Alcoholism: The Science Made Easy This publication includes a compilation of alcohol-related Addiction Science Made Easy articles from the ATTC National Office. Original source documents from Alcoholism: Clinical and Experimental Research, the official journal of the Research Society on Alcoholism. ATTC National Office • Kansas City, Missouri 2 2 2 Published in 2004 by the Addiction Technology Transfer Center (ATTC) National Office University of Missouri-Kansas City 5100 Rockhill Road Kansas City, Missouri 64110 This publication was prepared by the Addiction Technology Transfer Center (ATTC) Network under a cooperative agreement from the Substance Abuse and Mental Health Services Administration’s (SAMHSA) Center for Substance Abuse Treatment (CSAT). All material appearing in this publication except that taken directly from copyrighted sources is in the public domain and may be reproduced or copied without permission from SAMHSA/CSAT or the authors. Citation of the source is appreciated. Do not reproduce or distribute this publication for a fee without specific, written authorization from the ATTC National Office. Limited copies of this document can be ordered from the ATTC National Office by phone at 816-482-1200. Copies of Addiction Science Made Easy (ASME) articles can be downloaded from the Internet at www.nattc.org/asme. At the time of printing, Charles G. Curie, MA, ACSW, served as the SAMHSA Administrator. H. Westley Clark, MD, JD, MPH, served as the CSAT Director, and Karl D. White, EdD, served as the CSAT Project Officer. The opinions expressed herein are the views of the ATTC Network and do not reflect the official position of the Department of Health and Human Services (DHHS), SAMHSA or CSAT. No official support or endorsement of DHHS, SAMHSA or CSAT for the opinions described in this document is intended or should be inferred. I IIntroduction ntroductionntroduction 4 4 HOW TO USE THIS PUBLICATION This publication was created so the ongoing series of research based articles called Addiction Science Made Easy (ASME), could be easily distributed and used for educational purposes. Although these articles are available on the In- ternet, our vision was to create another way for educators and practitioners to access them. Whether educating students in a formal setting, delivering con- tinuing education courses, or discussing findings with colleagues, it is our hope that you will use this book to inform others. There are approximately 100 articles included in this document, and we have broken them into 10 major categories. Many articles could “fall” under several different category headings. For example, the article entitled Promising New Treatment Options for People With Co-Existing Alcohol Use and Psychiatric Disorders could have been placed in the Prevention, Intervention and Treatment category or in the Mental Health category. For this reason, we have included a number of ways for you to locate articles. The table of con- tents located on the next page includes page numbers for each of the primary categories. Then you’ll find a listing of all the article titles with their corresponding page numbers and category headers. At the back is a key word index to help you locate specific topics of interest. Please use these articles as you wish. Each page is perforated and three-hole punched for easy copying and storage. Please use these articles as the basis for presentations and handouts in trainings and classrooms. Tear out the pages, make copies, post them in your break room, pass them out to students, etc. We do ask that you site the original source whenever possible. ARTICLES ONLINE AT WWW.NATTC.ORG/ASME • More than 200 ASME articles • Searchable by key word • Research based, easy-to-understand 5 5 TABLE OF CONTENTS Listing of All Articles.....................................................................................6 Preface ......................................................................................................... 10 Acknowledgments ....................................................................................... 12 Adolescents.................................................................................................. 17 Biology – Neurobiology ..............................................................................35 Gender, Ethnicity & Culture ...................................................................... 63 Genetics & Other Risk Factors .................................................................... 79 Mental Health ........................................................................................... 109 Pharmacology ............................................................................................ 127 Physical Health.......................................................................................... 143 Pregnancy, Prenatal Exposure & Parenting ............................................. 165 Prevention, Intervention & Treatment ..................................................... 189 Violence & Injury ...................................................................................... 211 Key Word Index ........................................................................................ 227 6 6 LISTING OF ALL ARTICLES Articles in the Adolescents Category 1. Binge Drinking Among Jewish and Non-Jewish College Students ........................... 19 2. Binge Drinking: A Dangerous Rite of Passage ........................................................... 21 3. College Students May Be Drinking More Alcohol Than Even They Realize ............. 23 4. Adolescents With Alcohol Problems: Redefining the Basics ..................................... 25 5. Impulsiveness, Aggression, Alcohol and Adolescents ............................................... 27 6. Alcohol, Automobiles and Youth ................................................................................ 29 7. Teenagers, Drinking and Driving: A Quick Trip to the Grave ................................... 31 8. Tracking the Long-Term Functioning of Adolescents with Alcohol Problems ......... 33 Articles in the Biology – Neurobiology Category 1. Alcohol-Damaged Brains “Recruit” New Brain Regions to Perform Simple Tasks ...... 37 2. How Alcohol Gives and Then Takes Away ................................................................. 39 3. How Sensitive Is Your Brain to Alcohol-Induced Damage? ...................................... 41 4. The Brain Risks of Binge Drinking ............................................................................. 43 5. Abstinence May Make the Brain Grow Stronger ....................................................... 45 6. Cognitive Neuroscience Takes on Alcohol ................................................................. 47 7. Just a Spoonful of Thiamin? ....................................................................................... 49 8. Alcohol and Thiamin Deficiency Together: A Dangerous Combination? ................. 51 9. Chronic Drinking Increases Cortisol During Intoxication and Withdrawal ............. 53 10. Repeated Alcohol Detoxifications Can Impair Cognitive Function ........................... 55 11. Blocking Selected Neurotransmitter Activity May Decrease Alcohol Consumption .... 57 12. Probing the Role of the Delta Opioid Receptor in Alcohol Consumption ................. 59 13. Behavioral Sensitization: A New Perspective on Alcoholism .................................... 61 Articles in the Gender, Ethnicity & Culture Category 1. Women Who Drink May Be at Greater Risk of Cardiovascular Complications Than Men ........................................................................................... 65 2. Specifying Alcohol-Related Brain Damage in Young Women ................................... 67 3. African American Alcoholics: At Greater Risk for Immune Disorders?.................... 69 4. Liver Cirrhosis Is No Longer a “Black” Disease .......................................................... 71 5. Ethnic Difference in DUI Arrests and Use of Health Care Services in California ..... 73 6. Re-Examining Alcohol Problems Among American Indian Communities ............... 75 7. The Genetic Complexities of Sensation Seeking Behavior in Alcoholic Men ............ 77 7 7 Articles in the Genetics & Other Risk Factors Category 1. A Neurogenetic Approach to Alcoholism ................................................................... 81 2. Untangling the Matrix of Risk Factors for Alcoholism .............................................. 83 3. Using Brain Activity to Identify Risk for Disorders ................................................... 85 4. Searching for Biochemical Markers in Children of Alcoholics .................................. 87 5. The Eyes Have It: Seeking Expressions of the Genetic Risk for Developing Alcoholism ............................................................................................... 89 6. On the Cutting Edge of Brain Gene Analysis ............................................................. 91 7. Genetic Contributions to Alcohol Sensitivity ............................................................. 93 8. Investigating a “Protective Gene” Against Alcoholism .............................................. 95 9. Bridging the Gap Between Genetics and Motivations to Drink Alcohol ................... 97 10. When Alcohol and Nicotine Interact .......................................................................... 99 11. Exploring the Genetic Commonality of Alcohol and Tobacco Abuse ....................... 101 12. Abnormalities in Stress Hormone Response Among Alcoholics ............................. 103 13. Taste Testing May Help Identify Alcoholism Risk ................................................... 105 14. A Sweet Tooth May Be a “Marker” for the Genetic Risk for Developing Alcoholism ................................................................................................................ 107 Articles in the Mental Health Category 1. Alcoholics Have Blunted Responses to Psychological Stressors Such as Public Speaking.......................................................................................................... 111 2. Alcoholics With Antisocial Personality Disorder Have Blunted Emotional Reactivity ................................................................................................................... 