisolation greater improvement over a 4-year period from one another has become more difficult. than patients who received insight-oriented Many studies reported in the literature Involve therapy (Olson et al. 1981). adding a treatment of Interest to a facility's Extinction.--Recent experiments have shown standard therapeutic program, or are descrip- that alcohol-related stimuli (such as the sight tive evaluations rather than clinicaltrials or smell of an alcoholicbeverage) can induce comparing one or several treatments with the both physiolobical changes and altered absence of treatment. Studies discussed here behavior In alcoholic patients (Kaplan et al. generally employed an experimental method- 1983; Pomerleau et al. 1983). Because condi-

109 1.1 toning processes related to alcohol craving moderately 6 months after treatment and of and tolerance developmentmay affect the maintaining moderation up to 12 months later. rapidity of relapse after a period of absti- More recently, Moos, Finney, and Chan (1981) nence, some have proposed that conditioned foundthat 12 monthsafterabstinence- extinctionbe made anessentialpartof oriented treatment, 25 percent of therecov- treatment (Hinson and Siegel 1980). Extinction ered patients were drinking in moderation. It of the effectiveness of alcohol-relatedcues is should be noted that the term moderation In achieved by repeatedly presenting themun- these studies refers toan average consumption accompanied by either alcohol ingestionor of less than 5 ounces of absolute alcoholper intoxication. This may theoretically weaken day, in the absence of alcohol-relatedsymp- the link between these stimuli and drinking toms, work problems, or rehospitalizations. behavior, with a consequent improvement in Several explanations for these findingsseem treatment outcome. To date, a few successful to be emerging from studies employing longer case studies have been reported (e.g., Blakey followup intervals and more refinedassess- and Baker1980).Additional systematic in- ments of patient characteristics. The second vestigationshouldclarifythese data from part of the Rand study (Polich et al.1981) clinical research studies. revealed that the relapse rate 4 years after Coping skills training.-- Behavior therapists treatment was higher(41percent) among have recognized the importance of teaching those who had been drinking moderatelyat 18 new, adaptive coping skills to patients who months than among those who had been ab- engage in dysfunctional behaviors. These skills stinent at that time (30-percent relapse rate). include altering conditions beforeor after Other research (Orford et al. 1976; Finney and drinking, as well as developing alternative Moos 1981), as wellas the Rand studies, sug- ways of coping with persons, events, and feel- gests that those individuals characterized as ings that may have served to maintain abusive moderate drinkers at followup tend to have drinking (Miller and Mastria 1977). A number had less severe alcohol dependence and fewer of studies have demonstrated the benefits of drinking problems prior to treatment. A 2-year teaching social and other coping skills (e.g., followupofpatientsreceivingabstinence- Ferrell and Galassi1981; Oei and Jackson oriented treatment (Finney and Moos 1981) 1980,1982), although others havenot con- compared persons drinking moderately at 6 firmed these findings (c.f., Sanchez-Craig and months following treatment withpersons who Walker 1982). Chaney et al. (1978) have tested abstained. Those who returned to moderate a cognitive-behavioral model of treatment, drinking soon aftertreatment were more characterized as "relapse prevention" because likely to relapse to heavy drinking than those of its focus on identifying highrisk situations. who remained abstinent for 6 months and who Patients given skills training had lesssevere then attempted moderate drinking. Thus, while (though nolessfrequent)relapse episodes, moderate drinking seems possible forsome were more likely to be employed, and attended patients following treatment, this phenomenon aftercare moreregularlythan patientsin may be explained by the highly variable course control groups. A replication with alcoholic of alcoholism over time (some alcoholics take persons of higher socioeconomic status than longer to relapse than others), and by the the population originally studied found both existence of individual differences amongpa- skilltraining anddiscussion groupsto be tients in severity of alcohol dependence, social superior to a minimal-treatment group, but supports for moderate drinking, and a variety not different from each other (ones et al. of other mitigating factors. 1982). Further study should capitalizeon the Another possible explanation liesInthe increasingly widespread use of these methods. nonstandard interpretation of the term alcoholic. In many studies that report moderate Selecting Treatment Goals drinking by alcoholics, little information has been provided about the patients' severity of Interest in therapies withalternative dependence, history of alcohol abuse, orex- drinking goals was sparked in part by findings tent of alcohol-related disability. In studies that a small proportion of treated alcoholics reporting such data, moderate drinkingpa- reportedly were able to return to moderate tients tend to be less "alcoholic" at the time drinking without serious problems (Pattison they enter treatment. Had stringent criteria 1976). The Rand study (Armor et al. 1978), for for alcohol dependence been applied,itis example, reported that some "definitely al- conceivable that the drinking problems of coholic" persons were capable of drinking many of these patients would be classified as

110 134 alcohol abuse rather than alcoholism.Similar In summary, the Issues surroundingmoder- semantic problems cloud the meaningof mod- ate, nonproblem drinking as a viable treatment eration. Several studies (Armor et al.1978; option for nonalcoholic problem drinkers are Moos et al. 1981) have Included amounts of up not likely to be completelyresolved until to 5 ounces of absolute alcohol per daywithin progress i as been made In those areas most their definitions of moderate drinking.While relevant to this controversy: improved nomen- many patients weredrinking far below this clature, more precise diagnostic criteria, new limit, the use of such a high cutoff pointwould techniques for differential assessment, earlier tend to Inflate estimates of the proportionof treatment Interventions, better matchingof moderate drinkers. Furthermore, to the extent client needs to specific *,eatments, and im- that cognitive Impairment and otheralcohol- proved research methodo ;es.It should be related disabilities may result from consuming clear that while continue 'xploration and these amounts (Wilkinson and Sanchez-Craig assessment of a variety of .atment options 1981),thisliberal definition of moderation and goals for nonalcoholic and/or prealcoholic may be questionedin terms ofitshealth persons are appropriate endeavors, the con- implications. sensus of clinical opinionis that the most The controversies generated by such studies appropriategoalforalcoholicpersonsis as the Rand reports(Armor et al. 1978; Polich abstinence. etal.1981)illustratethe need to apply sophisticated and systematic research methodology to explorations of the following ques- Alcoholics Anonymous tions: In the small number ofalcoholic subjects who have reportedly established a pattern of moderate drinking,how stable is that With nearly 50 years of service to alcoholic pattern over time? How much Isthis drinking persons and their families, thefellowship of pattern altered by stress, anxietyreactions, Alcoholics Anonymous (AA) has not been the and environmental factors, such asmedia ad- subject of systematic research to studyits vertising and the cost of alcoholic beverages? long-term and short-term efficacy. To this What are the risks of resuming drinking com- end, Glaser and Ogborne (1982) reviewedthe pared with abstinence in this group? What are clinicaland researchliterature, andhave the characteristics of patients who havede- proposed a number of research questionsand veloped moderate drinking patterns in terms designs to highlight the most effective ele- those ofage,sex,socioeconomiclevel,marital ments of the AA program and describe status, and drinking history? To whatextent persons for whom AA participationisthe does the existence of a belief inmoderate preferred approach. drinking increase the risk of relapse in alco- Efforts to identify patients who are best far holic patients? suited to the AA approach have thus Despite questions raised about treatment sought to identify characteristics of thosewho goals for alcoholic persons, research has nev- have become actively InvolvedInthe AA ertheless proceeded on the effects of teaching program (e.g., Boscarino 1980; O'Leary etal. moderation to socially stable problem drinkers 1980).Some common characteristicshave (Heather and Robertson 1981). Pomerleau et been identified, Including need for structure al. (1978) have demonstrated thatbehavioral and for affiliation with a group. As yet, no treatment can be used effectivelyfor teaching consistent profile has emerged to characterize moderationtomiddle-Incomenonalcoholic successful AA members In terms of degree of problem drinkers, while others haveexplored impairment,socialstability,oremotional some dimensions ofteaching nonproblem al- disruption. This state of affairs has been at- cohol consumption skills.Effective elements tributed to inconsistencies of findings among of treatment that have been Identifiedinclude studies, differing focuses of attention across modeling and repeated practice of aclearly studies, and methodological Inadequacies delineated pattern of moderation (Strickler et (Ogborne and Glaser 1981). al. 1981), and empathy on the part ofthera- Alcoholics Anonymous is a major voluntary pists(Miller etal.1980). These must be resource in the treatmentof alcoholism, with viewed as suggestive findings, since theresults a reported membership of476,000Inthe of these treatment studies have yet tobe con- United States and Canada In 1980. The most firmed withvarious subgroupsof problem comprehensiveinformationonmembership drinkers, in natural environment settings, or comes from the organization Itself(Alcoholics with studies of long-term outcomes. Anonymous 1981). The triennial sample sur-

135 veys conducted since 1968 profile characteristics and trends of the membership. For ex- Family Treatment ample, membership has increased from 170,000 in 1968 to 476,000 in 1980; theproportion of women Increased from 22 percent in The accumulating evidence documenting the 1968 to 31 percent In 1980; the proportion of deleterious effects of alcoholismon families people 30 and under has increased to 14.7 has prompted heightened interest infamily percent in1980 from 11.3 percent in 1977 treatment of alcoholism, as described insome when this trend toward younger membership detail in the Fourth Special Report (USDHHS was first noted; and the proportion who state 1981). Although the therapeutic value offam- counseling agencies and treatment facilitiesas ily treatment Is well documented and heralded important in their attending their first AA for many related problem behaviors (Stanton meeting increased from 19 percent in 1977to and Todd 1982), Its unique contribution and 26 percent in 1980. (Of those members be- efficacy with alcoholism treatment remainto ginning AA since the 1977survey, 33 percent be fully demonstrated and evaluated (Stein- indicate counseling and treatment referrals glass 1979; Pattison and Kaufman 1981). Pre- were most responsible for first attendance.) liminary res..:ts froma study comparing degrees of spouse involvement In outpatient alcoholism treatment indicate certain advantages for marital therapy, but 18-monthout- Dynamic Psychotherapy and Group Therapy come datahavenotyetbeenreported (McCrady and Noel 1982). Considerablework Numerous descriptions of the application of In evaluating family therapy with alcoholic dynamic psychotherapy to the treatment of families Is needed, especially effortsto match alcoholism exist (Bean and Zinberg 1981; Zim- specific treatments to the problems presented berg1982), but almostno outcome studies by different families. evaluating this approach to treatment have been conducted. In recent years, psychother- apeutic approaches have given way to,or have Phimnacotherapy been combined with,behaviorallyoriented treatment in many settings. Some clinicians have argued against the use of psychotherapy The value of pharmacological agents suchas on the grounds that It may strip patients of disulfiram(Antabuse)as adeterrentto defense mechanisms that could be used in the drinking and various patient factorsassociated service of sobriety (Wallace 1978), and that it with favorable outcome is of continuingre- makes demands that alcoholics are unready to search interest. In recent work, Fuller and meet in the early phases of recovery (Valliant Roth (1979) randomly assigned 128men to 1981). Nevertheless, thereare indications that receive either a standard dose of disulfiram,a psychodynamicallyorientedgrouppsycho- pharmacologically inactive dose, or a daily therapy may in fact be preferred for certain dose of the vitamin riboflavin. The standard subgroups of alcoholic persons (Kissin 1977). dose of disulfiram was more effective than A considerable body of literature describes riboflavininproducing abstinence after 1 group therapy techniques in the treatment of year, although differences were small (Fuller alcoholism (e.g.,Vannicelli1982), but with and Williford 1980). only a few evaluative studies to support Its One aspect of treatment with disulfiram has efficacy. A recent study by Oei and Jackson been patient noncompliance, that is, thepa- (1980) compared group with individual therapy, tient's unwillingness to continue regular inges- each of these approaches being used to provide tion. Azrin et al. (1982) studied compliance- socialskillstraining to some patients and enhancement procedures with patients ina traditional supportive therapy to others. Sig- rural outpatient clinic. A behavioral "disul- nificant improvement was found only inpa- firam assurance" program, involving fiveses- tients given social skills training, with greater sions of stimulus control training, role playing, improvement in those trained in a group set- and communication skills training,was highly ting than among those treated individually. effective in promoting abstinence in married Giventhepotentialcost-effectiveness clients, but had little effecton single clients. group therapy, as well as its widespread However, the addition of behavior therapy these findings shouldbe followed up with (training indrink refusal, socialskills, and comprehensive evaluative studies. muscle relpation,j and counseling inrecrea-

112 tion activities and job-finding) was sufficient Factors Affecting TreatmentOutcome to produce nearly complete abstinencefor single clients. These are intriguing results, especially since they were obtained in rela- monthly tively few sessions and with only Quality of Treatment followup contacts thereafter. Another study tested the effects of a compliance-enhancement procedure In an Indus- As In other areas of psychotherapy, treat- trial setting (Robichaud et al. 1979) and dem- ment outcome in alcoholism isaffected by the onstrated the effectiveness of closely super- perspectives and attitudes of the therapists, vised Ingestion of disulfiram for reducing ab- which in turn are functions of their training, senteeism,butonlyduringthetreatment experience, and self-esteem (Cartwright period.Thefindingsregardingdisulfiram 1980). Treatment outcome is also affected by should be regarded as preliminary, but they do theinterpersonalskillsofthealcoholism suggest that disulfiram may have auseful role counselor. Valle (1981) evaluated treatment in treatment If compliance can be ensured. outcomes in patients randomlyassigned to Future studies of compliance with broader eight recovered alcoholic counselors andfound ranges of clients are needed and maybe fa- that counselors having a higher level ofin- cilitatedby newly developed methods for terpersonal functioning tended to have pa- monitoring use of disulfiram (e.g., Paulson et tients who drank less, relapsed less often, and al. 1977; Neiderhlser and Fuller1982). recovered more quickly after a relapse. A possible role for lithium in the treatment Evaluations of training programs for alco- able of alcoholism has been consideredbecause of holism counselors indicate that they are its effectiveness Intreating affective dis- to achieve gains in such areas asparticipants' orders and the relatively high incidenceof knowledge, attitudes, ego strength,capacity findings thus forself-disclosure, and effectivenessof these disorders in alcoholics. The of far have been equivocal.In one study, de- counseling (Gideon et al. 1980). The success pressed patientstakinglithiumhad fewer alcoholism counselor training programs has drinking episodes compared with placebo con- prompted their use as a treatment method trol patients, but without any greateralle- with chronic alcohol- and drug-dependent in- viation of the depression than occurredIn the dividuals, with positive results sustained for at control patients (Kline et al.1974). In other least 1 year (Kahn and Stephen 1981). studies, however, depressed patients did not during lithium therapy consume less alcohol Response to Treatment (Pond etal.1981). The possible value of lithium In treating alcoholics thus remains uncertain, with more definitivestudies re- Treatment research has increasingly focused quired, employing double-blind proceduresand onidentifyingpersonaland environmental comparisons with other forms of treatment factorsthatpredictpositiveornegative (McMillan 1981). treatment outcomes. Positive outcomes are no Ciraulo and Jaffe (1981) have reviewed the longer conceived solely in terms of total abuse of tricyclic antidepressantsin alcoholics stinence from alcohol, since posttreatment and report success in treating initial symptoms functioning in such domains as physical health, of withdrawal, such as anxiety, depression,and psychological adjustment, social functioning, somatic discomfort, only within thefirst 2 to and occupational performance may not de- to 3 weeks after cessation ofdrinking. In a sub- teriorateautomaticallywithrelapse sequent study, however,they demonstrated drinking (Finney et al.1980); moreover, suc- that alcoholics show greater clearanceand cessful abstinence is not necessarily associ- lower plasma levels of irnipramlne than non- ated with good functioning in other areasof alcoholics,suggesting that previous studies adjustment. which found persistent restlessness and mal- One form of negative outcome is attrition, aise may have utilized dosages that werein- that is,failure to complete the treatment adequate for alcoholics (Ciraulo et al.1982). program. Client factors found tobe related to Future studies should seek to definesubtypes attritionincludeinadequatefinancialre- of depression in alcoholics, monitorplasma sources, low social stability, andyouth (Welte drug et al. 1981; Kell and Esters1982). Treatment levels of antidepressants, and evaluate of effects both on depression and ondrinking variables such as program duration and size alsocaninfluencethe behavior. treatmentgroups

113 137 dropoutrate (Schroeder etal.1982). Un- Matching Patients to Therapies doubtedly,attritionresults from aninter- action between individual and program factors The emerging concept that alcoholism Is not and may be reduced by Improvements inpro- a unitary disorder has stimulated renewed ingram design and the method of assigning pa- terest in delineating different subgroupsor tients to treatments. types of alcoholic persons. As discussed pre- It is generally believed that treatment out- viously, the goal of this research is to facil- come is affected less by the treatment process itate treatment planning and Improve treat- itself than by the personalresources and ment outcome by matching types of alcoholic characteristicstheclientbringstothe persons with the most appropriate treatment treatment situation. Numerous studies have interventions. Although this typologicalap- shown good prognosis to be associated with proach is not new to the field of alcoholism, social stability and marital adjustment recent studies have benefited from improve- (Baekeland 1977). Personalcharacteristics ments in assessment technology (Meyer et al. recently reported to be associated withpoor 1981)and from the applicationofmore prognosis include cognitive impairment (Ab- sophisticatedstatisticaltechniques (Skinner bott and Gregson 1981) and depression (Hat- 1982). sukami et al.1981). While client character- Attempts to differentiate alcoholicson the istics seem to be Important determinants of basis of personality characteristics account outcome regardless of the quantity or quality for most typological research efforts (Morey of treatment, other research has shown that andBlashfield1981).Severalindependent this effect may be mediated indirectly by the studies have denoted two common subgroups: environment to which the client returns after (1) passive-dependent alcoholicpersons char- residentialtreatment(CronkiteandMoos acterized by antisocialpersonality disorder 1980). Another study found that three situa- and (2) neurotic alcoholic persons whomay use tional factors (negative mood states, inter- alcohol as a coping mechanism. In a study de- personalconflicts,andsocialpressureto signed to explore the often-noted association drink) were most likely to precipitate relapse between alcoholism and antisocial (psycho- after treatment (Cummings et al. 1980). These pathic)personality,Hesselbrock etal.(in studies indicate that therapeutic efforts must press) compared alcoholics havingan early deal not only with the individual character- history of social deviance with those whowere istics of the patient, but also with the envi- relatively free from problems before the onset ronmental contexts in which the patientis of alcoholism. Alcoholics with antisocialper- expected to function after treatment. sonality were found to have an earlier onset of With thisin mind, some have advocated alcoholism, as well as a more rapid andsevere giving more attention to restructuring of the progressionofdrinkingproblems.Several client's environment through marital or family other studies (McLellan et al.1981; Zivich therapy, while others have called for a more 1981) suggest the Importance of psychiatric general approach focusing on frequent after- disturbance,particularlyinthealcoholic's care contact in the period after treatment response to treatment. Alcoholic subgroups (Costello 1980). As a neglected dimension in characterized by poor psychological adjust- the treatment system, aftercare consists of (a) ment were found to show little or no Im- ongoing supportive activities, such as profes- provement following treatment, whereas These sionalandself-helpprograms designedto having high adjustment levels showed signif- maintain treatment gains, (b) prevention of icant improvement. McLellan etal.(1981) costly rehospitalizations, and (c) Improvement conclude that because patients havingless insocialand occupationalfunctioning.At' severe psychological disturbance respond to present, the resources most frequently most kinds of treatment, cost considerations available to fulfill these functions are halfway would recommend this subgroup to outpatient houses, AA groups, and program-sponsored settings. support groups.Ingeneral,affiliationwith The probability of a genetic predisposition aftercare groupsis associated with better to alcoholism has prompted the search for an treatment outcome (Costello1980). Further alcoholic subtype related to family pedigree. research is needed to determine the relative One study of more than 7,000 alcoholic men efficacy of different kinds of aftercare, the found that those with a family history of al- optimal frequency and duration of aftercare, coholism had more severe symptomatology, and how clients can be induced to comply with more antisocial behavior and other psycho- aftercare without dropping out. pathology, less stable employment histories, 3 s 114 and more severe physical symptoms (Frances promise as an avenue to improved treatment et al. 1980). Another approach to the classi- efficacy,the systematic study of patient- fication of alcoholics is based on certain in- treatment interactions will have to await the dicators known to predict treatment outcome. development of better typologies and One study (Gibbs 1981) classified alcoholics on improved scientific research methodology. the dimensions of social stability and intellectual functioning and showed that mutually Emerging Trends and Future Directions exclusive types were often assigned to the same treatment regimen despite their widely different rehabilitation needs. A consensus appears to be developing among In an attempt to directly test the clinical clinicians, researchers, and policymakers that implications of differentiating subgroups of treatment research is passing through a tran- alcoholics, several investigators have studied sitional period during which basic assumptions how certain types of patients respond to dif- are being reevaluated and a new approach to ferent treatments. Using a classification sys- treatment efficacy is emerging. The elements temthatdifferentiateschronicalcoholics of this trend include refinements in the defi- from a less severe type of behaviorally im- nition of terms, improvements in the tech- paired drinker, Brown and Lyons (1981) found nology of diagnosis, a more sophisticated ap- that alcoholics do slightly better in programs proach to the planning of treatments, and a having a high medical orientation, while the new awareness of the complexity of evaluation behaviorally impaired drinkers respond better methodology. to treatment having a high psychological re- The advances noted in this chapter in the habilitationorientation.Usingadifferent areas of conceptualization, assessment, and classification scheme, Finney and Moos (1979) treatment intervention can only serve to en- studied the treatment response of alcoholics hance the quality of services available to al- classified in terms of high or low social com- coholic persons. The notion that different de- petence. Contrary to the findings of Brown grees of alcohol dependence can be measured, and Lyons (1981), no evidence was found to that different types of alcoholic persons can indicate that various treatment programs were be classified, and that different types of dis- differentially effective for different types of ability can be diagnosed has important im- patients. plications for treatment and research. Recent Althoughevidencesupportingtreatment reviews of treatment-related priorities con- matching remains equivocal, there may be ducted by the Institute of Medicine (1980), the important methodological reasons whythe Journal of Studies on Alcohol (Keller 1979), matching hypothesis has not been adequately and the World Health Organization (Edwards tested.First, despite improvements inthe et al.1981) suggest that these themes will methods and theory of classification, the op- constitute a promising but ambitious agenda timal classification system has yet to be de- for the 1980s. As articulated in the writings of veloped. Even though family history, psychi- many specialists in the field, a new approach atric disorder, alcoholic symptomatology, and isemerging regarding the ways inwhich organic brain dysfunction seem to be prom- treatment is conceptualized, conducted, and ising differentiating characteristics, there has evaluated. been little attempt to integrate information The traditional model, which still dominates from these disparate levels of analysis into much thinking about alcoholism treatment, more comprehensive typologies. Second, many describes how heterogeneous groups of pa- matching studies have not been designed to tients are assigned to multimodal treatment detect predicted interactions. In a recent re- programs. After a period of time, the relative view of the matching literature (Skinner 1981), success or failure of treatment is evaluated itwas found that evidence supporting the primarily on the basis of the proportion of matchinghypothesis cameprimarilyfrom patients remaining abstinent, and secondarily those experimental studies that randomly asby global assessments of functioning in other signed patients to treatment conditions, while areas of living. Because both treatment vari- the results of nonexperimental correlational ables and client variables are aggregated in studies tended to be less supportive. Finally, in this approach, treatment effects may be ob- a number of studies it is possible that the as- scured when the improvements of some pa- signed treatments were not sufficiently dis- tients are averaged with the lack of improve- tinct to produce a differential effect. Thus, ment or even deterioration of other patients. whilethematchinghypothesisstillholds Even when treatment effects are observed, it

115 3 9 Is not clear which parts of the treatment come to realize that multiple patterns of al- process are responsible.In addition to the cohol use may result in multiple forms of conceptual limitations of this model, much of disability. Accordingly, a new emerging model the evaluation research conducted within this of treatment stresses the heterogeneousna- tradition is difficult to interpret becausepa- ture of the client population, the need for tient characteristics differ from one study to more specific and efficient treatments, and another, outcome criteria have not been suf- the importance ofmaintaining gains after ficientlyspecified, comparison groups have treatment. This model differentiates among not been included In the research design, and alcoholics (e.g., depressedvs. nondepressed) the treatment process has not been adequately and attempts to match each type with the described.Furthermore,theposttreatment most appropriate combination and configu- environment has not been taken into account, ration of treatments. and there have been unrealistic expectations Recognizing the Importanceofaccurate about what the treatment will accomplish. patient descriptions, the American Psychiatric In contrast to the traditionalmodel of Association has developed systematic criteria treatment, the emerging model stresses the for classifying alcoholic patients along a num- heterogeneous nature of the client population, ber of dimensions. The technique, a part of the need for more specific and efficient in- DSM III(Diagnostic and Statistical Manual of terventions,the importance ofmaintaining Mental Disorders) promises to providemore treatment gains In the posttreatment envi- standardized and comprehensive patient ronment, and the diversities of different out- diagnoses. comes (Skinner 1981; Cronkite and Moos 1980). Severalmethodsarecurrentlyusedto This model differentiates among types of al- identifyalcoholicsbeforethey comefor coholic persons (e.g., less dependent or more treatment.Laboratorytestsforbiological dependent, depressed or not depressed,cog- markers or indicators can be a powerful aid to nitively impaired or not impaired) andcon- detecting alcoholism. Current research on the jointly attempts to match each type with the use of biochemical indicators in the early de- most appropriate combination of treatment tection of alcoholism suggests that a single interventions (e.g., pharmacotherapy, behavior specific biochemical marker for alcoholism therapy, family treatment, etc.). The efficacy may be elusive. The combination of GGTP, of various treatment combinations is evalu- MCV, and several other tests, however, ap- ated by comparing patients who are matched pears to offer, at relatively low cost, a strong to appropriate treatments with those who are indication of recent excessive alcohol con- mismatched or assigned randomly to a stand- sumption. In addition, a widely used and val- ard package of interventions. Within thenew idated self-administered test,the Michigan model, greater attention is given to evaluating AlcoholismScreeningTest (MAST),elicits changes in behavior, attitudes, physical health, responses to medical, social, and behavioral andpsychosocialfunctioningtakingplace statements. The MAST is rapid, inexpensive, during the process of treatment. Anotherarea and relatively accurate. of focus Is the posttreatment environment, Studies show that untreated alcoholics and where the patient's recovery may be impeded their families are disproportionately high users or supported by what takes place in the family ofmedicalservices.Insuranceprograms, setting or in the job situation. Ideally, the especially HMOs, In recognition of the cost treatment process would continue during the implications have begun to target alcoholism posttreatment period in the form of various for increased attention. Preliminary studies kinds of specialized aftercare. Finally, the suggest that partial hospitalization or out- new model recognizes that outcome may vary patient programs may be as effective as in- along a variety of dimensions, and that ab- patient programs for some patients; moreover, stinence is just one goal of a more ambitious the lower costs of the former may lead to in- treatment strategy that Includes rehabilitation creased use. in other important areas of functioning. Treatments continuetorelylargelyon psychotherapy and behavior therapy (including social skills and assertiveness training, self- Stunmary control training, cognitive restructuring, and aversion therapy, which pairsalcoholwith The traditional concept of alcoholism as a unpleasantstimuli).Inaddition, group ap- unitary disease has been challenged. Over the proacheslikeAlcoholics Anonymousare past decade, researchers and clinicians have widespread. Behavior therapy in conjunction