113 3. Childhood Abuse May Predict Social Phobia, Agoraphobia and Post Traumatic Stress Disorder Among Adult Alcoholics ........................................ 115 4. Searching for Anxiety Relief in Alcohol Can Be Dangerous ..................................... 117 5. Suicidal Behavior Among Alcoholics ......................................................................... 119 6. Adult Alcoholism and Attention Deficit Hyperactivity Disorder Are Connected .... 121 7. Alcohol Impairs Executive Cognitive Functioning Much Longer Than Expected ...... 123 8. Alcohol Damages Day-to-Day Memory Function .................................................... 125 8 8 Articles in the Pharmacology Category 1. Searching for New Detoxification Strategies ........................................................... 129 2. Fine-Tuning Naltrexone Treatment for Alcoholics ................................................... 131 3. Searching for New Medications to Treat Alcoholism .............................................. 133 4. Using Naltrexone to Treat Alcoholics With a “Mediterranean Drinking Pattern” ..................................................................................................................... 135 5. Behavioral Therapies Plus Pharmacotherapies Can Add Up to Success ..................137 6. An Anti-Nicotine Drug Reduces the Rewarding Effects of Alcohol......................... 139 7. Promising New Treatment Options for People with Co-Existing Alcohol Use and Psychiatric Disorders ..................................................................... 141 Articles in the Physical Health Category 1. Alcohol Abuse May Increase Susceptibility to HIV Infection .................................. 145 2. Alcohol and Cancer ....................................................................................................147 3. Can Heavy Alcohol Use Lead to Some Kinds of Cancer? ......................................... 149 4. Alcohol May Hasten the Progression of Cancer ........................................................ 151 5. Is There a Link Between Alcohol and Allergies? ...................................................... 153 6. How to Build Strong Bones: Get Milk, Lose the Booze ............................................. 155 7. Alcohol, Sodium Sensitivity and Blood Pressure ...................................................... 157 8. Alcohol’s Effects on Testosterone ............................................................................. 159 9. Moderate Alcohol Consumption After Meals Can Decrease Levels of Insulin ......... 161 10. Chronic Alcohol Abuse Damages Regulating Hormones ........................................ 163 Articles in the Pregnancy, Prenatal Exposure & Parenting Category 1. Alcohol Consumption During Pregnancy Alters Thyroid Function ........................ 167 2. Alcohol, Women and Pregnancy .............................................................................. 169 3. Pregnancy, Drugs and Alcohol, Emotional Instability: What Nightmares Are Made Of ................................................................................. 171 4. Exploring the Complexities of Prenatal Alcohol Exposure.......................................173 5. Drinking During Pregnancy: Information May Not Be Enough .............................. 175 6. Drinking During Pregnancy: American Indians and African Americans ................. 177 7. Genetic Protection Against Fetal Alcohol Syndrome? ............................................. 179 8. Light to Moderate Drinking During Pregnancy Can Effect Adolescent Growth ...... 181 9. Light to Moderate Drinking During Pregnancy May Lead to Learning and Memory Deficits in Adolescents ........................................................................ 183 10. The Power of the Mother-Child Bond ...................................................................... 185 11. Parenting, Stress and Your Child’s Risk for Alcoholism .......................................... 187 9 9 Articles in the Prevention, Intervention & Treatment Category 1. Alcohol and Drug Treatment Among HMO Patients ................................................ 191 2. Examining the Effects of Managed Care on Alcohol and Other Drug Treatment ... 193 3. Doctor, Counselor, Cost-Cutter ................................................................................ 195 4. Finding Sobriety and Saving Money Through Spirituality ...................................... 197 5. Comparing Screening Instruments for Alcohol Dependence and Abuse ................ 199 6. Brief Mail- and Computer-Generated Interventions Work Best for Problem Drinking Among Young People ................................................................................ 201 7. Educational Attainment May Predict Drinking Outcomes Following Alcohol Treatment .................................................................................................... 203 8. Alcohol and Smoking: Why They Go Together ........................................................ 205 9. Nicotine Patch Treatment Works for Smokers with Long-Term Sobriety .............. 207 10. Alcohol, Friends and Courtship ................................................................................ 209 Articles in the Violence & Injury Category 1. Alcohol, Drugs and Violence Between Intimate Partners ....................................... 213 2. Alcohol, Interpersonal Violence and Mexican American Women ........................... 215 3. Alcohol Consumption and Intimate Partner Violence..............................................217 4. Marriage, Alcohol and Violence ............................................................................... 219 5. Alcohol’s Double Threat: A Greater Chance of Crashing and More Severe Injuries .......................................................................................................... 221 6. Alcoholics May Be More Injury Prone Than Illicit Drug Users ............................... 223 7. Drinking and Drugging Can Be Painful.................................................................... 225 KEY WORD INDEX BEGINS ON PAGE 227. 10 10 PREFACE Many professionals in direct treatment settings do not have the resources or time to read research journals; nor do their agencies have the money to subscribe to these publications. In addition, research is typically written in a technical manner which is difficult to use in every day prevention and treatment practice. In an effort to bring current research findings to direct service providers, individuals at three organizations came together in an unprecedented manner. In 1999, staff from the Addiction Technology Transfer Center (ATTC) National Office, the Research Society on Alcoholism (RSA) and the journal, Alcoholism: Clinical and Experimental Research (ACER), decided to partner in an effort to translate and disseminate current research on alcoholism. Their goal was to provide frontline staff, educators and the public easy-to-read, concise research findings. Through the synergy of these three organizations, the Addiction Science Made Easy (ASME) project was born. Since that time, more than 215 alcoholism research articles have been disseminated throughout the world. Each month a science writer reads and summarizes the main findings from ACER and “translates” them into easy-to-understand articles. EurekAlert! The ASME articles are first distributed to journalists online through EurekAlert! (www.eurekalert.org), an online press service created by the American Association for the Advancement of Science. The primary goal of EurekAlert! is to provide a forum where research institutions, universities, government agencies and corporations can distribute science-related news to the media. Once released, these articles are made available to the public. More than half a million public visitors, and almost 20,000 registered journalists have viewed ASME articles via the EurekAlert! Web site. Several articles can be directly linked to international news coverage by a variety of media groups including the New York Times, BBC, Reuters, CBC, International Herald Tribune, Yahoo News, CNN International, MSNBC and WebMD. 11 11 Distribution by the ATTC ASME articles are available online at the ATTC Network Web site (www.nattc.org). From the home page, users can click on the Addiction Science Made Easy link. Once there, they can search a database of all ASME articles by keyword, or simply view the most current articles. The ATTC also distributes ASME articles through its free electronic magazine Eye on the Field. This e-zine is published by the ATTC National Office each month, and is sent to more than 9,500 subscribers. Each issue features information relating to substance use disorders and includes four ASME articles, useful tools for practitioners, information about educational events, pertinent Web sites and timely news. Those interested can subscribe to Eye on the Field at www.nattc.org. Similarly, the ATTC National Office highlights ASME articles in its bi-annual newsletter, The ATTC Networker. This free publication is mailed to approximately 5,000 subscribers. Each issue highlights an important theme relating to addiction treatment (such as co-occurring disorders), and then profiles trends, statistics, trainings, treatment methods and other publications relating to that theme. To subscribe, contact the ATTC National Office at 816-482-1200 or visit www.nattc.org. Finally, the ATTC Network highlights ASME articles at trainings delivered across the country. The concise, easy-to-understand style of these articles is perfect for practitioners, educators and the public to receive at conferences and educational events. ARTICLES ONLINE AT WWW.NATTC.ORG/ASME • More than 200 ASME articles • Searchable by key word • Research based, easy-to-understand 12 12 ACKNOWLEDGMENTS Since its inception, there have been many important contributors to the ASME project. It continues to be a truly collaborative undertaking. First and foremost, we want to thank the researchers for their tireless efforts – the steadfast scientists who spend their lives studying the effects of alcohol on the human body, mind and spirit. Their work is ground-breaking and ultimately contributes to saving lives. Many individuals were