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120 144 tionnaire to measure severity of alcohol depend- Sanchez-Craig, M., and Walker, K. Teaching coping ence.BritishJournalofAddiction74:79-87, skills to chronic alcoholics in a coeducational halfway house: I. Assessment of programme ef- 1979. fects. British Journal of Addiction 77(1)05-50, Strickler, D.P.; Bradlyn, A.S.; and Maxwell, W.A. 1982. Teaching moderate drinking behaviors to young Saxe, L.; Dougherty, D.; Esty, K.; and Fine, M. The adultheavy drinkers:The effectsofthree Effectiveness and Costs of Alcoholism Treat- training procedures. Addictive Behaviors 6(4): ment. Health Technology Casestudy 21 Report 355-364, 1981. No. OTA-HCS-22. Washington, D.C.: Congress of Swint, J.M., and Nelson, W.B. Prospective evalu- the United States, Office of Technology As- ation of alcoholism rehabilitation efforts: The sessment, 1983. 108 pp. roleofcost-benefit and cost-effectiveness Schroeder, D.J.; Bowen, W.T.; and Twemlow, S.W. analyses. 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Relevance and Oran es: A ConitirlsonofIn21,..__Itand of brain dysfunction to treatment objectives: Outpaten:4giarrCer City, Minn.: Hazel- Should alcohol-related cognitive deficits influ- treatment? Addic- den Foundation, 1981. ence the way we think about Spitzer, R.L.; Williams, J.B.W.; and Skodol, A.E. tive Behaviors 6(3):253-260, 1981. DSM-III: The major achievements and an over- World Health organization. Diagnosis and Clas- v ev7777kmerican Journal of ftychiatry137(2): sification of Mental Disorders and Alcohol and utS-nrnaries of working 151-164, 1980. Drug-Related Problems. Stanton, M.D., and Todd, T.C. The Family Therapy papers from an international conference,Co- of Drug Abuse and Addiction. New York: Guil- penhagen, Denmark, April 1982. ford Press, 1982. Zimberg, S. Office psychotherapy of alcoholism. In: Steinglass, P. Family therapy with alcoholics: A Solomon, J., ed. Alcoholism and Clinical Psy- review. In: Kaufman, E., and Kaufmann, P.N., chiatry. 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121 145 Chapter VIII

Prevention: A Broad Perspective

This chapter will describe current perspec- Inaddition,significantgrassrootsgroups tives on prevention of alcohol-related prob- concerned about alcohol problems have de- lems, summarize recent research findings,and veloped over the past fewyears. Some of highlightactivitiesatnational,State, and these have focused national attentionon and community levels to reduce alcohol-related stimulated nationwide action to reduce alco- problems. hol-related highway accidents. Others have focused on education, mutual supportgroups, Current Perspectives server responsibility, concern about alcohol beverage advertising, and support foraddi- tional enforcement and legislative actions that Within recent years, prevention of alcoholhave prevention potential. related problems has emergedas a key issue Empirical research on alcohol-related prob- not only in the United States but interna- lems among special populationgroups (e.g., tionally as well (Mosher 1981). Therehas been women, young black men, Hispanic Americans, enormous growth of attention on the part of American Indians and Native Alaskans, and the many countries asitbecomes increasingly elderly) indicates a need for andhas contrib- clear that few, if any, countriesare free of uted to a growing interest in prevention ef- problems associated with the consumption of forts for specific at-risk populations. alcohol.Legislators, educators, researchers, Furthermore, research in a number ofareas and others throughout the worldare seeking offers significant promise for futurepreven- ways to reduce alcohol-related problems and tion efforts. These areas include: to decrease the personal, social, and economic costs associated with them. The effects of alcohol consumptionon The emerging focus on prevention is related neurotransmitters in the nervous system to a number of factors. One is the realization that the treatment system alone cannot be Means for manipulating tolerance to al- expectedtodealwithallalcohol-related cohol in the brain problems (USDHHS 1981). Another is thatnot only heavy chronic drinkerscause and suffer Genetic factors or markers thatmay help from alcohol problems. The National Academy to explain why individuals seem to differ of Sciences' report, Alcohol and Public Policy: In their vulnerabilities to the problems Be and the Shadow of Prohibition (Moore and associated with alcohol consumption Gerstein , tndicates that: Role of known risk factors in the devel- Chronic drinkers with high consumption opment of alcohol-related problems both cause and suffer farmore than their numerical share of the adverseconse- Assessment of the impact of legislative quences of drinking, (but) their share of and regulatory measures alcohol problems is still onlya fraction- - typically less than half--of the total. Al- Early identificadon and diagnosis of al- coholproblemsoccurthrow houtthe cohol problems drinking population.. . at ower rates but among much greaternumbersas one Increased awareness of the need to fur- moves from the heaviest drinkers to more ther evaluatevariouseducational and moderate drinkers. (p. 44) community approaches

122 Since the Fourth S ecial Re ort to Congress (Moore and Gerstein 1981). This section of the (USDHHS 1 , t ere appearstoaveeve - chapter will set forth findings of research on oped an emerging consensus that the public two major instruments for preventingalcohol- health approach can provide a useful concep- related problems: (1) education, information, tualframeworkfordevelopingprevention and training and (2) law and regulation. strategies. This model derives from epidemiological studies of communicable disease indicating that proper planning requires knowl- Education, Information, and Training edge not only of host, agent, and environment, but also of their interaction. Concurrent with the growing acceptance of this approach, there has been a significant School-Based Alcohol Education Programs publicand privateeffortdirectedtoward health promotion and disease preventionand Alcohol education programs for youths 18 growing evidence ofeffectiveness.Several years of age and younger havefocused on both recentpublicationshavedocumentedim- general unselected youth populations and those provements in the Nation's health over recent atrisk for alcohol problems (Hewitt1982). years, as well as gains that maycontinue. Alcohol education programs for the former Among these improvements are: have ranged irom those delivering only alcohol-related information to those with little or The proportion of adults who smoke has no alcohol-related content,and those designed declined by more than 20 percent over the to foster the personal developmentof par- past 15 years. ticipants to reduce the likelihood of later alcohol problems. Several programs have com- The proportion of the population with high bined alcohol-specific education withpersonal serum cholesterol levels has declinedby development (NIAAA 1979, 1981b). 12-22 percent. Educational efforts also have been directed at groups of adults who interactwith young The proportion of adults who exercise people and who are in a position to influence regularly has increased by as much as 100 their drinking (Hewitt 1982). Programsfor par- teachers, percent. (USDHHS 1982) ents and other family members, other community professionals, and lay people Appliedtoalcohol-relatedproblems, the have been developed, on the assumption that public health approach directs simultaneous providing these key "gatekeepers" with infor- attention to (1) individuals at risk for devel- mation on alcohol and alcoholism may wellaf- oping problems, (2) the availability and dis- fect the youth for whom they areresponsible. tribution of alcohol, and (3) the drinking en- Evaluations of alcohol education programs vironment. Objectives of the Nation for 1990 indicatethat:(1)significantincreasesin include more than a dozen specificallyrelated knowledge about alcohol are oftenobserved to alcohol (see box, page124) and reflect (Fullerton 1979; Staulcup et al. 1979; Wittman attention to each of these three areas. 1982); (2) less dramatic but nonetheless real The Alcohol, Drug Abuse, and Mental Health changes in attitudes toward alcohol ortoward Administration(1981)hasdefinedprimary self and others also occur, especially when prevention as actions or interventionsdesigned attitude change Is an explicit goal of the pro- to reduce the incidence ofalcohol disorders gram (Evans et al. 1979;Weisheit et al. 1979; and related problems. (Secondary prevention, Wittman1982);(3)difficult-to-Interpret or or intervention, isconcerned with the early modest changes in actual drinking behavior Identification and treatment ofthesedis- occur, although fewer programsset out to orders, to reduce their prevalence or the measure behavioral change thanchanges in prevalence of dysfunctional behaviors asso- attitudes toward or knowledge aboutalcohol ciated with them.) (Fullerton 1979; Staulcup et al. 1979; Wittman In 1981, the National Academy of Sciences 1982); and (4) although evaluation designs are completed a study (under contract toNIAAA) becoming more sophisticated, futurestudies of alternative approaches to the preventionof will need to develop measurable and precise alcohol-related problems. Based on thisstudy, program objectives and goals(Wittman 1982). the Academy concluded that: The possibilities modest Elementary-agechildren.--Thisgroupof for reducing the (alcohol) problem are focus of in- but real and should increase withexperience children has recently become the

123 14 7 1990 Objectives Alcohol Abuse and Alcoholism

.By 1990, fatalities frommotor vehicle accidents involving drivers levels of .10 percent with blood alcohol or more should be reduced to fewer than 9.5per 100,000 population per year. (In 1977, there were 11.5per 100,000 population.)

. By 1990, fatalities from other(non-motor-vehicle accidents, indirectlyattributable to alcohol use, e.g., falls, fires,drownings, ski mobile, aircraft) shouldbe reduced to 5 per 100,000 population peryear. (In 1975, there were 7 per 100,000 population.)

. By 1990, the cirrhosis mortalityrate should be reduced to 12per 100,000 population. (In 1978, the rate was 13.8per 100,000 population.)

By 1990, the incidence of infantsborn with fetal alcohol syndromeshould be reduced by 25 percent. (In977, the rate was 1per 2,000 deaths, or approximately 1,650 cases.) . By 1990, per capita consumption ofalcohol should not exceed thecurrent levels. (In 1978, about 2.82 gallons of absolute alcoholwere consumed per year per person aged 14 and over.)

6. By 1990, the proportion ofadolescents 12 to 17 years old who abstainfrom using alcohol (or other drugs) shouldnot fall below 1977 levels. (In 1977, theproportion of abstainers was 46 percent for alcohol.)

.By1990,the proportionofadolescents12to 17 yearsoldwho reportacute drinking-related problems during the previousyear should be reduced to below 17 percent. (In 1978, it was estimatedto be 19 percent based on 1974 data.)

. By 1990, the proportion of problemdrinkers among all adults aged 18 andover should be reduced to 8 percent. (In 1979, itwas about 10 percent.) 9. By 1990, the proportion of women of childbearing age aware of risks associatedwith pregnancy and drinking--in particular, the fetal alcoholsyndrome--should be greater than 90 percent. (In 1979, itwas 73 percent.)

10. By 1990, the proportion of adultswho are aware of the added risk of headand neck cancer for By 1990, the proportion of adultswho are aware of the added risk ofhead and neck cancer for people with excessive alcohol consumptionshould exceed 75 percent. (No baseline data are available.)

11. By 1990, 80 percent of high schoolseniors should state they perceivegreat risk associated with alcohol intoxication. (In 1979, only 35percent perceived "great risk" associated with having five or more drinksper occasion once or twice each weekend.)

12. By 1990, the proportion of workersin major firms whose employersprovide a substance abuse prevention and referralprogram (employee assistance program) should begreater than 70 percent. (In 1976, 50 percent ofa sample of the Fortune 500 firms offeredsome type of employee assistance program.)

13. By 1990, a comprehensivedata capability should be establishedto monitor and evaluate the status and impact of misuse of alcohol (anddrugs) on: health status,motor vehicle accidents, accidental injuries in additionto those from motor vehicles, interpersonal aggression and violence, sexual assault,vandalism and property damage,pregnancy outcomes, and emotional and physical development ofinfants and children.

NOTE: Acute drinking-relatedproblems have been defined driving while intoxicated, as problems such as episodes of drunkenness, or drinking-related problems with alcoholauthorities.

124 14 1982). These findings emphasize the complex creased prevention activities.Bartlett's (1981) for youth analysis of alcohol education programsand phenomena that prevention programs high school should address, as well as the specialchar- their impact on elementary and adoles- age youth cautionsagainst overemphasizing acteristics and changing needs of the teach- cent problem drinker. cognitive learning and lecture-oriented Mas- ing methods, failing to assiststudents' recep- The CASPAR program in Somerville, tivity to the material and toappreciate the sachusetts, took this complexity into consid- problems caused by the "captivepopulation" eration when it Included teachertraining, peer Importance of teaching programs, and an alcohol-specific syndrome, and overlooking the problem coordinating alcohol education programswith curriculum to teach decisionmaking, solving, and coping skills. It foundsubstantial related community resources.Nontraditional atti- programs that involve studentsin curriculum increasesin knowledge and improved design and interactive learning seemmost tudes. The peer leadership training wasfound effectiveInraisinglevelsofself-esteem, successful. and opti- Oneinnovativepreventionapproachto feelings toward home environment, grade-school children--the Alpha Center Pre- mism. A significant inverserelationship was levelsofself-esteemand ventionModel--isinplaceintwo Florida foundbetween counties (Pringle et al. 1981). Thismodel is likelihood of problem drinking(NIAAA 1979). based on the assumption that alcoholabuse, Changes in drinking behavior did occur in the derives from experimental group as comparedwith the like other behavioral problems, control group, which was not exposed tothe early developmental problems.Students aged 8 maladaptive behaviors at program over a period of3 years (Wittman to 12 who display high home and school attend specialclasses to im- 1982). These effects decayed when junior academic skills. Their teach- youth moved into the highschool, however. prove social and high a level behaviormanagement The experimental group showed as erslearnclassroom did the control techniques and interpersonalcommunication for alcohol-related problems as skills, and a counselor works with parentsat group in high school(NIAAA 1979). remains The Here's Looking AtYou curriculum home. The Alpha Center concept found similar essentially unproven, however. program in Seattle, Washington, results with a multifaceted programthat paid particular attention to the alcoholdiscussion Adolescents.--Most youth begin to drinkin content of the curriculum inrelation to the developmental age of the child. The most en- adoescence. This is also thetime when youth couraging of the findings was thatfor the age are most atrisk for the most catastrophic longitudinal of drinking: alcohol-related cohortsixth-eighthgrade (the consequences subsample first measured while they werein traffic accidents. alcohol abuse sixth grade and then during thesucceeding 2 A recent study on adolescent curriculum was relevant to prevention effortsfound that (1) years), the impact from the by youth found not only in knowledge, butalso in inalcohol is the most widely used drug improving between the ages of 12 and17 (making this creasing self-esteem and, in some, target), (2) prob- decisionmaking skills (NIAAA 1981b).Further group an obvious prevention to yield lem drinking increases sharplywith advancing study of this curriculum is expected (3) adolescent problem more knowledge aboutthe impact of the cur- age during adolescence, and actual drinkers use illicit drugs much moreoften than riculum on intervening variables nondrinkers, (4)heavy drinking during ado- behavioral outcomes. by other One program for high-riskyouth at the high lescence is typically accompanied in terms of antisocial behaviors, (5) bothparental and peer school level has proven effective drinking, behavioralchange. The Student Assistance influences strongly affect problem Program, Implemented in 23 schoolsin West- (6)adolescent problem drinkersdiffer and chester County, New York, has aprimary pre- from non-problem-drinkingadolescents--they deviance, less successful vention component aimed at newcomers, sen- are more tolerant of people in school, and prize morehighly independence iors, children of alcoholics, and young problems.Usingsmall than academic success(Braucht 1982).Re- withinterpersonal and prob- groups facilitated by atrained counselor, the search on self-reported drug usage effective In reducing the lem behaviors indicates significantassocia- program has proven and use of al- incidence of both alcohol problemsand ab- tions between such behaviors alcohol and cohol, tobacco, illicit drugs,painkillers (e.g., senteeism (often associated with aspirin), and tea or coffee(Hundleby et al. other drug problems) (NIAAA1983).

125 149 Another innovative program focusing on a alcohol education projects thatassessed be- high-risk group of delinquentadolescents in- havior change and clearly cluded an intensive training found evidence of program for the change, it deserves carefulscrutiny and pos- staff of the Partners Pr3grarn, a nonprofit sible replication. volunteerorganizationdesignedto provide Goodstadt and Sheppard (1983)also recently services to youths in troublewith the law in compared three short-term Denver, Colorado (Resource programs--a cog- Alternatives nitive program, a decisionmakingprogram, and Corp. 1982). Another essentialcomponent of a values-clarification program--for highschool the programwas peer education. Thepro- students. The cognitive gram's evaluation study program Improved design provided for levels of alcohol knowledgesignificantly more three control groups, allof whom were en- than the other programs, rolled in theprogram before the alcohol edu- even though there was no change in behavioral expectationsor cation/preventiontrainingcomponent was attitudes. The decisionmaking provided to the staff. Results program was of the evalua- successful in leading studentsto a better un- tion revealed that youths'perceptions of the derstanding of major decisionmaking negative consequences of drug concepts, and alcohol use demonstrating the viability of thisprogram in increased after theircounselors had been ex- teaching about decisionmaking.The values- posed to alcohol education.More important, the experimental clarification programwas most likely not ap- groups experienced less se- propriate for the target audience,so no gen- vere alcohol and other drug problemsthan did eralizations could be made. the control group (NIAAA 1981a). The authors did draw, A project conducted jointly however, some sig- by the American nificant conclusions. They found,for instance, Medical Association and theAmerican Asso- that while attitudes ciationof were not changed by these MotorVehicleAdministrators programs, attitude change is positively related (Flames and Petrucelli 1980) was based on the to reduced alcohol consumption.They also assumption that teenagers inthe process of getting their driver's found that those who improved Intheir use of licenses are maximally decisionmaking concepts weremore likely to motivated to cooperate withan alcohol edu- show a shift toward less pro-alcohol cation program attached attitudes. to that process. The Theyconcludedthat"whereasbehavioral programrequiredteenagers applyingfor outcomes area desirableobjective,they license in New York,Wisconsin, or Oklahoma to view an alcohol education probably represent unreasonableexpectations film in high for interventions of such shortduration, al- school driver education classes,after which though they would continue they were tested for knowledge to be significant increase and long-term objectives and worthyof examina- retention. Results indicatedthat the infor- tion" (Goodstadt and Sheppard 1983). mation was retained at leastfor a short time; however, the impact of the program on sub- College-age youth.--An effortto stimulate sequent ratesof drunken drivingwas not prevention and intervention assessed. programs has been made at the college levelin recognition of One of the most thoroughstudies of the both the paucity of such impact ofalcohol education programs to this time on adolescents and the differences in approachand strategy (Stuart 1980) included lecturesgiven to almost required for effective prevention 1,000 junior and senior high and inter- school students on vention with this population (Bryan1982; Dean the physiology and pharmacologyof drugs in- 1982). cluding alcohol and the legal,social, and psy- Several interesting approaches chological ramifications of their to prevention use. While with college-age youth havebeen reported. A information levels increased, drugand alcohol use also increased. survey of 457 Memphis State Universitystu- dents and 30mentalhealth A study by Goodstadtand his colleagues professionals working In the university settingrevealed that (1982) found that educating7th to 10th grade the students, unlike theprofessionals, con- students on myths aboutalcohol,beverage sidered substance abuse problems advertising, reasons for drinking, to be the and effects most serious of 24 mental healthproblems of alcohol on the family,driving, sports, fit- experienced by ness, and sexuality improved their knowledge students (Henggeler etal. but 1980). Evaluations of alcoholeducation pro- had mixed effectson theirattitudes grams at the University of Virginia (Portnoy toward alcohol. Moreover, during the program, 1980) and Saint Mary's College(Leavy 1980) the students decreased theiralcohol consumption. Since this is both demonstrated the apparentease with one of the few adolescent which the student's information,based on al- 1 5 9 126 cohol knowledge, can be changed--and the real NIAAA's recent mass media campaignclearly difficulty in changing actual drinking behavior. indicates that such efforts can stimulatein- Similar results were obtained at Brown Uni- terest in both the preventionof alcohol pre,- and versity by a "sons and daughters ofalcoholics" lems and communitywide organization group designed as a preventionand interven- development toward this end (NIAAA 1982). tion strategy (Donovan 1980). Between 1975 and 1980, a comprehensive Education Programs About Other alcohol education program for collegestudents Health Hazards was developed, implemented,and evaluated at the University of Massachusetts(Kraft 1982) Recently, attention has been devoted to and somewhat later replicated and extended at determining what can be learned about pre- the University of North Carolina(McCartney ventionofalcohol-relatedproblemsfrom and Humbert 1983; Mills et al.1983). These carefully developed programs intended to re- two projects were among the mostcarefully duce other health hazards(Hochheimer 1981). evaluated of all large-scale prevention proj- And some have concluded thatthemost ects directed at this populationof drinkers. promising prevention technique for the 1980s The University of Massachusetts project pro- is the community-based modelthat blends a host, gramed mass media messages to raise aware- varietyof approaches aimed at the address the com- ness of drinking anddriving, and sponsored agent, and environment to development plexities and needs specific to the community group discussions and community and techniques designed to influence ways inwhich (Hochheimer 1981; Wittman 1982; Holder alcohol was consumed by collegestudents. As Blose 1983). a result of theseefforts, knowledge and at- One design that combined mass media cam- titude changes took place; however, no posi- paigns with intensive interpersonaltraining at ob- the local level was the Stanford HeartDisease tive changes in drinking behavior were This served (Kraft1982). The evaluation design, PreventionThreeCommunityStudy. however, was invalidated, since duringthe study had the following fivegoals: generate program the minimum purchase age waslow- awareness about the programand its focus, ered in Massachusetts.Itisimpossible to increase the knowledge of the audience, mo- behavioral changes oc- tivate people to adopt new behaviors,teach know, therefore,if skills curred as a result of the program. people new skills, and reinforce the new and behaviors so they would bemaintained (Hochheimer 1981). Their findings showed that Mass Media Campaigns dietary changes and exer 'se werelearned and Far- The consensus about mass mediainforma- through mass media alone (Maccoby tion campaigns is that: (1) suchefforts are quhar 1975). However, other behaviors,such as and smoking, changed onlywheninterpersonal largely limited to increasing knowledge and be- reinforcing established attitudes andbehavior training (based on the social learning 1977), and (2) havior work of Bandura 1977,1978, 1979, and patterns (Blane and Hewitt (McAlister et al. slight alteration on changing drinking patterns Goodstadt 1978) was included this effect is indeter- 1979). After 2 years, the overall decreasein may occur, although in the minate (Blane 1976). However,Wallack (1981) risk of heart disease was 16-18 percent experimental sites, compared with 6.5 percent notes that: for the control group. A review on the effects of massmedia In Project CLASP (CounselingLeadership About Smoking Pressures), which wasbased on would lead one to a healthy skepticism McAlis- regarding the effectiveness ofsuch a previous smoking and health research, trainedseveral program Implementationtechnique. This terand colleagues(1979) skepticism must be tempered becauseof teams of five to seven highschool students to have gen- lead classroom sessions for juniorhigh school the flawed evaluations which to erated the body of effectiveness data....lt students. The objective of the sessions was may be that determiningthe effects of increase students' commitment not to start mass media is a functionof broadening smoking and topsychologically "Inoculate" research questions to gain better under- them againstpressuresto smoke.Similar alco- standing of the wider view, ratherthan activities aimed at deterring the use of narrowing them further to assessindi- hol and other drugs also were added.When the vidual exposure and reaction in greater experimental and control schools were compared following 21 months oflongitudinal ob- detaiL (p. 230)