instrumental in developing the innovative partnership that made the ASME project possible five years ago. Specifically, we are greatly indebted to Carlton Erickson, PhD, director of the Addiction Science Research and Education Center at the University of Texas and associate editor of Alcoholism: Clinical and Experimental Research (ACER). Dr. Erickson, along with Ting-Kai Li, MD, director of the National Institute on Alcohol Abuse and Alcoholism (NIAAA) and the immediate past editor of ACER, approached ATTC National Office staff with their resourceful idea which resulted in the ASME project. Their ardor for making research accessible to frontline workers is evident, and their expertise and communication styles continue to build bridges between the research and treatment communities. We also want to thank Victor Hesselbrock, PhD, president of RSA, the RSA board of directors, and countless others from RSA, who have been supportive of the ASME project since the beginning. RSA’s monetary contribution continues to make these articles possible. Similarly, we greatly appreciate the new editor of ACER, Ivan Diamond, MD, PhD, who supports this partnership and continues to allow us to “translate” research from the journal. Additionally, without copyright permission from the journal’s publisher Lippincott, Williams and Wilkins, none of this would be possible. Next we commend our science writer, Sherry Wasilow-Mueller. Each month she reads, interprets and summarizes each ASME article for dissemination to the field. We applaud her ability to capture the essence of new research and to clearly translate technical content. Her enthusiasm for this work is evident in the excellence of her article summaries. We believe her concise writing style will help change the way practitioners view research. It was the insightful vision of Mary Beth Johnson, MSW, director of the ATTC National Office, to create this book for educators and practitioners. 13 13 A thank you also goes to Jennifer Tate Giles, MSW, and to Angie Olson, MS, associates of the ATTC National Office, who organized, edited and designed this publication. In addition, Carla Ingram, CSACII, LCSW, associate director of the ATTC National Office, helped review and categorize the articles. Finally, we are grateful to Iris Wilkinson, EdD, associate professor in the Human Services Department at Washburn University, and Amy Leary, LPC, counselor team leader at ReDiscover Mental Health Services, who both took the time to read and score each article for inclusion in this publication. Their insights helped us organize a final product that will be maximally useful to users. Sherry Wasilow-Mueller – ASME Science Writer As stated previously, we appreciate the invaluable work of the ASME science writer, Sherry Wasilow-Mueller. Each month, she takes four current ACER research articles selected by an ACER associate editor and creates feature stories. To develop the ASME features, she uses input from the corresponding authors and other scientists who comment on the value of the research being presented. Her articles highlight scientific findings from the ACER journal in an easy-to-read, concise manner. More than simple press releases, each feature provides a broad perspective beyond simple reporting. In June 2001, Wasilow-Mueller was presented with the second annual RSA Journalism Award. Carlton Erickson, PhD, ACER Associate Editor and a national researcher on alcoholism, believes Wasilow-Mueller’s work is impressive. “Sherry has done a superb job of bringing newsworthy research to the public’s attention,” he said. “Her work is characterized by its accuracy, understandability and a talent for condensing large amounts of information into scientifically accurate, interesting articles.” Wasilow-Mueller is married with three small boys, and hopes to eventually earn a doctorate. 14 14 THE ASME PARTNERS This project was made possible through the vision and synergy of three organizations: the Addiction Technology Transfer Center (ATTC) National Office, the Research Society on Alcoholism (RSA) and its journal, Alcoholism: Clinical and Experimental Research (ACER). Each organization contributes time and resources to make this project possible. Addiction Technology Transfer Center (ATTC) National Office University of Missouri – Kansas City 5100 Rockhill Road • Kansas City, Missouri 64110 816-482-1200 • www.nattc.org The Addiction Technology Transfer Center (ATTC) Network is dedicated to identifying and advancing opportunities for improving addiction treatment. The Network’s vision is to unify science, education and services to transform the lives of individuals and families affected by alcohol and other drug addiction. The Network is funded by the Substance Abuse and Mental Health Services Administration (SAMHSA) to upgrade the skills of existing treatment practitioners and other health professionals, and to disseminate the latest scientific findings to the treatment community. Serving the 50 U.S. States, the District of Columbia, Puerto Rico, the U.S. Virgin Islands and the Pacific Islands, the ATTC Network operates as 14 individual Regional Centers and a National Office. The ATTC National Office (National Office) supports the ASME partnership in a number of ways. The largest contribution is by contracting with a science writer to summarize the findings of four ACER journal articles each month. In addition, the National Office disseminates ASME articles in key ATTC publications, maintains an ASME area on the ATTC Network Web site, and developed, published and disseminated this ASME publication. 15 15 Research Society on Alcoholism (RSA) 7801 North Lamar Boulevard, Suite D-89 Austin, Texas 78752-1038 512-454-0022 • www.rsoa.org The Research Society on Alcoholism (RSA) was established in 1975 to encourage scientists to use research to investigate solutions for alcohol-related problems. It is a fertile meeting ground for scientists and promotes research and the acquisition/dissemination of scientific knowledge. RSA’s current membership of more than 1,600 people is drawn from countries all over the world. Membership consists of regular scientific members, associate members and student members. RSA provides support for the ASME partnership by contracting with the EurekAlert! Web site which allows ASME articles to be accessed by journalists throughout the world. In addition, RSA contributed funds to publish this ASME book. Alcoholism: Clinical and Experimental Research (ACER) www.alcoholism-cer.com Alcoholism: Clinical and Experimental Research (ACER) was founded by the National Council on Alcoholism and Drug Dependence (NCADD). In the 1980s, RSA assumed publication of the journal, and it became the Society’s official journal. Each month, this publication brings health care professionals the latest clinical studies and research findings on alcoholism, alcohol-induced syndromes and organ damage. Each month, ACER Associate Editor, Carlton Erickson, PhD, reviews embargoed articles from the journal and chooses four to be rewritten by the ASME science writer. Erickson oversees the work of the science writer, and then submits the four feature articles to the EurekAlert! Web site for posting. 16 16 16 The following is an alphabetical list of everyone who has been instrumental to this ASME project: Ivan Diamond, MD, PhD Founding Director, Ernest Gallo Clinic and Research Center School of Medicine, University of California, San Francisco Editor in Chief, Alcoholism: Clinical and Experimental Research (ACER) Carlton Erickson, PhD Director, Addiction Science Research and Education Center and Pfizer Centennial Professor of Pharmacology/Toxicology College of Pharmacy, University of Texas at Austin Associate Editor, Alcoholism: Clinical and Experimental Research (ACER) Jennifer Tate Giles, MSW Contractor, Addiction Technology Transfer Center (ATTC) National Office University of Missouri – Kansas City Victor Hesselbrock, PhD Scientific Director, Alcohol Research Center and Physicians Health Services Professor of Addiction Studies University of Connecticut Health Center, Farmington, Connecticut President, Research Society on Alcoholism (RSA) Carla Ingram, CSACII, LCSW Associate Director, Addiction Technology Transfer Center (ATTC) National Office University of Missouri – Kansas City Mary Beth Johnson, MSW Director, Addiction Technology Transfer Center (ATTC) National Office University of Missouri – Kansas City Amy Leary, LPC Counselor Team Leader, ReDiscover Mental Health Services Kansas City, Missouri Ting-Kai Li, MD Director, National Institute on Alcohol Abuse and Alcoholism (NIAAA) Bethesda, Maryland Immediate Past Editor, Alcoholism: Clinical and Experimental Research (ACER) Lippincott, Williams and Wilkins Publisher Baltimore, Maryland Angie Olson, MS Contractor, Addiction Technology Transfer Center (ATTC) National Office University of Missouri – Kansas City Sherry Wasilow-Mueller, MA Science Writer, Editor, Researcher Lethbridge, Alberta, Canada Iris Wilkinson, EdD Associate Professor, Human Services Department Washburn University, Topeka, Kansas A AAdolescents dolescentsdolescents ADOLESCENTS ADOLESCENTSADOLESCENTS Articles in the Adolescents Category 1. Binge Drinking Among Jewish and Non-Jewish College Students 2. Binge Drinking: A Dangerous Rite of Passage 3. College Students May Be Drinking More Alcohol Than Even They Realize 4. Adolescents With Alcohol Problems: Redefining the Basics 5. Impulsiveness, Aggression, Alcohol and Adolescents 6. Alcohol, Automobiles and Youth 7. Teenagers, Drinking and Driving: A Quick Trip to the Grave 8. Tracking the Long-Term Functioning of Adolescents with Alcohol Problems BINGE DRINKING AMONG JEWISH AND NON-JEWISH COLLEGE STUDENTS BINGE DRINKING AMONG JEWISH AND NON-JEWISH COLLEGE STUDENTS • Americans who frequently attend religious services have lower rates of alcohol use and misuse. • The same relationship has not been found among Jewish Americans. • Heavy drinking and alcoholism are less common among Jews than Christians. In the United States, religious commitment, as measured by service attendance, has an inverse relationship with alcohol consumption and alcohol problems. In other words, individuals who frequently attend religious services tend to have lower rates of alcohol use and misuse. The same association has not, however, been consistently found among Jewish Americans. A study in the December issue of Alcoholism: Clinical and Experimental Research (ACER) examines the relationship between religious variables and binge drinking among Jewish and non-Jewish college students. It also examines the association between binge drinking and genetic, cultural and religious variables in the Jewish sample alone. “Binge drinking is a growing focus in the alcohol research literature, especially among college students,” said Susan E. Luczak, assistant project scientist in the department of psychiatry at the University of California, San Diego and first author of the study. “It has been related to many negative social, academic, and physical problems. Other measures of problems, such as abuse and dependence symptoms, are also important, but less prevalent in college samples.” Luczak added that even though researchers have traditionally found a strong association between “religious service attendance” and fewer alcohol problems among Christians, heavy drinking and alcoholism are less common among Jews. “There is something about being Jewish that seems to protect people from heavy drinking and drinking problems,” she said. Perhaps this ‘protection’ is rooted in cultural differences, she noted, or perhaps ‘religious service attendance’ may have different meanings across religious groups. Researchers examined two groups: 132 (68 female, 64 male) Jewish and 147 (72 female, 75 male) non-Jewish White college students. Participants reported their alcohol consumption for the previous 90 days and provided information about their religious affiliation and the number of religious services attended in the previous year. Study subjects also had blood drawn for genotyping at the alcohol dehydrogenase (ADH2) locus, one of several genes that encode the major enzymes involved in alcohol metabolism, and which has been associated with protection from alcoholism. Jewish study participants completed the Jewish Identity Scale, developed and published by researcher Itai Zak in Psychological Reports in 1973. The scale measures the degree to which being Jewish plays a part in one’s life, the importance of belonging to the Jewish community, and the closeness one feels to Jews in the world. “This study has three key findings,” said Luczak. “First, religious service attendance is associated with lower rates of binge drinking in non-Jewish college students, but not in Jewish college students. This is consistent with previous research. Second, being religiously 19 continued ~ 20 20 BINGE DRINKING AMONG JEWISH AND NON-JEWISH COLLEGE STUDENTS Jewish, as compared with secularly Jewish, relates to lower rates of binge drinking, but Jewish cultural identification does not. Third, in the combined sample of Jewish and non-Jewish students, those who possessed the ADH2*2 genetic variation were approximately half as likely to binge drink as those who did not possess the variation.” Luczak said, that for the Jewish sample alone, these findings suggest that religious, and not just cultural, Jewish affiliation is related to lower levels of alcohol consumption. Although this may seem to contradict earlier findings of a weak relationship between religious commitment and lower rates of alcohol use and misuse among Jews, Stephen Maisto, professor and director of clinical training in the department of psychology at Syracuse University, believes that the answer may lie in the design of a fundamental measure – defining religious commitment by service attendance. “Perhaps it would have been more useful to define types of services attended and their meaning to the participants, rather than just a count of the number of services attended,” he said. The ‘religious affiliation’ variable, which summarizes a complex set of practices and beliefs regarding the Jewish religion, he noted, may have tapped into religious practices that affect overall life-styles, including alcohol consumption. “Future research definitely needs to conduct more studies that can address the mechanisms underlying drinking pattern differences according to religious affiliation,” he said. “The correlation between the two is established. The task now is to achieve a better empirical understanding of the association.” Luczak said the study’s genetic findings are related to previous reports that found a relationship between ADH2*2 and less frequent drinking among Jews, and lower rates of alcohol dependence in Asians and non-Jewish whites. She said, “The current study examined binge drinking, which is more related to drinking problems, and is a different measure than alcohol dependence. Although these findings may not add to the literature on alcohol depen-Article is based dence, they do provide evidence that ADH2*2 also relates to a on the following measure of heavy alcohol use in a combined sample of Jewish published research: and non-Jewish whites.” Luczak, S.E., Shea, S.H., Carr, L.G., Luczak and her colleagues will continue to examine drinking T.-K. Li, Wall, T.L. behavior in Jewish and non-Jewish college students. “We are (December 2002 ). also examining the role of culture, religion and genetic varia-Binge drinking in tions in these and other ethnic groups including Koreans and Jewish and non-Jewish Chinese,” she said. White college students. Alcoholism: Clinical and Experimental Research, 26(12), 1773-1778. BINGE DRINKING: A DANGEROUS RITE OF PASSAGE BINGE DRINKING: A DANGEROUS RITE OF PASSAGE • Adolescence is a time when many begin experimenting with alcohol. • Some adolescents binge drink, that is, drink heavily during a short period of time. • Adolescent brains may be particularly vulnerable to the neurotoxic effects of alcohol. • Binge drinking during adolescence may have long-term disruptive consequences for memory. Adolescence is often a time of fashion consciousness, learning how to drive a car and exploring the limits of parental patience and endurance. Adolescence is also a time when most people begin drinking, often drink the most, and for some, experiment with binge drinking. A study in the August issue of Alcoholism: Clinical and Experimental Research (ACER) explores the long- term neurobehavioral consequences of binge drinking during adolescence. Binge drinking can be loosely defined as an intense bout of drinking during a single session, such as a single evening. For males, that can mean five or more drinks in one sitting; for females, it can be four or more drinks. Several studies have found that a significant percentage of teenagers report regular bouts of drinking in which high blood alcohol levels are attained. Furthermore, when the above definitions are used, recent data from the Harvard School of Public Health College Alcohol Study indicates that roughly 45 percent of all college students binge drink. According to Aaron M. White, research associate in the department of psychiatry at Duke University Medical Center and first author of the ACER study, roughly 23 percent of all college students are frequent binge drinkers, meaning that they binge three or more times in a two-week period. White and his co-authors used rodents to test for the effects of binge-pattern drinking. “We were particularly interested in knowing whether these treatments produced different effects in younger rats than in older rats,” he said. After a regimen essentially comparable to multiple instances of binge drinking in humans, both adolescents and adults were tested for anxiety and learning. Following the initial alcohol exposure phase, no effects were found. However, when a later, moderate dose of alcohol was given to all of the rats, those that had previously received the adolescent alcohol exposure showed the greatest disruption of working memory. These results suggest that binge-pattern exposure to alcohol during adolescence does something to the adolescent brain that leads it to respond differently – more sensitively – to alcohol in the future. “We believe that the adolescent brain is more vulnerable to the neurotoxic effects of alcohol than the adult brain,” White explained, “and this could account for the findings of our study. Alcohol impairs activity at a receptor called the NMDA receptor. These receptors are highly concentrated in the hippocampus, a brain region critically involved in learning and memory. During withdrawal from alcohol, NMDA receptors can become overly active, which can make the brain more vulnerable to cell death. We are currently investigating whether adolescent 21 continued ~ 22 22 BINGE DRINKING: A DANGEROUS RITE OF PASSAGE brains exhibit greater withdrawal-induced hyperactivity at NMDA receptors than adults, and if such hyperactivity leads to greater cell death in adolescent than adult subjects.” “The implications of this study,” said David L. McKinzie, senior biologist at Lilly Research Laboratories and adjunct assistant professor at the Indiana University School of Medicine, “are that teenagers who drink heavily may be especially susceptible to the neurobehavioral effects of alcohol than adults with similar drinking experiences. Of special concern is the possibility that the effects of early chronic alcohol drinking may have long-lasting consequences, both as a general insult to the brain as well as changing the individual’s later reactivity to alcohol.” Although White cautioned against generalizing from a small sample of rats to the entire human population, he noted that the findings are consistent with previous research on alcohol abuse during adolescence. McKinzie concurred. “The few animal studies to date have consistently suggested that developing brains are especially sensitive to the toxic effects of alcohol,” said McKinzie. “This type of study is particularly important because a large percentage of adolescents consume alcohol. Unfortunately, relatively little is know about the long-term consequences of chronic alcohol drinking in adolescent individuals. If this age group is indeed found to be especially vulnerable to alcohol and its long-term effects, as this study suggests, we may need to concentrate our efforts on preventive strategies.” Article is based on the following published research: White, A.M., Ghia, A.J., Levin, E.D., & Swartzwelder, H.S. (August 2000). Binge pattern ethanol exposure in adolescent and adult rats: Differential impact on subsequent responsiveness to ethanol. Alcoholism: Clinical and Experimental