127 151 servation, the experimental school's students In addition, they are assistedin improving were found to be smoking and drinking sig- self-image, making Informed choices, andre- nificantly less than students In the control sisting pressure to smoke. Advertisingtech- school, who had receivedan intensive course niques, verbal and nonverbal communication in health education butno peer-group sessions skills, and appropriate and effectiveuse of with high school students. Further evaluation assertiveness also are examined. The material is needed to ,see if this effectpersists over Ineach ofthesesessionsistransmitted time and to gain a better understandingof through discussion, demonstration, and role these efforts. playing, and oftenIs notsmoking-specific, Other prevention programs basedon social although connections are made whereappro- learningtheory(Bandura 1977)emphasize priate. Students also participate Ina self- strategies encouraging young peopleto refuse improvement program in which they identifya drugs. Significant positive resultshave been skill they want to improveor a behavior they found in university-based research anddemon- want to change and then set long- and short- stration programs aimed primarilyat smoking range goals for accomplishing this. Botvin and prevention. Other research has supportedthe Eng (1982) have found that the assumption that rehearsing program in- responses to det- creased knowledge and reduced by 58percent rimentalhealthinfluencesincreases the the onset rate of smoking. In addition, the likelihood that these responses willbe used in experimentalgroupexpressed less social appropriate situations (McGuire 1969). anxiety and were more resistant to influences Most refusal programs incorporatethree than the control group. components: strategies that increaseyoung Wellness programs may offer additionalop- people's knowledge by providing information portunities for alcoholism preventionat the about both the hazards of drugs and their ef- worksite. Wellness programspositive lifestyle fects, and about peer pressure and other in- change programsoffer healthy employeesthe fluences to use drugs; techniques for expand- opportunity to modify lifestyles that might,at ingone'sspecificbehaviorrepertoirefor a future date, cause health problems. Smoking saying "no"; and training in life skills (e.g., cessation, exercise, stress values management, clarification,enhancing self-esteem, weight control, and nutritionprograms are assertiveness training, problem solving, and typically offered inthe effort to promote coping abilities). As a wide body of research healthier lifestyles, improve quality of lifeat has shown, each plays a part ina person's present, and reduce health risks in the future. choice toadopteitherlife-enhancingor A number oflargecorporations,including health-risking behaviors (Bandura 1969; Rotter Johnson & Johnson and Control Bata, have put 1972; Jessor and Jessor 1977; Perry 1981). wellness programs into place. Theseprograms In one such program--Project SMARTat the may, but typically do not,provide alcohol University of Southern California- -the prin- corn nents, relying instead on existingem- cipal objective has been to implementand ployee assistance programs (EAP)to reach study a school-based preventionprogram de- employees with alcohol problems. Whenno signed to offset peer pressure through theuse EAP exists to address stigmatized problems, of positive strategies to refusedrugs and its inclusion may greatly enhance thecom- thereby reduce cigarette smoking and alcohol pany's human wellness program. However, the and marijuana use in the sixth through ninth existence of comprehensive positive lifestyle grades. In Project SMART, two curriculums change programs may affect drinkingprac- have been developed; one focuseson social tices and general awareness of healthylife- resistanceskillstraining, andtheother styles, thereby preventing alcohol problems stresses self-managementskillsandvalues from developing in some individuals. Empirical clarification. Both use peer leaders. Pretest studies of the impact of theseprograms on the findings indicate that it may be importantto prevention of alcohol problemsare necessary begin the intervention at a point where the before their role and widespread implementa- target audience begins to perceive itselfat tion in the worksite can be determined. risk, and that youth preventionprograms are more effective whenfacilitatedbypeers Programs for Populationsat Special Risk (Johnson et al. 1981). In the Life Skills Training Program,a simi- Women.--Inthe past, few preventionap- lar program developed at the Cornell Univer- proaches have been designed specifically for sity Medical School, studentsare Informed women. These usually provided assertiveness about myths and realities relating to smoking. training, exercises for enhancing self-esteem,

128 5 2 they drink more and stress management seminars(Irwin 1976; whites, when theydrink Sandmaier 1976). To date, neither theunder- heavily, thus increasing the likelihoodof cer- with lyingassumptionsnorthe program effec- tain negative consequences associated tiveness of these types of programs havebeen heavy drinking (Rolzen 1982). Ameri- confirmed empirically. Rates of alcoholism among Hispanic One program currently beingevaluated is cans appear to be higherthan the national the Alcoholism Center for Women, LosAnge- average (Garza 1979). Variablesthat may ex- les County, which recentlydeveloped a sys- plain these elevated rates of alcoholabuse tematic community approach foridentifying Include sociocultural norms and valuesthat and delivering prevention activities toadult encourage heavy drinking,especially by men, women at high risk foralcohol problem's.. Spe- minority group status, problems of accultur- cial attention was paid to developing amethod ation and their associated stresses, and pos- high-risk women and sible biochemical and physiologicalfactors. to identify populations of factors, theirpsychological and sociologicalpredis- Causalrelationship between these position to alcohol abuse. Using thisinforma- singly or together, and alcoholism,in either this tion, the Alcoholism Center designedand Im- individuals or groups of individuals, has to plemented a multimedia,multifaceted pre- time only been inferred. HispanicAmericans, vention strategy, which is being tested. likeotherminority groups, underutilize treatment and rehabilitation resources,and Minorities.--For many years, accurate data few prevention programs have beendesigned on the nature and extentof alcoholism among for them (Alcocer 1982). this coun- ethnic and racial minorities within exists try were unavailable, makingthe task of tar- Elderlypersons.--Strongevidence geting prevention efforts within andbetween that the percentage of drinkersbegins to de- better cline at age 50, and at age 60 to 65,the per- these groups difficult. Now, however, males drops data are available on alcoholism andproblem centage of heavy drinkers among drinking among black,Asian,Hispanic, and even more sharply.From age 50 on, however, Native Americans. An important issuerelated some older people whohave been lifelong ab- variationsamongethnic stainers or moderate social drinkersbecome tounderstanding Brody groups in use of alcohol andincidence of al- problemdrinkers (NASADAD 1981; cohol problems has been whether thesevari- 1982).. But the negative attitudes of many sociocultural, bio- mental health professionals towardolder per- ations derive more from prevention and chemical,orphysiologicaldifferences.Al- sons seeking help make the attribute predominant treatment of alcoholism in theelderly very though current data for influence to sociocultural differences difficult. One solution may be support the determination of sig- self-help groups--older persons helpingthose (Schaefer1982), in need--as well as a greateremphasis on nificant genetic contributions to alcoholism affect use risk indicates the need to morefully examine preretirement planning that may (Gomberg 1982). Loss, biochemical andphysiologicalparameters. and abuse of alcohol Thus, a final answer to the questionawaits such as that reflected in retirement, appears methods and more to be an impetus for developingalcohol prob- more sensitive bioassay isolation is sophisticated sociocultural surveydesigns. lems in this age grc up. In addition, While drinking behavior of youth andthe of particular significance for prevention pro- communityremains gramers, e.g., how to reach thelarge numbers elderlyintheblack experi- largely undocumented, the findingsfrom a few of women in this age group who have prevention programs for black youth(Crisp enced loss and who are living alone. (Gaines An assessment model to help plan treatment 1980; Miranda 1981) and black women elderly has 1976) have been reported. Suchprojects need and prevention services for the to be studied in depth toempirically assess been proposed (Kola and Kosberg1981). De- their effectiveness. Of particular concernfor signed to consider the specialneeds of the that young elderly for prevention and treatmentservices, prevention programers is the fact importance of in- black males (aged 25-34) In metropolitan areas the model recognizes the times more likely than tegrating these services into existing commu- are as much as 10 An young white males ofthe same age to die from nity treatment and prevention resources. cirrhosis of the liver. This disproportionately example of a self-help programeffectively the Increased rate remains higher for blackmales integrated into its community is located at 1982). In addition, Eagleville Hospital and Rehabilitation Center, until age 65 (Malin et al. prevention although it appears that blacks drinkless than where it began drug and alcohol

129 5 3 services to the elderly in Montgomery County, visit to an obstetric clinic,women fill out a Pennsylvania, in1978(Leigh 1980). structured health history thatelicits information on alcoholuse as well as other items. Infants.--Alcohol consumption during preg- Women who reported consumingmore than45 nancy poses a significant risk for the unborn drinks per monthwere counseled in a noncon- child, with consequences includingincreased frontative manner about thebenefits of de- spontaneous abortion, decreased birthweight, creasingalcohol major and minor birth defects, consumptionforhaving and mental healthier babies. Fetaloutcomes were mark- retardation. edly superior for those heavy These effects of alcohol drinking women on the developing who decreased alcoholconsumption or ab- human fetus are detailed elsewherein this stained during the remainder volume (see chapter 5). Some of the pregnancy occur in children to those for heavy drinkers who didnot change whose mothers, duringpregnancy, consume their drinking behavior. Of particular alcohol In amounts consistent interest, with a diagnosis the Boston study tentatively concludedthat of alcoholism. Someoccur In children whose either the later pregnancy period mothers drink moderately. All ismost of them are crucial for alcohol teratogenicity,or revers- completely preventable. ibility of injury Is possible if A variety of prevention heavy drinking is approaches will be terminated early enough duringthe pregnancy necessary to reach social or moderate drinking course. Further work may clarify exactly when women and women who drink heavily. The prevention effortscan be implemented for Surgeon General's health advisoryon the risks optimal effectiveness. of alcohol consumption duringpregnancy, is- A recent cross-sectional sued in 3uly 1981 (FDA), pointed study compared up the need drinking patterns duringpregnancy over a 6- to prevent alcohol-derived birth defects.This year interval (Streissguth et al. advisory urged physicians and 1983).Dif- other health ferent samples of pregnantwomen were in- professionalstoadvise patientswhoare terviewed in1974and 1975 and in1980 pregnant or considering pregnancy and not to drink 1981. In the interim period, the studypopula- alcoholic beverages. tion was exposed to public media One of the best documented fetal and educa- alcohol tional programs on alcohol andpregnancy. syndrome (FAS) preventionprograms is the Although the proportion of Fetal Alcohol Syndrome women drinking Demonstration Pro- during pregnancy was foundto have decreased gram at the University of Washington (Little during the 6-year interval, the etal. proportion of 1980; McIntyre1980). This program women drinking at least an ounce of absolute aimed at providing model public and profes- alcohol per day was relativelyconstant. Since sional education on FAS, clinicalservices for it is precisely this limitedproportion of the pregnant women, assessment services for FAS population thatincurs the highest children, riskof and ongoing evaluations of these alcohol-related birthdefects, activities. Compared with theseresults a control communi- highlight the need formore intensive preven- ty, there was a significant increase inthe tion efforts. number of women who agreedto become abstinent during pregnancy. However,the program was lesssuccessfulinreachingthe pregnant "excessive drinker" whowas drinking Law and Regulation at levels reported to posea risk to the fetus. Thus, it may be indicated thatsome women who are exposed to programs on alcohol and Since the publication of the FourthSpecial pregnancy will decrease their drinking, while Report to Congress (USDHHS 1981),a number other women who drinkmore heavily may re- of studies have been published, quire specialized services such exploring the as those of- implications of legislative and regulatoryap- fered by the obstetrical communityin terms proaches for the prevention of of screening techniques for early alcohol-related Intervention problems. The findings of thesestudies are and subsequent referral fortreatment (Little summarized here. in press). Other efforts--one in Goteborg,Sweden, and oneinBoston--havereportedhighlysuc- International Studies cessful outcomes utilizinga secondary prevention approach (Olegardet al. 1979; Rosett In collaboration with the World et al. 1980e 1983). During their first Health Or- prenatal ganization (WHO), the InternationalStudy of 15 4 130 Alcohol Control Experiences (ISACE)reviewed alcohol Intoxication in the Americas is the historic.1patterns ofalcohol consumption, most neglected alcoholissue;(2) increased problems, policies, and their effects in Fin- Interest in group-oriented measures aimed at land, Ireland, the Netherlands, Canada, Po- preventing alcohol-related problems should be land,Switzerland,and theUnitedStates developed;(3)available empirical evidence (specifically, California). suggests that a number ofprevention-oriented, The study, entitled Alcohol, Society and the legislatively based policies should integrate State (Make la et al. 1981), found that "growth public health and economic development ben- iliaTeohol consumption was accompanied by an efits and costs with the social, cultural, and increase in a broad variety of problems related political societal values; (4) public and gov- to drinking....This holds not onlyfor conse- ernmental awareness must precede implemen- quences of prolonged drinking, butfor social tation of effective policies; and (5) while the and health problems related to single drinking experiences of one country can assist others, a episodes as well." Noting that "from a policy country's alcohol-related prevention strategies perspectiveitis perfectly legitimate to be must be shaped by its own uniquesocial, cul- interested in the autonomous impact of alco- tural,political, and economic situations hol control on consumption and problems," the (Institute of Medicine 1982). authors state that "from a historical per- The ANSVAR Mutual Insurance Company, in spective, the notion of effect is problematic.... connection with the 1981 annual conference of Most of the time, changes in policy measures the International Council on AlcoholAddic- have, in fact, been one facet of the same tions, published Alcohol in the World of the general social processes, and changes in con- 80's:Habits, Attitudes, Prevention Policies sumption, another." (p. 109) and Voluntary Efforts (Armyr et al.1982). This The report also concluded that (1) "a re- broad inquiry detailed conditions in 23 coun- organization of responsibilities among tries or groups of countries with respect to branches of government may be required to drinking habits, alcohol control policy, eco- achieve a successful combination of economic, nomic issues, and efforts from the voluntary health, and social considerations;" (2) "pre- sector. This review concurred withthe find- ventive alcoholpolicies should...be given a ings of ISACE and also concluded that, In the high priority as an alternative to the morally coming 5 years, alcohol consumption was more inspiredcontrolofproblemdrinkers;"(3) likely to increase than decrease, along with "policy changes on alcohol should be made many Indicators of alcohol-relatedproblems. with caution and a sense of experiment;"(4) "while control of availability should receive a high priority, itIs Important to consider gov- Taxation ernmental powers to manipulate the environment of drinking so as to lower therisk of adverse consequences" (e.g., trafficfatalities As the ISACE study noted, there is a"rel- andalcohol-relatedviolence);(5)"interna- atively large econometric literature on the tional organizations should give close atten- relation of alcohol taxes and prices to con- tion to existing and future tradepolicies and sumption" (Makela et al. 1981, p. 89). Recent arrangements with a potential foraffecting studies attempt to address more clearly the the availability of alcoholic beverages"(Ma- relationship of alcohol taxes to alcohol-related kela et al. 1981, pp.110-112). problems. InJune1982,the National Academy of In particular, Cook and Tauchen (1982) es- Sciences published the proceedings of an In- timate that an increase in the liquor excise gallon (viz., stituteofMedicine(IOM)- supportedinter- tax by $1 (1967 prices) per proof American workshop entitled Legislative 64 ounces of ethanol) would reduce the liver Approaches to Prevention of Alcohol-Related cirrhosis mortality rate by 5.4 percent in the Problems. The purpose of this workshop was to short run and perhaps by twice that amountIn explore the issue of economic growth, alco- the long run.Cook also offers a historical holism, and alcohol-related problems by re- example: When France imposed stringent wine viewing available data and the experiences of rationing In 1942, the cirrhosis mortality rate other countries to help policymakers in the inParisfell from 35/100,000in 1941to Americas understand the complexities gov- 6/100,000 in1945-46, only to return toits erning public policy decisions. The consensus previous higher levels when rationing ceased in emerging from the conference participants 1948. Other work (Mello1972; Nathan and was that: (1) the cost to societyfrom episodic Lisman1976) offersclinicalevidence that