Research, 24(8), 1251-1256. COLLEGE STUDENTS MAY BE DRINKING MORE ALCOHOL COLLEGE STUDENTS MAY BE DRINKING MORE ALCOHOL THAN EVEN THEY REALIZE • Most of what is known about alcohol consumption by college students comes from self-reports. • New research shows that college students overestimate what is meant by “standard” drink sizes. • These findings suggest that students drink significantly more than they report. Most of what is known about alcohol consumption by college students comes from survey data. Yet much of what is known about college drinking may be underestimated, according to findings published in the November issue of Alcoholism: Clinical and Experimental Research (ACER). An examination of college students’ ability to define “standard drinks” suggests that college students drink significantly more than they think they do. “For some reason, we’ve all just sort of assumed that we can take students’ responses on surveys at face value,” said Aaron M. White, assistant research professor in the department of psychiatry at Duke University Medical Center and first author of the study. “[We’ve believed] that if they say they had three drinks, then they really had three drinks. This study suggests that it’s just not that simple. Students tend to have pretty liberal views about what constitutes a single drink. In fact, if a student tells us they had three drinks, there’s a good chance it was more like five or six. This is a big difference, particularly if we’re trying to figure out how many students qualify as ‘binge drinkers’ based on their self-reported drinking habits.” White and his colleagues asked 106 undergraduate students (54 males, 52 females) to complete a 12-item survey. The survey was designed to gather basic information about students’ current drinking habits and three tasks relating to drink size. The tasks involved free-pouring according to each subject’s estimation of a standard drink size: 1) beer, 2) a shot of hard liquor and 3) alcohol for a mixed drink into cups of different sizes. The student-poured volumes were then compared to volumes of standard drinks used in the Harvard School of Public Health College Alcohol Study survey(s). For every cup size in each of the three tasks, students overestimated how much fluid they would need for a standard drink size. “Regardless of which type of drink we asked students to pour,” said White, “they almost always poured too much. When asked to pour a standard size beer into a 32-ounce cup, some students filled the cup to the top! For these students, each of their drinks actually equaled 2.5 standard drinks.” Furthermore, in all three pouring tasks, the magnitude of the discrepancy increased with cup size. “These findings suggest that students drink more than they think,” said White, “which means that survey data probably underestimate actual drinking levels on college campuses. This is obviously not good news, neither for those of us who use surveys in our research, nor for those of us trying to deal with alcohol misuse on college campuses. The scale of the problem could be bigger than we thought.” 23 continued ~ 24 24 COLLEGE STUDENTS MAY BE DRINKING MORE ALCOHOL THAN EVEN THEY REALIZE “The fact that many students probably consume more alcohol than their survey responses suggest could help explain some of our previous findings about the consequences of drinking,” added Courtney Kraus, second author for the study. “We’ve observed that a surprisingly high percentage of college students experience alcohol-induced memory blackouts, more than might be expected based on their self-reported consumption. The high incidence of blackouts makes more sense if students are actually drinking more than they think.” “We need to repeat this study with a larger random sample of students,” said Ralph Hingson, professor of social and behavioral sciences and associate dean for research at the Boston University School of Public Health. “When they’re collecting information about drinks in these surveys, they ought to provide more information about what a ‘standard’ drink really is. In addition, we ought to study if alcohol-related problems are associated with miscalculation of the amount of alcohol that it takes to make a standard drink. For example, are the people who underestimate the amount of alcohol in a standard drink the ones who are more likely to be dependent, who drive after drinking, ride with drinking drivers, or engage in other alcohol- related behaviors that pose risks to themselves and others?” “We somehow need to teach students, health educators, administrators, and anyone else involved in dealing with college-drinking issues how to accurately define a drink,” added White. "Until then, we have to be cautious about the conclusions that we draw from survey data, and about the levels of consumption that we promote to college students as ‘safe’ or ‘normal.’ Telling a student that his or her peers typically drink three or four drinks when they go out could do some damage if that kid defines a drink as a 10-ounce cup of booze with a splash of Coke.” Article is based on the following White also suggested a new kind of beverage labeling. “When published research: someone picks up a box of cookies or a bag of potato chips,” he White, A.M., Kraus, C.L., said, “one of the first things they often do is look for information McCracken, L.A., about serving sizes, calories, etc. Doesn’t it make sense that these Swartzwelder, H.S. labels, or at least a rudimentary form of them, should be placed (November 2003). on drinks that contain alcohol? Otherwise, how is a person to Do college students know how many standard servings of alcohol are present?” drink more than they think? Use of a White spoke of an Australian government initiative requiring free-pour paradigm information about serving sizes on all alcoholic beverages. “By to determine how doing this, the government can now have meaningful dialogue college students define with the populace about healthy and unhealthy drinking levels, standard drinks. and can measure alcohol consumption more accurately. Why Alcoholism: Clinical the beverage industry does not voluntarily place this informa-and Experimental tion on their products [in the U.S.] is beyond me. My guess is Research, that the public would really appreciate it.” 27(11), 1750-1757. ADOLESCENTS WITH ALCOHOL PROBLEMS: REDEFINING ADOLESCENTS WITH ALCOHOL PROBLEMS: REDEFINING THE BASICS • The Diagnostic and Statistical Manual of Mental Disorders - Fourth Edition (DSM-IV) is widely used to define alcohol abuse and dependence. • Yet little is known about the validity of DSM-IV criteria for alcohol use disorder (AUD) diagnoses when applied to adolescents. • Researchers applied a statistical method called latent class analysis (LCA) to DSM-IV AUD criteria. They found that “milder” and “more severe” categories derived from LCA provided better coverage of symptomatic adolescents than DSM-IV alcohol abuse and dependence categories. For some nosologists – people interested in the classification of diseases – the Diagnostic and Statistical Manual of Mental Disorders - Fourth Edition (DSM-IV) lies somewhere between serving as a valuable diagnostic tool and one in need of revision. Of special concern is the validity of DSM-IV alcohol use disorder (AUD) diagnoses when applied to adolescents. A study in the December issue of Alcoholism: Clinical and Experimental Research (ACER) uses an advanced quantitative technique called latent class analysis (LCA) to examine the utility of new ways of classifying adolescent alcohol problems. “There is controversy regarding the use of DSM-IV criteria with adolescents,” said Tammy Chung, assistant professor of psychiatry at the University of Pittsburgh Medical Center and lead author of the study. “For example, existing criteria include symptoms that are not commonly experienced by adolescent problem drinkers, which limits their utility when applied to this age group. Symptoms such as alcohol withdrawal and alcohol-related legal problems typically occur only after years of heavy drinking. Conversely, other DSM-IV-defined symptoms, such as alcohol tolerance, generally tend to have a high prevalence in adolescent drinkers, and do not clearly distinguish between adolescents with and without drinking problems. In certain cases, individuals may have alcohol-related symptoms, but fail to meet DSM-IV AUD criteria for a diagnosis. We need to remember that these criteria were developed for use with adults, and little is known about their validity when applied to adolescents. Although a few papers have addressed this topic cross-sectionally, this study is among the first to address this issue in adolescents using longitudinal data.” “There are all kinds of problems with DSM-IV when applied to adolescents,” agreed James Langenbucher, associate professor at the Center of Alcohol Studies at Rutgers University. “One of these is that the way in which we diagnose alcohol and drug problems, and even gambling problems and eating disorders, is based on the prototype of a middle-aged White man, probably a patient in a Veterans Affairs hospital during the 1960s to 1970s. This prototype gave us all the ideas that have filtered down and been codified. No one had in mind a 17-year old Latino kid in Philadelphia when deciding what were the essential characteristics of alcohol and drug abuse disorders.” 25 continued ~ 26 26 ADOLESCENTS WITH ALCOHOL PROBLEMS: REDEFINING THE BASICS The first DSM was published by the American Psychiatric Association in 1952. Diagnostic criteria for alcohol and other drug problems were added in 1980 (DSM-III). In general, there are three DSM-IV categories of substance-use disorders: no diagnosis, abuse, and dependence. Alcohol abuse and dependence are defined by mutually exclusive criterion sets. Alcohol abuse is diagnosed by meeting at least one of four symptoms representing recurrent hazardous use and negative psychosocial consequences resulting from drinking. Alcohol dependence requires meeting three of seven symptoms within a 12-month period, precludes a diagnosis of abuse, and includes symptoms related to physical dependence, impaired control over drinking behavior, and increased salience of alcohol consumption. For the Chung study, researchers used LCA to identify subgroups of adolescents who share a common pattern, profile of symptoms or other characteristics. They then used the subgroups’ symptom profiles to refine the DSM-IV criteria used to diagnose AUDs. “We were able to develop severity-based categories of adolescents with milder and more severe alcohol-related problems,” said Chung. “The milder and more severe categories derived in this study provided better coverage of symptomatic individuals than DSM-IV alcohol abuse and dependence categories, suggesting that some reorganization of DSM-IV AUD criteria may improve the identification of individuals who may benefit from treatment. In addition, longitudinal data indicated an overall decrease in the severity of adolescents’ alcohol-related problems one year after substance abuse treatment.” “Another important finding,” said Langenbucher, “is that case severity in this data seems to be carried by the number, not the type, of symptom. It’s the overall number of symptoms that best accounts for the severity of the case. This argues for a dimensional system that relates abuse to dependence, perhaps not different categories, but different ranges on the severity continuum.” Chung said, “These results suggest that a proportion of symp-Article is based tomatic adolescents who may benefit from intervention, may not on the following published research: meet criteria for a DSM-IV AUD diagnosis, and thus may not be eligible for third-party reimbursement for substance abuse treat- Chung, T., & Martin, C.S. ment. As our own findings confirmed, treated adolescents tended (December 2001). to show reductions in alcohol-related problems one year after Classification and substance abuse treatment, a finding that does not support the course of alcohol notion of an inevitable progression to more severe problems.” problems among adolescents in “What we want to eventually do,” said Langenbucher, “is de-addictions treatment. velop DSM-V. That version should be out toward the close of Alcoholism: Clinical this decade. We want improved diagnostic rules for all kinds of and Experimental psychiatric diagnoses including major depression, schizophre-Research, nia and also substance-use disorders.” 25(12), 1734-1742. IMPULSIVENESS, AGGRESSION, ALCOHOL AND ADOLESCENTS IMPULSIVENESS, AGGRESSION, ALCOHOL AND ADOLESCENTS • Adolescents with alcohol problems often manifest impulsive, aggressive and antisocial behaviors. • One type of adult alcoholism (Type II) is likewise characterized by antisocial behavior, and may be linked to a decrease in function of the neurotransmitter serotonin. • A recent study has found that adolescents with both alcohol and antisocial problems show an increase in serotonin function. • Serotonin dysregulation, rather than high or low levels, may be key to high-risk behaviors. Alcohol use disorders are nearly as common among older adolescents as among adults. Adolescents who abuse alcohol or are dependent on alcohol often manifest impulsive, aggressive, and antisocial behaviors. A study in the November issue of Alcoholism: Clinical and Experimental Research (ACER) examines the possibility that variations in brain chemistry can set the stage for risk-taking behaviors. More specifically, it studies the role that dysregulation of central serotonergic function may play in impulsiveness, aggression and conduct disorders in older adolescents (between 16 and 21 years of age) with alcohol problems. “Impulsive and aggressive personality traits, as well as impulsive-aggressive behavior,” explained Paul Soloff, professor of psychiatry at the University of Pittsburgh School of Medicine and lead author of the study, “are temperamental traits that lead to socially disinhibited behavior, also called ‘behavior undercontrol.’ Kids with behavior undercontrol are more likely to develop alcohol use disorders than non-impulsive-aggressive kids.” One type of adult alcoholism, referred to as Type II, is defined by antisocial behavior, including many expressions of behavior undercontrol, as well as early onset (before age 25), and male predominance. (This is in contrast to Type I alcoholism, which is found in both males and females, occurs later in life and is not associated with antisocial traits.) Research suggests that there is a biologic (and possibly hereditary) basis for the temperament of impulsivity that is related to dysregulation of the neurotransmitter serotonin in the parts of the brain that inhibit impulses. Studies of adults with alcohol use disorders have found evidence of decreased serotonin function, especially those with Type II alcoholism (identified by antisocial behavior). Similarly, studies of impulsive-aggressive individuals, independent of alcohol use disorders, have found diminished serotonin function. “We looked at adolescents who already had developed alcohol use disorders to see if they had higher levels of impulsivity and aggressivity than healthy control subjects, and to also see if they had lower central serotonergic function,” said Soloff. “We measured central serotonin function by giving them a single dose of a medicine called fenfluramine, which releases serotonin in the brain, and then looked for effects of that release in the blood.” Serotonin itself cannot be measured in the blood. However, serotonin release in the brain causes a rise in the hormones prolactin and cortisol in the blood. “The changes in prolactin and cortisol provided an index of serotonin responsiveness,” he continued. continued ~ 27 IMPULSIVENESS, AGGRESSION, ALCOHOL AND ADOLESCENTS 28 “In adults with alcohol use disorders,” said Duncan Clark, director of the Pittsburgh Adolescent Alcohol Research Center, “the serotonin system is relatively insensitive or unresponsive to stimulation. In this study, the serotonin responsivity results were somewhat different than would be expected from studies of adults.” Neither Soloff nor Clark were surprised that older adolescents with alcohol use disorders had more impulsivity and aggressivity than control subjects. The boys tended to be more aggressive in general than the girls, but both had equally high levels of impulsivity. Furthermore, overall the two groups (alcohol users and control subjects) did not significantly differ on their prolactin or cortisol responses. This suggests that not all youth with significant alcohol use disorders early in life have a dysregulation of serotonin metabolism. However, the most extreme subjects – nine boys with both alcohol use disorders and the most antisocial traits (which were diagnosed as conduct disorder) – had a significant elevation in cortisol response, which correlated with measures of aggressivity. “These findings may be interpreted to show that the serotonin system was more responsive in these subjects,” said Clark. “[This may reflect] an earlier stage of neurobiological development. Increased responsiveness of the serotonin system in adolescence may be followed by decreased responsiveness in adulthood. However, the level of responsiveness may not be as important as the ability of the brain to regulate the response to stimulation. While not in the same direction as with adults, these results are still consistent with the idea that individuals with these high-risk behaviors have serotonin dysregulation.” Soloff plans to further study the serotonin system using positron emission tomography (PET) neuroimaging, where metabolic changes can be “visualized.” He believes this research will ultimately reveal more about where in the brain impulsivity is controlled, how serotonin is regulated in Article is based these individuals, and whether this dysregulation can be rem-on the following edied. published research: Soloff, P.H., Lynch, K.G., Clark noted, “We need to know more about the development of & Moss, H.B. the serotonin system from childhood through adolescence and (November 2000). into adulthood. New brain imaging techniques may allow us to Serotonin, impulsivity, study brain chemistry directly rather than relying on measure-and alcohol use ment of effects of brain chemistry on blood chemistry. Through disorders in the older an understanding of the brain and behavior, better approaches adolescent: to identifying children at risk, better prevention programs and A psychological study. more effective treatment interventions may be developed.” Alcoholism: Clinical and Experimental Research, 24(10), 1609-1619. ALCOHOL, AUTOMOBILES AND YOUTH ALCOHOL, AUTOMOBILES AND YOUTH • Underage drinking and driving continue to cause significant numbers of injury and death. • Riding with drinking drivers may be even more dangerous for adolescents than drinking and driving. • New findings indicate that drinking and driving, and riding with drinking drivers, may be particularly problematic among Latino youth. Although the message of “don’t drink and drive” has been a common refrain for the past two decades, much less attention has been given to the risks of riding with a drinking driver. A study in the August issue of Alcoholism: Clinical and Experimental Research (ACER) examines ethnic differences among adolescents who engage in driving after drinking (DD) and riding with drinking drivers (RWDD). Findings indicate there is a distinct need to direct prevention efforts toward Latino youth. “Adolescent alcohol use, driving after drinking, and riding with drinking drivers are significant public health problems,” said Samantha Walker, associate research scientist at the Prevention Research Center and corresponding author for the study. “Consequences can include automobile crashes, physical injury and possible death.” In 2000, according to the National Highway Traffic Safety Administration (NHTSA), 21 percent of young drivers who were killed in crashes were intoxicated with blood alcohol concentrations of 0.10 g/dl or greater. Among those drivers who had been drinking, three percent were involved in property damage-only crashes, five percent were involved in crashes resulting in injury, and 22 percent were involved in crashes resulting in fatality. RWDD is a less-recognized practice than DD, yet may be even more dangerous for adolescents. “The percentage of adolescents riding with drinking drivers is frighteningly high, with approximately half of all youth reporting such experiences in the past 12 months,” said Brenda A. Miller, a senior scientist at the Prevention Research Center. “This study clarifies that a greater proportion of our adolescents are at risk for injury or death due to riding with drinking drivers as compared to driving under the influence.” Researchers used random-digit dialing procedures to recruit 1,534 15- to 20-year-olds (839 females, 695 males) living in California to participate in a telephone survey. Latinos, African Americans and Asian Americans were oversampled to allow cross-group comparisons. “Our findings indicate that DD and RWDD may be particular problems for Latinos,” said Walker. “That is, Latino youth appear more at risk for these behaviors than are other youth at similar levels of alcohol consumption.” The study found low prevalence rates of DD and RWDD among Asian American youth, which may indicate the presence of protective factors – whether social or environmental – at work within the Asian American community. 