131 155 alcoholic persons do reduce their alcohol con- reported 'had been drinking' (HBD)crash sumption as a function of thebeverage costs. involvement among Cook (1981) also found that 18-20-year-olddri- increases in the vers, an (annual] reduction of 31percent tax rate of spirits will reduce boththe auto fatality rate and the cirrhosis occurred in the first 12 months afterthe rate. Smith drinking age was raised from18 to 21 in (1981) draws thesame conclusion. Two reviews of these relationships December of 1978. Analyses oflate-night, worldwide (WHO 1979; single-vehicle crashes witha male driver, Colon 1980) suggest that whilealcoholic bev- of which a majority have erages behave as other market commodities been consist- do ently identified as involvinga drinking (inthat consumptionis affectedI)) nrice), driver, reveal a significant there are also complicated reduction of interactions be- 18percent among drivers aged18-20 tween the availability of alcoholsupplied by after the higher legal drinking the distribution networkand the pricing of age was alcohol. implemented. (Wagenaar 1980,p. 148) Cook and Tauchen (1981) also note that the In another study (Maxwell 1981),made after Federal tax on alcoholicbeverages has re- Illinois raised its minimum legal mained constant in nominal drinking age terms since 1951. in January 1980 from 19to 21 years, data for Thus, the real price of alcoholicbeverages has actually declined in recent single-vehicle, nighttime, male-driverinvolve- years, such that ments occurring between 8p.m. and 3 a.m. between 1960 and 1980 the real priceof liquor were used as a surrogate for alcohol-involved declined 48 percent, beer 27 percent, and wine accidents. This study, comparing1980 with 20 percent. 1979 accident data, concluded that On balance, the weight of raising the opinion (Cook legal drinking age lawwas effective in re- 1981) appears to be thatconsumption is af- ducing the single-vehicle, fected by price, and data exist nighttime, male- in support of driver Involvement for driversaged 19 and 20. this view. Moreover, thepreviously held view For 1980, the percentage of that reducing overall reduction attrib- consumption does not utable to the law changewas 8.8 percent. affect consumption by theheaviest drinkers The Michigan and Illinois (Make la1975)is studies looked at being challenged andre- all accidents--fatal, injury, andproperty dam- evaluated (Make la1980; Smart 1982). Many age. Another study (Williams et al. 1983), countries already have adopted us- the view that ing data from the Fatal AccidentsRecords increasing the price of alcoholicbeverages is a System(FARS)ofthe viable control strategy. Sweden NationalHighway (Somervuori Traffic Safety Administration,looked at nine 1977), Finland (Koski 1977),Australia (Luey States that raised their legal 1979), Poland (Malec 1980), minimum age. and some Euro- Eight of the nine States experienceda reduc- pean Common Market countries(Sulkunen tioninnighttime 1978) employ fatalcrashinvolvement some form of price policy asa among drivers in the affectedage group; the consumption control. average annual reduction was 28 percent. A recent study (Wagenaar et al.1981) on the effects of raising the minimumage in Michi- Minimum Drinking Age gan and Maine concluded that Michigan drivers aged 18-20 experienceda net reduction of approximately 20 percent in the Thereis frequency of considerable evidencethatin- Involvement In creasing the legal alcohol-related injury- age for possession, pur- producing crashes due toa raised drinking age chase, consumption, or sale of alcoholic bev- from 18 to 21; in Michigan, therewas a 17- erages can be an effectivemeasure to reduce percent decrease in alcohol-relatedcrashes drunk driving accidentsamong youth (Douglass et al. 1974; Wagenaar 1980; damaging property for thesame age group; Wagenaar et al. and in Maine, 18- to 19-year-oldswere in- 1981; Maxwell1981; Williams etal.1983; volved in Hingson et 20 percent fewer alcohol-related al.1983). A study by Wagenaar crashes damaging property. (1980) analyzeda random sample of 20 percent Therealsoisevidencethatcontiguous of all reported accidents (i.e.,fatal, Injury, Stateswithdifferential and property damage) in Michigan minimum drinking from Jan- ages create problems with cross-borderpur- uary 1972 to December 1979. It concluded that: chase of alcohol by youth (Lilliset al. 1982). Based on these studies, the NationalTrans- Controllingfortrends,seasonally, and portation Safety Board recommended other patterns in the frequency In 1982 of police- that all States raise the minimum legalage for

132 156 drinking or purchasing all alcoholic beverages Current Activities to 21. Several States have done so, and many Introduced this kind of legislation in 1982 and 1983. World Health Organization In 1979, the World Health Assembly recog- nizedthatproblemsrelatedtoalcohol- - excessiveconsumption,inparticular--rank Highway Safety among the world's major healthproblems. A In seeking to reduce injuries and fatalities resolution was passedurgingthe member from alcohol and highway traffic accidents, States to take all appropriate measures to deal the legislative area has received increased with the increasing problem and requestingthe attention. New laws are mandating stringent directorgeneraltostrengthentheWorld minimum penaltiesforintoxicateddriving Health Organization's (WHO) capacity to this offenders and supporting more intensive en- end (WHO 1979, 1980). forcement of existing intoxicated driving laws. At the 1982 World Health Assembly, tech- These legislative approaches are being taken nical discussions involving 300 delegates from to establish new limits on driving anddrinking 100 countries were held on the topic"Alcohol and to decrease the incidence of driving while Consumption and Alcohol-Related Problems: intoxicated. Development of National Policies and Pro- A recent review of intoxicated driving lit- grams." The need for national alcohol policies erature (Borkenstein 1981) suggestedthat the to overcome future problems wasaccepted by role of alcohol in traffic accidents canbe every discussion group, as wasthe need to curtailed by (1) reducing per capita alcohol mobilize "political will" to overcome the in- consumption (by increasing price or raising evitabledifficultiesindevelopingnational this political drinking age);(2)constructingstreets and alcoholpolicies. Furthermore, highways that place fewer demands on drivers willmust springfrom the grassroots and the so the effects of alcohol are not as severe;and should represent the community as well as (3)increasing enforcement tobringabout Nation. A major recommendation emanating general deterrence of drinking and driving. fromthesediscussionswasthatalcohol- In Survey and Deterrence of theDrinking related problems be given their vitallyImpor- Driver: An International Survey, Ross(1981) tant place in all strategies forreaching the reviewed the experience of various countries goal of "Health for All by the Year 2000." in adopting the Scandinavian model,which In 1983, the World Health Assembly passed a combines the principles of deterrence with resolution reiterating the firm conviction that laws related to drinking and driving.He con- problems relating to alcohol consumption rank cludes that "enactment and enforcementof among the world's majorpublic health con- drunk driving laws are most successful intheir cerns and constitute aserious hazard for hu- initialdeterrenceofdrinking and driving. man welfare.This resolution recommended When certainty of punishment for drinkingand that member States formulate explicitand driving violations Is low, however, this initial comprehensive national alcohol policies with deterrent effect disappears. A reasonable in- prevention as a priority within the framework terpretation of the results of this review is of the strategy of "Health for All by theYear that Scandinavian-type laws deter whenIni- 2000." The resolution also asked WHO notonly of to continue but to intensify its program on tiated because of exaggerated perceptions of the risk of apprehension and punishment.Since alcohol-related problems as an integral part they appear to increase the real risksmuch the strategy and to strengthen Its capacity to States to more moderately, thedeterrent accomplish- respond to requests from member ment rests not on a firmfoundation,but support their efforts in dealingwith alcohol- rather on a temporary scaffold thatbecomes related problems. undermined through experience." Furthermore, Ross suggests that "research Is needed tode- National termine the function of the componentsof behaviorof Health promotion. --To achievethe1990 legalthreatInaffectingthe within the drinking and driving, particularly therelation health objectives, many agencies between actual and perceivedcertainty, se- Department of Health and Human Services collaborative verity,and celerityofpunishment(Gibbs (DHHS) areincreasingtheir activities. For example, the NationalCancer 1975); and the interaction between certainty of de- and severity of punishment." Institute and NIAAA are In the process

133 1 5 7 termining the appropriateness ofand strategies for a public education developed a plan of actionaddressing this effort designed to problem. The Council'sprogram, consisting of raise awareness aboutrisks of alcohol-related six measures, including cancers. public education,is intended to continue thenational momentum Furthermore, specific DHHSagencies are against intoxicated driving. working withtheDepartment of Defense The Alcohol Traffic Safetyand National (DOD) to introducea comprehensive health Registration Act of 1982 (Public promotion effort that includes Law 97-364) preventing al- authorizes incentivegrants to the States to cohol abuse and alcoholismwithin the mili- tary, as well as with DOD developers encourage the establishment of effectiveal- of a cohol safetyprograms. Administered by the curriculum guide foruse in dependent schools National Highway Traffic overseas. Safety Administra- tion (NHTSA), the lawprovides a basic grant to States that meeta minimum set of stand- Youth.In 1982, the Secretary ofDHHS un- ards and a supplemental deFfrkoanInitiativeon Teenage grant when additional Alcohol provisions are Incorporated.National Drugged Abuse to address the risksassociated with the and Drunk Driving Awareness consumption of alcohol by Week, also en- youth. This effort, acted by Congress, stimulateda sense of na- which was supprted by theDepartments of tional priority about this Transportation (DOT) and problem during the Education (DOE), week of December 12-19,1982. included dissemination ofmodel programs, Withinthe Federal Government, joint initiatives with the private several sector, re- agencies and departmentshave joined to in- gional prevention and treatmentconferences, creaseefforts and a national conference toreducealcohol-related held In Washington, highway accidents. For D.C., designed to draw national instance, NIAAA and attention to NHTSA and the Departmentof Defense have the work of a growing numberof youth- strengthenedinteragencycollaborationto directed drinking and drivingprograms. The Initiative will be continued prevent such accidents. NHTSA'sapproach through efforts vigorously supportsa six-step countermeasure directed at youth at highrisk for development model. of alcohol problems. In addition, DHHS andDOE are collabora- ting to explore the role of Policyconference.--As notedearlier,in schools in pre- 1981, the National Academyof Sciences pub- venting adolescent health problems.The Ado- lished a report on its study lescent School Health Promotion of alternative ap- Demonstra- proachestopreventiontoalcohol-related tion Program will focuson ways to improve problems (Alcohol and Public the integration of alcohol, drug Policy: Beyond abuse, and the Shadow of Prohibition).In May 1983, under mentaland generalhealthpromotion/prevention contract to NIAAA, NM conveneda cross principlesintoschool management section of national, State, and policies, health services, and local leaders to curriculums. examine the study's conclusionsand to distill ideas for future research Highway safety.--Subsequent and effective pre- to theini- vention measures. Discussionscentered on the tiatives of grassrootsmovements at the local supply of alcohol, communicatingabout alco- and State levels, e.g., MothersAgainst Drunk hol, and community Drivers cooperation to reduce (MADD),StudentsAgainstDrunk alcohol problems. Driving (SADD), Remove The participants--rep- Intoxicate Drivers resenting Government, business,State legis- (RID), PARK IT, and Citizensfor Safe Drivers, latures, public Interestorganizations, and the a number of activities have taken placeat the scientific community--agreed national level. The Presidential that a "network Commission on of policies" and nota single-focus strategy Drunk Drivingwas created in April 1982 to could be effective in reducing heighten publicawareness of the seriousness alcohol-related problems. The proceedings ofthis conference of the drunk driving problem,persuade States will be published in late 1983. and communities to strengthentheir law enforcement and trialprocess, and encourage State and Local State and local officialsto accept and use the latest techniques and methods to solve the The Omnibus BudgetReconciliation Act of problems and to generatesupportforin- 1981 incorporated creased law enforcement. The Federal resources for Commission's alcohol-related prevention and treatment final report will be completedby the end of services into the Alcohol and 1983. Recently, the National Drug Abuse and Safety Council Mental Health Services BlockGrant. Of the