29 continued ~ 30 30 ALCOHOL, AUTOMOBILES AND YOUTH “These results suggest that some ground work needs to be done to better understand why Latino youth are more vulnerable to these risks and whether our prevention message needs to be presented in a different manner that would be better heard by Latino youth,” said Miller. “We need to be cautious, however, about concluding that all Latino youth are more susceptible because the findings do not support this conclusion. Only when we account for drinking behaviors and driving practices do we see an increased risk for Latino youth.” Miller added that although many parents likely already know that children who drink frequently are at higher risk for either DD or RWDD, they may not know that risky driving and the number of days driven are also related to an increased risk for DD or RWDD. “Risky driving is probably part of a constellation of high-risk behaviors,” said Miller. “The total number of days driven may be related to control or ownership of a car that provides the means to engage in drinking and driving more readily. We know that parents who monitor their children are less likely to have children who engage in alcohol or drug use. However, monitoring teenagers’ behavior is increasingly more complex, especially when the access and availability of vehicles adds to freedom and independence from parental controls.” Walker said that future research will explore some of these complexities, specifically, “clarifying the relationships among drinking patterns, driving practices, social and environmental influences such as drinking locations, and DD and RWDD, particularly among Latino youth.” Miller suggested that future studies also explore strategies to help adolescents avoid those situations in which drinking and driving occur, especially scenarios in which they are passengers riding with a drinking driver. “For many adolescents, the automatic loss of their license or a Article is based zero-tolerance policy of any alcohol use while driving provide a on the following powerful external control over DD behavior,” said Miller. “Howpublished research: ever, the issue of RWDD is not so easily addressed. Our preven-Walker, S., Treno, A.J., tion strategies should make it easier for adolescents to negotiate Grube, J.W., Light, J.M. difficult social situations that may emerge in their lives, such as (August 2003). what to do when a friend that drove you to a party has too much Ethnic differences to drink. Particularly important is the need to provide construcin driving after drinking tive strategies rather than messages that simply admonish against and riding with such behavior. And ultimately, providing adolescents with an drinking drivers ability to handle these difficult social problems will provide them, among adolescents. hopefully, with the strengths they need to negotiate other social Alcoholism: Clinical problems in their lives.” and Experimental Research, 27(8), 1299-1305. TEENAGERS, DRINKING AND DRIVING: A QUICK TRIP TO THE GRAVE TEENAGERS, DRINKING AND DRIVING: A QUICK TRIP TO THE GRAVE • Motor vehicle crashes are the leading cause of death for 15- to 20-year-old youth in the U.S. • More than one quarter of the drivers killed in crashes had been drinking. • One alcohol-prevention curriculum was found to significantly reduce first-year serious traffic offenses. • The curriculum seemed to be particularly effective for kids who drank very little. Motor vehicle crashes are the leading cause of death for 15- to 20-year-old youth in the United States, according to mortality data from the National Center for Health Statistics. More than one quarter of the drivers killed in crashes had been drinking. While all school-based alcohol prevention programs strive to minimize alcohol use and/or misuse, little is known about the actual effects of these programs, particularly on students’ driving. A study in the March issue of Alcoholism: Clinical and Experimental Research (ACER) examines the effects of a high school- based alcohol misuse prevention program on participants’ subsequent driving behaviors. “A law setting a minimum drinking age of 21 years exists in all the states,” explained Jean T. Shope, senior research scientist with the Transportation Research Institute at the University of Michigan and lead author of the study. “Although it has reduced underage drinking and driving fatalities, we still have a problem.” In 1999, according to the National Highway Traffic Safety Administration, 3,561 drivers 15 to 20 years old were killed – and an additional 362,000 injured – in traffic crashes. Of those young drivers fatally injured, 29 percent had been drinking. Although driving after drinking is potentially deadly under any circumstances, it is particularly dangerous when teenagers do it. “It’s important to look at the context of this behavior,” said James Hedlund, a consultant in traffic safety for Highway Safety North. “Not only is their drinking illegal, because the minimum drinking age in the United States is 21 years of age, but so too is their driving after drinking. Every state has a zero-tolerance law.” Under these laws, teenage drivers detected with a blood alcohol concentration of 0.02 grams per deciliter or above will lose their driver’s licenses. “So driving after drinking is doubly illegal,” he said. “There are two overall methods to change someone’s behavior: enforcement and education,” added Hedlund. “Legal interventions have been evaluated best, because they go into place at one given time, all over a state. But a high school prevention program doesn’t work that way. It’s usually put into place in one high school, often for a short period of time, and it’s very difficult to measure its effects. One of the really good things about Shope’s study is that she finds effects in long-term traffic offense data.” Shope’s research is a follow-up to the Alcohol Misuse Prevention Study, in which five hour’s worth of alcohol-education sessions were given to 10th grade Michigan students during each of the 1988-1989 and 1989-1990 school years. For this study, Shope and her colleagues examined 31 continued ~ TEENAGERS, DRINKING AND DRIVING: A QUICK TRIP TO THE GRAVE 32 students’ driving histories for roughly seven years following licensure, which typically occurs during or shortly after 10th grade. The study had three main findings. “They found that the curriculum reduced serious traffic offenses, both alcohol-related and other offenses as well, by about 20 percent in the first year these kids were licensed to drive,” said Hedlund. “Second, the effect disappeared after the first year of driving. Third, the effect in the first year was strongest in two particular groups of students: those who didn’t drink very much, and those who had parents who didn’t seem to disapprove much of teen drinking.” “I think it’s important that the prevention program seemed to work best among the group that had not yet started to drink,” Shope said. “This is a typical finding in prevention. To get to them at the right time makes all the difference. It’s just like trying to prevent smoking; you need to stop them before the age of 13. We already know that drinking increases very much during high school. If you’re going to do prevention, you have to get in there before the behavior starts, otherwise you’re doing treatment or harm reduction, not prevention.” “This is one of the few studies I know that looks at an educational program and actually finds some bottom-line results of observable behavior,” said Hedlund. “It gives some scientific data that say you really can teach high school kids something. I’m saying that only somewhat facetiously. This is a very difficult group to try to educate, especially in ways that are socially responsible, when a lot of these kids are looking for ways to be socially irresponsible. So it’s good news that this study gives us some indication that education about socially acceptable behaviors may indeed make a bottom-line difference. The results aren’t conclusive, but they are very promising.” Article is based “There really needs to be more follow-up or long-term evalua-on the following tion of prevention programs,” Shope said. “We also need longer-published research: term intervention or teaching. Why would a five-hour program Shope, J.T., Elliott, M.R., in 10th grade, with no revisiting of the topic … why would that Raghunathan, T.E., have much of an effect? Sometimes these school programs are & Waller, P.F. just a drop in the bucket when there’s a lot of other stuff going (March 2001). on in a young person’s life. You can’t really expect a whole lot of Long-term follow-up change from a tiny little effort. One more thing, while schools of a high school alcohol may be very convenient places to reach groups of young people, misuse prevention many of these programs would work much better if the same program’s effect on message were also being delivered from the home, family, students’ subsequent community, youth organizations and the media. Prevention can driving. be somewhat ‘swimming up stream’ when it’s not really being Alcoholism: Clinical reinforced anywhere else.” and Experimental Research, 25(3), 403-410. TRACKING THE LONG-TERM FUNCTIONING OF ADOLESCENTS TRACKING THE LONG-TERM FUNCTIONING OF ADOLESCENTS WITH ALCOHOL PROBLEMS • Standard treatment may not be enough for some adolescents with alcohol problems. • A significant proportion of adolescents continue to drink and/or use other drugs, have poor relations with family and friends, and experience academic problems following