134 158 amount used In any fiscal year foralcohol or ganizing and expanding programs for persons drug abuse activities, the States must use not arrested for driving while Intoxicated (DWI). less than 20 percent for alcohol and other drug Some States and local communities have found abuse prevention and early Intervention. A that organizing a task force on Intoxicated report Including information on services pro- driving can be Instrumental In eliciting coop- vided under this block grant will be submitted eration. For example, the Governor's Alcohol to Congress In January 1984. and iiighway Safety Task Force In New York Through the combined efforts of manyState was co-chaired by the director of theDivision Alcohol Authorities and NIAAA, a publicedu- of Alcoholism and Alcohol Abuse andthe cation campaign directed at women and youth commissioner of the Department of Motor wassuccessfullyimplemented.Ittargeted Vehicles. This task force established one goal: alcohol problems among women, alcohol con- "to reduce dramatically theincidence and sumption during pregnancy, and alcoholprob- tragic consequences of drunk driving in New lems among youth,includingdrinkingand York State." To achieve this goal, a compre- driving. Television, radio, and print materials hensive systems approach was recommended. were disseminated through amultilevel strat- The task force's recommendations resulted in egy designed to encourageboth State and local legislative changes, the most significant being collaboration and involvement from a wide user funding for DWI programs. consortium ofgroups Interestedinalcohol The State of South Carolina also has been problems. The States provided resourcesfor especially active in the area of drunk driving dissemination of the materials, organizedthe through the appointment of four regional task campaign efforts, and developed local pro- forces that will use community-based involve- grams. Furthermore, manyStates and local ment to work on reducing the growing problem communities developed additional public ser- of drinking and driving in the State. The State vice announcements and print materials. Government also has introduced a Thousands of people became involved in this comprehensive legislative package that would effort across the country, and process evalu- raise the legal drinking age to 21, prohibit the ation indicates that the campaign was cost- possession of an open container of beer or efficient and successful in reaching the target wine in a moving vehicle, provide that a blood audiences. More than $10 million was donated alcohol concentration of .10 percent or more by the private sector for airing of alcohol- Is legal evidence of impairment, and require relatedtelevisionpublicservice announce- that offenders render services to their comments during the first 11 months of the1982 munity (NASADAD 1983). campaign, at a cost of less than 1.1 cent per Other States -- Michigan, California, Mary- person. Twenty percent of thepublic service land, Maine, Vermont, and Massachusetts, for announcements were broadcast betweenthe example--have implemented campaigns and hours of 5:00 p.m. and 11:30 p.m., one of the. programs within their communities.The year- prime viewing times for women and youth end figures for 1982 showed that more than ( NIAAA 1983). 5,000 fewer fatalities were recorded than in A national prevention network, composed 1981. This also represents a 14-percent de- primarily of State prevention coordinators, has crease since 1980 (NHTSA1983). NHTSA re- been formed as part of the National Associa- cently selected 10 cities, counties, and States tion of State Alcohol and Drug Abuse Direc- to undertake special efforts to removein- tors (NASADAD). This group represents an toxicated drivers from the highways. The 10 important prevention resource for the Nation. sites have been designated "targets of oppor- It is now formalizing organization and devel- tunities," a concept developed to promote the oping operating procedures and agendas adoption of comprehensive, community-based, (NASADAD 1983). general deterrence alcohol programs. The re- Many States are particularly aggressive in sults of this effort hold potential for future their pursuit of preventing drinking and driving prevention of public health problems. accidents and fatalities. During the 1983 leg- An important point made about State and islative session in the States, 378 separate I. cal prevention programs is that there is a lag pieces of legislation related to alcohol and/or in prevention programing and prevention out- drugs and highway safety were introduced In come. According to the CONSADResearch 37 States, and 38 laws wereenacted Report on Prevention (McCartney and Hum- (NASADAD 1983). bert 1978), prevention must involve a large A number of States have been active in enough population base, over time, to actually gathering data on the problem and then or- affect social norms. An example that proves

135 153 the point,theCottageMeetingProgram izations and 200 local public broadcaststa- (Boswell 1983), found that after 10years It tions (PBS) across the country. Each had changed community partici- norms and attitudes, pating PBS station and communityvolunteers resulting in an increased demand forpreven- organized town meetings to watch thepro- tion services. grams and discuss community solutions unique to the problems of particular communities. Private Sector The project was produced andpilot-tested by WQED InPittsburghwith funding by the In 1982, the National Councilon Alcoholism Richard King Mellon Foundationand the Met- (NCA), which pioneered theconcept of alco- ropolitan Life Foundation(WQED 1983). holism as a disease and a major health prob- The private sector is becoming lem, adopted a position increasingly paper on prevention involved in national, State, and localpreven- (NCA1982; Tofany 1983). This paperexpresses tion activities. Insurance companies,the mo- NCA support for a wide variety ofapproaches, tor vehicle industry, soft drink producers and including education,informationprograms, distributors, tire manufacturers, sportsteams, regulatory measures includingadvertising privately owned print and broadcastoutlets, curbs, an increase in Federal excisetaxes on producers and distributors of alcoholic bever- alcoholic beverages, a nationwide legal ages, and a wide range of other private sector drinking age of 21, and a series of rotating businesseshavecontributedto)revention health warning notices regardingthe conse- efforts. quences of alcohol consumption. The message communicated bythese efforts Through the 1982 NIAAA public education Indicates that there is and must continueto be campaign and outreach efforts conducted by a shared responsibility for preventionamong the National Clearinghouse for Alcohol In- different groups at all levels. Thisenviron- formation (NCALI), major voluntary associa- ment of concern has the potential forgener- tions embarked on alcohol abuse prevention ating additional enthusiasm, commitment,and for the first time. For example, the YWCA, resolve to address alcohol problems. with...assistance from NCALI, developeda curriculum and provided technical assistance for the potential implementation ofa pre- Summary vention program in 900 local chapters. Many voluntary organizations included comprehen- The intent of this chapter has beento de- sive prevention programs and activitieson scribe current perspectiveson prevention, to their agendas at the community level,thus summarize available research, andto describe Increasing visibility for alcohol-related prob- currentpreventioneffortsandinitiatives. lems and prevention programing at the local While national,State, and local prevention level. Many businesses also joined this effort activities - -oftenstimulated by at the State and local levels. grassroots movementsmay be implemented withouta In addition, in 1982, parentgroups began to scientifically based and sound methodological seek ways to prevent illegal and harmful al- design, description of these effortsdoes sug- cohol use and misuse by youth. The previous gest Ideas for future prevention research. focus of these groups was on the prevention of Clearly, advances have been made inpre- drug use; more recently, this attention has ventionsincetheFourthSpecialReport focused on alcohol and alcohol in combination (USDHHS 1981)was pullished. Previous re- with other drugs. search efforts focusedon measuring the im- In the area of drinking and driving, other pact of single variables to determine changes adult and youth community groups proliferated in behavior and often failed to demonstrate to prevent alcohol-related motor vehicleac- significant differences. A broaderrange of cidents. These various groups work to createa prevention approaches Isnow being tested, climate in which the communityas a whole however, and evaluationsare being designed to can be activelyconcernedaboutcertain test models in which myriad factors andvar- alcohol-related problems. iables interactincontributingto alcohol- Probably one of the largest private sector related problems. initiatives to prevent alcohol and other drug Although definitive answersmay not be problems among youth has been "The Chemical forthcoming In the immediate future, research People," a two-part television broadcast aired findings suggestthat both educationalap- in November1983in conjunction with the proaches and laws and regulations contribute participation of more than 25 nationalorgan- to a reduction of alcohol problems. For these

136 160 to be effective, however, public support must drinking practices, and interventionsin be generated and sustained. theenvironment mediating between Given the complexity and interaction of drinking and certain of its consequences factorsaffectingdrinkingpatterns, occur- represent valid approaches with promise rences, and consequences, nosingularpre- for sustained improvement. Each detailed vention strategy is likely to be optimal or element will fail or succeed only as it is universally generalizable. What is becoming implementedproperly andthoroughly; eminently clear from previous and recent re- tactics that are undertaken as part of a search is that a combination of diverse strat- broad and coordinated approach are more egies must be employed. In this regard, a re- likely to be effective than ones under- port entitled Beyond the Shadow of Prohibition taken in isolation. (Moore and Gerstein published by the National Academy of Sci- 1981, p. 116) ences in 1981 states that researchers: Itis hoped that these combined approaches are convinced that the regulationof sup- will be effectiveinreaching the alcohol- ply, legal and educational approaches to related health objectives of the Nation. References

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141 165 Index

Abstinence Alcoholism (see also Alcohol abuse; Alcohol and cognitive deficits, 27, 28 dependence) with disulfiram treatment, 112-113 as cause of death, 6-7 and healthy offspring, 69, 76, 130 cognitive effects of, 27 vs. moderate drinking, 1 1 1 and depression, 29 and psychiatric symptoms, 29 diagnosis of, xiii, 101-103 as treatment outcome, 105, 113, 115 and family problems, 89 Accidents, alcohol-related hospital discharges with, 8, 9 airplane, 85 and rape, 89 home and recreational, . subtypes, heritability of, 18-19 pedestrian, xix, 85 theories traffic (see also Driving and drinking), xix, 9-11, denial of responsibility, 91 83-84 disinhibition, 87, 89, 91 work-related, xix, 85-86 interactive drinking/violence, 91 Adolescents social learning, 89, 91 alcohol education programs for, xxii, 125-126 and traffic accidents, 84 consumption patterns in, xiii, 3-5 Alcoholism counselors, xi, 113 Initiative on Teenage Alcohol Abuse, 134 Alzheimer's disease in single-vehicle fatal accidents, 9-11, 83 compared with alcoholic brain injury,xv, 28 tobacco education programs for, 127-128 Animal studies Age (see also Drinking age, minimum) on alcohol and cancer, 59 and AA membership, 112 on alcohol and digestive system, 45, 46, 47-48 and alcohol education programs, 123, 125-127 on alcoholic blood disorders, 53-54 re alcohol and homicide, 87-88 on alcohol metabolism, 48 and brain scan measurements, 27 on alcohol-related birth effects, 71-72, 73, 74, and early detection of alcoholism, 104-105 75, 77 as factor in consumption, 2-3, 4 on alcohol withdrawal, 35 in fatal traffic accidents, 9-11, 83 on calcium uptake and binding, 34 interaction with alcohol consumption, 26 on cognitive skills, 26, 28 re suicide, 92-93 on electrical activity in neurons, 33 Alcohol abuse (see also Alcoholism) on genetic susceptibility to alcoholism, 21 based on reinforcement theory, 37-38 on heart effects of alcohol, 52 costs of, v, 93-95, 96 on hormonal changes, 56, 57-58 definitions regarding, xiii, 101 on reinforcement theory, 37-38 historical perspective on, x on sexual dysfunction, 55-56 and psychiatric illnesses, 29, 114 on tolerance, 21, 35, 36 Alcohol dependence (see also Alcoholism) Antabuse (see Disulfiram) defined as syndrome, 101-103 early detection of, 104-105 Beverage type related to tolerance, 36-37, 101, 102 in birth effects, 77 Alcohol, Drug Abuse, and Mental Health in consumption per capita, 1 Administration (ADAMHA) Biochemical markers for alcoholism prevention definitions, 123 In early diagnosis, xii, xxi, 104-105 role in lCD development, xx, 101 elevated AANB (alpha amino N-butyric acid) in Alcohol metabolism blood, 49 genetic variation, 20, 21 elevated GGTP (serum gamma-glutamyl inability in heart, 52 transpeptidase), xxi, 104 in Orientals ("flushing"), 20, 21 elevated MCV (mean corpuscular volume), xvii, role of liver in, 48-50 54, 104 and sexual dysfunction, Birth effects, alcohol-related (see also Fetal TIQ formation and uncon ad drinking, xvi, alcohol syndrome) 38 in animal studies, 71-72, 73, 74, 75, 77 Alcoholic Rehabilitation Act, enactment of, x low birth weight, xviii, 69, 73-74, 76 Alcoholics Anonymous (AA), xi, xxii, 111-112, 114 fetal alcohol syndrome, xviii, 70-71

142 16' 6 Birth effects, alcohol-related (cont.) Costs of alcohol abuse hyperactivity, xviii, 69, 74 economic infant mortality, 69 of birth defects, 71 mental retardation, xviii, 74 illness - specific estimates, 94, 95, 96 motor development scores, xviii, 74 population-specific estimates, 94 neural development, 75 In work productivity, 93-94 problems with human studies, 71 effect of treatment on, 106-107 spontaneous abortion, xviii, 69, 72 under Blue Cross/Blue Shield, 107 Black Americans within health maintenance organizations males and suicide, 92 (HMOs), 107 pregnancy and drinking, 6 social, 94 prevention programs for, 129 Counselors, alcoholism, xi, 113 Blood Crime, role of alcohol in abnormalities with liver disease, 49 homicide, xix, 87-88, 90 disorders from alcohol other, 89, 90 elevated MCV (mean corpuscular volume), 54 rape, xix-xx, 88-89, 90 altered clotting factors, 54 leukopenia, 54 Dementia, alcoholic megaloblastic anemia, 53 chronic organic brain syndrome, 28-29 vitamin deficiencies, 53 DSM-III evaluation, 101 effects of heavy alcohol use on, xvii Dependence (see Alcohol dependence) Blood alcohol concentration (BAC) Depression legal standard for intoxication, xix and alcohol use, xx, 29, 30 levels in fatal accidents, 9-11, 83-86 and suicide, 92 level of impairment, 25 Detoxification Brain (see also CAT scans; Cognition; EEG In nonhospital ("social") settings, xxi, 106 recordings) and regaining cognitive skills, 27 damage in alcohol-affected fetuses, 74 Diagnosis of alcoholism effects of alcohol on, xv-xvi biochemical markers, xii, xxi, 104 measurement for alcohol dependence, 27 difficulty in, 84, 100, 115 DSM-III, role of, xx, 101-103 1CD, role of, xx, 101 psychosocial indicators Caffeine Michigan Alcoholism Screening Test (MAST), as antidote to alcohol, 26 104 Cancers and alcohol Munich Alcoholism Test, xxi, 104 of digestive tract, xvi, 45, 46, 59 unitary disease concept, 100, 114 of liver, 59 binary classification rule, 100 of pancreas, xvii, 48, 59 continuum of severity, 100-101 CAT (computer-assisted tomography) scans Diet in measuring brain for alcoholism, xv, 27 and alcoholic brain injury, xv Children and blood disorders, 46, 53 alcohol education programs for, 123, 125 contribution to alcoholism, 27-28 of alcoholics, 91-92 and liver damage, xvii, 48, 49 conduct disorders as alcoholism predictors, 17 and pregnancy outcome, 72 Cirrhosis, alcoholic and vitamin deficiencies, xvi, 46 blood abnormalities in, 49 Digestive tract as cause of death, xvii, 6-7 cancers of, xvi, 45, 46, 48, 59 description of pathology, 50-51 effects of alcohol on, xvi hormonal changes in, 57, 58 esophagus, 45 hospital discharges with, 8, 9 intestine, 46-47 Cognition, effects of alcohol on mouth, 45 in alcoholics, 27 pancreas, 47-48 driving-related skills, xv, 25, 84 stomach, 45-46 role in treatment models, 110 Disulfiram (Antabuse) in social drinkers, 26 effectiveness as treatment, xxii, 112-113 and violent crime, 87, 88 Diuresis, alcoholic, 58 Consumption of alcohol Drinking age, minimum measured by sales, 1-2 effectiveness in prevention, xxii, 132-133 per capita, by State, xiii, 1-2, 3 Driving and drinking (see also under Cognition; per capita, by type, 1-2 Driving while intoxicated arrests) in pregnancy, 75-76 and fatal accidents, 83-85 self-reported, 2-6, 77 legal prevention, 133 surveys, 2-6 public reaction to, xi, 84-85, 122

143 1 67 Driving while intoxicated (DWI) arrests Heart (cont.) drivers in fatal accidents, 11, 84 cardiomyopathy, alcoholic, 51 prevention programs, 135 moderate alcohol use, benefits of, 51-52 and violent crime, 88 Hepatitis, alcoholic DSM-III (Diagnostic and Statistical Manualof blood abnormalities in, 49 Mental Disorders) description of pathology, 50-51 definitions, alcohol-related, 101 Heredity (see also Genetic factors; Pregnancy differential assessment, 103 outcome) evaluation axes, 101 role in predicting for alcoholism, xii, xiii-xv interview schedules, 101 Hispanic Americans uniform standards for diagnosis, xx, 102 pregnancy and drinking, 6 rates of alcoholism, 129 Education programs treatment programs for, 108-109 and drinking during pregnancy, 76, 78 Hormones effectiveness in prevention, xxli, 123, 125-127 action In alcohol metabolism, 48 school-based altered by alcoholism,. ii-xvili for adolescents, 125-126, 127-128 glucagon, 58 for elementary-age children, 123, 125 growth hormone, 57 for young adults, 126-127 hypothalamus-pituitary-adrenal axis, 56-57 work-related wellness programs, 128 insulin, 58 EEG (electroencephalogram) recordings oxytocin, 58 average evoked response (AER), 31 parathormone, 58 and brain model of intoxication, 30 prolactin, 57-58 Elderly sexual dysfunction, 55-56 prevention programs for, 129-130 thyroid, 57 treatment needs of, 108 vasopressin, 58 vulnerability to alcohol, 26 Hospitalization Employee assistance programs alcohol-related causes of, 7-8 effect on productivity, 93-94 and cost-benefit analysis, 107 role in treatment, xi, xxi, 105 for detoxification, 106 wellness programs, 128 and treatment effectiveness, 107-108 Endocrine system (see Hormones) Hypocalcemia, alcoholic, 58 Environment Hypoglycemia, alcoholic, 58-59 in family alcoholism, 15-19 in fetal growth retardation, 73 in physiological responses, 19-20 and violent crime, 87

Family life, alcohol-affected Immune response children of alcoholics, 91-92 diminished In alcoholics, xvil separation and divorce, 89 role in alcoholic liver damage, 54 violence 1CD (International Classification of Diseases) child abuse, 90, 91 role in diagnosis, xx spouse abuse, 90-91 updating, 101 Fatty liver, alcoholic Insurance (see Health insurance) description of pathology, 50-51 Intervention (see Prevention; Treatment) Fetal alcohol syndrome (FAS) characteristics of, xviii, 70 Kidney economic impact of, 71 disease in alcoholics, 54 genetic factors and, 71 prevalence of, 70-71 Liver prevention programs on, 130 effects of alcohol on, xvii, 48-51 disease and behavioral deficits, 30 Genetic factors disease and glucose tolerance, 58 in alcoholic cirrhosis, 5! disease and sexual dysfunction, 55, 56 in alcoholic subtypes, 114 Lung in birth effects, 71, 77-78 disease in alcoholics, 54-55 in chronic pancreatitis, 48 vs. environment In family alcoholism, 15-19 among minority populations, 129 Mass media campaigns in physiological responses to alcohol, 19-21 effectiveness in prevention, xxii- xxlii, 127 for women and youth, 135 Health insurance Metabolism (see Alcohol metabolism) role in treatment, xi, xxi, 106-107 Minority and special populations (see Adolescents; Heart Black Americans; Children; Elderly; Hispanic effects of alcohol on, xv11 Americans; Native Americans; Orientals; cardiac arrhythmlas, 52 Women; Young adults)

144 1e& Moderate drinking Prevention of alcohol-related problems (cont.) and birth effects, 77 grassroots involvement, 122, 134 and relapse rate in alcoholics, 105, 110-111 law enforcement policy, xxii, 84-85, 130-131, 133 and social problems, 83 mass media campaigns, xxii-xxiii, 127 Muscle, skeletal National Academy of Sciences study on, 123 myopathy, alcoholic, 52-53 primary (with children), xi Muscle, smooth public health approach to, 123 in esophagus, alcohol and, 53 research findings on, 122 in uterus, alcohol and, 53 secondary (early intervention), 100, 104-105, 130 for special populations, 118-130 National Academy of Sciences through taxation, xxiii, 131-132 legislative approaches to prevention, 131 Psychiatric illnesses prevention policy, 123, 134 and alcohol abuse, 29, 114 National Center for Health Statistics Psychosis, alcoholic (Korsakoff's) Hospital Discharge Survey, 7-8 as cause of death, 6-7 pregnancy and drinking behavior surveys, chronic organic brain syndrome, xv, 28-29 5-6 hospital discharges with, 8, 9 National Council on Alcoholism, 136 National Institute on Alcohol Abuse and Alcoholism Sex (see also Women) (NIAAA) as factor in consumption, 2, 4 establishment of, x as factor in hospital discharges with alcoholism,8 fatal accident studies, 83 Sexuality national drinking pattern surveys, 2-3 altered by alcoholism, 55-56 pregnancy outcome and alcohol studies, 71 effects of alcohol on, xvii-xviii prevent ,n efforts, 127, 133-134 Suicide National Institute on Drug Abuse (NIDA) role of alcohol in, xx, 29, 92-93 alcohol consumption surveys, 3-5 Native Americans alcohol-related hospitalizations, 8-9 Taxation alcohol-related mortality among, 8 as prevention approach, xxiii, 131-132 treatment programs for, 108-109 Teenagers (see Adolescents; Young adults) Neurons (nerve cells) Teratology (see Birth effects, alcohol-related; in alcohol effects, 31 Fetal alcohol syndrome) in alcohol-related birth effects, 75, 77 Therapy (see Treatment) chemical transmission between, 34-35 Thiamine (vitamin B1) description and function, 31-33 deficiency in alcoholics, xv, 27-28, 46-47 electrical conduction in, 33-34 and heart disease, 51 neuronal membrane, xvi, 35-37 and Wernicke's encephalopathy, 28-29 Nutrition (see Diet) and Wernicke-Korsakoff syndrome, 20 Time of day/week Orientals, genetic studies, 20, 21 as factor in traffic accidents, 11, 12,84 Objectives for the Nation (In 1990), xii, 124 Tobacco combined effect with alcohol, xv, xvi, 26 Pancreatitis, chronic in digestive tract, 45, 59 in alcoholics, xvi, 47-48 in fatal fires, 86-87 and glucose tolerance, 58 in fatal traffic accidents, 84 Pregnancy outcome (see also Birth effects, in fetal abnormalities, 74 alcohol-related) in lung disease, 54 consumption patterns and, xi, xviii, education programs for adolescents, 127-128 5-6, 75-76, 77 Tolerance historical risks to, 69-70 in alcohol dependence syndrome, 101, 102 and paternal drinking, xviii, 76 and genetic influence, 21 and prevention efforts, 78, 130 and neurochemical changes in brain, 34 Prevention of alcohol-related problems role of hormonal systems in, 36 and birth effects, 78 role of learning in, 36 current activities Treatment of alcohol-related problems "The Chemical People," 136 approaches National Council on Alcoholism, 136 Alcoholics Anonymous, xxii, 111-112, 114 State and local efforts, 134-136 behavior therapy, xxii, 109-110 U.S. Government agencies, 133-134 family therapy, xxii, 112, 114 volunteer organizations, 136 job-related, 105 World Health Organization, 133 pharmacotherapy, xxii, 29, 3!', 112-113 educatior nrograms, xxii, 78, 123, 125-127, 128 psychotherapy, xxii, 112 drinking age, minimum, xxii, 132-133 cost-benefit analysis of, 107

1451 6 9 Treatment of alcohol-related problems (cont.) Withdrawal, alcohol detoxification, xxi, 106 in alcohol dependence syndrome, 101, 102 diagnosis and, xx, 100-104, 114-115 convulsions, 35 and early intervention, xxi, 104 and detoxification, 106 goals, 110-111 hormonal effects of, 56-57, 58 insurance coverage for, xi, xxi, 106-107 and treatment with tricyclic antidepressants, 113 multiple substance abuse programs, 109 Women (see also Pregnancy outcome) outcomes, 105, 112-116 alcoholics and depression, 92 recent developments In, xi, 100, 105, 114, and AA membership, 112 115-116 consumption patterns, 75-76 settings, 107-108 prevention programs for, 128-129, 135 targeted to special populations, xxi-xxii, 108-109 treatment needs of, 108 World Health Organization (WHO) current activities, 133 Uniform Alcoholism and Intoxication Treatment dependence syndrome, xxi, 101-103 Act and intern itional alcohol policy, 130-131 effect on treatment, 106 role in ICD development, xxi, 101 Veterans Administration (VA) alcohol-related hospitalizations, 8 Victims, alcohol in, 88, 89 Young adults Violence (see Crime) alcohol education programs for, xxii, 126-127, Vitamins and minerals (see also Thiamine) 135 In alcoholic hypocalcemia, 58 consumption patterns in, 2-5 deficiencies in alcoholics, 45-48, 53 In single-vehicle fatal accidents, 9-11 riboflavin as treatment, 112 Youth (see Adolescents; Young adults)

*U.S. GOYERNMENT PRINTING OFFICE 1984 442-667/18416 17 146