treatment. Standard treatment may not be enough for some adolescents with alcohol problems, say researchers. While many adolescents reduce their alcohol use and have fewer related problems following treatment, a significant proportion continue to drink and/or use other drugs, have poor relations with family and friends and experience academic problems. Scientists say that long-term studies of treated adolescents are essential for determining what impact treatment can have and what factors may change the severity of alcohol problems over time. These findings, gathered from four studies of adolescents who were followed for one to eight years after treatment, were presented at a symposium during the joint 2002 Research Society on Alcoholism/International Society for Biomedical Research on Alcoholism meeting. Symposium proceedings can be found in the February issue of Alcoholism: Clinical and Experimental Research (ACER). “We know very little about the impact that adolescent problem drinking has on academic achievement, relations with family and friends and employment through young adulthood,” said Tammy Chung, assistant professor of psychiatry at the University of Pittsburgh Medical Center and co-organizer of the symposium. “Longer-term studies can help us to understand how certain developmental milestones, such as full-time employment and independent living, affect the course of alcohol problems that begin in adolescence. Longer-term studies can also tell us which adolescents are most likely to continue or return to problem drinking and how treatment can be improved to more effectively meet their specific needs.” Findings presented at the symposium included: -Treatment works for many teens. At least half of the adolescents studied showed reductions in alcohol use and problems following treatment, with concurrent improvements in psychosocial functioning. -Treatment needs can change. The severity and frequency of alcohol problems among treated youth can fluctuate over the long term. “Researchers have identified multiple pathways of change in alcohol use and problems,” said Chung. “About half of the treated adolescents maintained low levels of alcohol use and problems through young adulthood, while some treated adolescents experienced continuing alcohol problems.” 33 continued ~ TRACKING THE LONG-TERM FUNCTIONING OF ADOLESCENTS 34 WITH ALCOHOL PROBLEMS -Use of other drugs following treatment is associated with greater alcohol use and related problems. “Adolescents who drank and used other drugs such as marijuana after treatment,” said Chung, “generally had poorer outcomes in the areas of family relations and academic achievement. These poorer outcomes appeared to last through young adulthood.” -Researchers and clinicians need to consider the impact of developmental milestones on the course of adolescent-onset substance use disorders. “We need to know more about the impact of certain developmental milestones – full-time employment, obtaining a driver’s license, independent living – on the course of alcohol problems in treated youth,” said Chung. “This will allow us to improve the timing, such as the addition of booster sessions and content of interventions for youth.” -The value of pretreatment characteristics, such as a family history of alcoholism, may become more evident as young people transition into adult roles. “The bottom line,” said Chung, “is that alcohol problems that begin in youth do not necessarily have a chronic course. If we can identify the risk factors associated with alcohol problems that continue into young adulthood among treated youth, we can improve the effectiveness of their treatment.” Article is based on the following published research: Chung, T., Martin, C.S., Grella, C.E., Winters, K.C., Abrantes, A.M., Brown, S.A. (February 2003). Course of alcohol problems in treated adolescents. Alcoholism: Clinical and Experimental Research, 27(2), 253-261. B BBiology – iology –iology – Neurobiology NeurobiologyNeurobiology BIOLOGY – BIOLOGY –BIOLOGY – NEUROBIOLOGY NEUROBIOLOGYNEUROBIOLOGY Articles in the Biology – Neurobiology Category 1. Alcohol-Damaged Brains “Recruit” New Brain Regions to Perform Simple Tasks 2. How Alcohol Gives and Then Takes Away 3. How Sensitive Is Your Brain to Alcohol-Induced Damage? 4. The Brain Risks of Binge Drinking 5. Abstinence May Make the Brain Grow Stronger 6. Cognitive Neuroscience Takes on Alcohol 7. Just a Spoonful of Thiamin? 8. Alcohol and Thiamin Deficiency Together: A Dangerous Combination? 9. Chronic Drinking Increases Cortisol During Intoxication and Withdrawal 10. Repeated Alcohol Detoxifications Can Impair Cognitive Function 11. Blocking Selected Neurotransmitter Activity May Decrease Alcohol Consumption 12. Probing the Role of the Delta Opioid Receptor in Alcohol Consumption 13. Behavioral Sensitization: A New Perspective on Alcoholism ALCOHOL-DAMAGED BRAINS “RECRUIT” NEW BRAIN REGIONSALCOHOL-DAMAGED BRAINS “RECRUIT” NEW BRAIN REGIONS TO PERFORM SIMPLE TASKS • Chronic alcoholism is known to damage the brain’s cerebellum and frontal lobes. • Researchers used brain imaging technology to watch abstinent alcoholics perform a simple motor task. • Alcoholics performed the task, finger tapping, slower than non-alcoholics. • Alcoholic brains also recruited other-than-normally activated regions of the brain to perform the task. Researchers know that many alcoholics continue to experience cognitive deficits even after long-term abstinence from alcohol. Results from a study in the April issue of Alcoholism: Clinical and Experimental Research (ACER) confirm that motor deficits also continue to plague abstinent alcoholics. By using functional magnetic resonance imaging (fMRI) to “watch” brain regions involved in a simple motor task – finger tapping – the study has found that the brain appears to compensate for alcohol-induced damage by “recruiting” other, unexpected brain regions. “We know from neuropathological studies that the two parts of the brain that are most often damaged in chronic alcoholics are the cerebellum and the frontal lobes,” said Peter R. Martin, professor of psychiatry and pharmacology, director of the Vanderbilt Addiction Center at the Vanderbilt University School of Medicine and corresponding author for the study. “Rapid self- paced motor activity such as finger tapping is a function of the motor cortex, the posterior part of the frontal lobe, which initiates a stimulus to the muscles of the hand, that is then coordinated by interplay between the cerebellum and the frontal lobes. In other words, I reasoned that there would probably be abnormalities in activation of these regions in alcoholics during finger tapping.” While undergoing MRI, two groups of participants performed repetitive, self-paced index finger- tapping exercises: eight (seven males, one female) alcohol-dependent patients after approximately two weeks of abstinence; and nine (seven females, two males) healthy volunteers or “controls.” Participants alternated between using their dominant hands (DH) and non-dominant hands (NDH) to perform the index finger-tapping exercises. Researchers used fMRI analysis to compare DH and NDH performance in each subject group in order to examine whether the groups differed in the patterns of activation they exhibited in the cerebral cortex and cerebellum. The detoxified alcohol-dependent patients performed the finger-tapping tasks significantly slower than the control group. However, contrary to expectations, the slower tapping was not accompanied by proportionately decreased fMRI brain activation in the cerebral cortex and cerebellum. Rather, the alcoholics had a significant increase of activation in the cortical brain region ipsilateral to (on the same side as) the active hand during DH tapping. In other words, the alcoholics had to use more of their brains to do less. 37 continued ~ 38 38 ALCOHOL-DAMAGED BRAINS “RECRUIT” NEW BRAIN REGIONS TO PERFORM SIMPLE TASKS “First, we found that alcoholics, generally speaking, tapped more inefficiently,” said Martin. “Second, in order to generate a single tap, an alcoholic would activate a larger part of their brain than a normal person. So, the results seem to indicate that even though alcoholics, as they recover from drinking, can probably demonstrate relatively normal tapping, they have to use more of their brain to generate the taps.” “This study underlines the importance of considering the operation of brain circuitry involved even in an ostensibly simple task,” said Edith Sullivan, associate professor of psychiatry at Stanford University School of Medicine. “Further, evidence for recruitment of brain regions that are not normally involved in a given task puts a person at risk for performance inefficiency for that particular task, other tasks that need to be done simultaneously, and more complex divided-attention tasks, such as driving.” Increased activity in the ipsilateral cortical region of the brain was highly unexpected, said Martin. “Normally, when I tap with my right hand,” he said, “it’s mostly my left motor cortex (part of the frontal lobes) that’s firing, in conjunction with my right cerebellum. ‘Ipsi’ means same side, ‘contra’ means opposite side. So, we’re talking about my contralateral cortex and my ipsilateral cerebellum. The significantly higher activity we found in the alcoholics was on the ipsilateral cortex, the side that we don’t normally expect to be activated. This finding is compatible with the idea that different regions of the brain are being called into activity that would not normally be activated in order to meet the behavioral demands. Furthermore, this sug-Article is based gests that even though alcoholics at some level may seem to be on the following performing normally, if you raised the level of complexity at published research: which they are being asked to perform, they may exhaust their Parks, M.H., capacities … there may be no more brain to bring in, to recruit, Morgan, V.L., to compensate.” Pickens, D.R., Price, R.R., Dietrich, M.S., These findings lead to new questions, said Martin. “If we study Nickel, M.K., patients as they progress with their abstinence, do these abnor- Martin, P.R. malities get better? It may be that the brain gets better at com (April 2003). pensating, but it doesn’t normalize, it just learns how to bring in Brain fMRI activation even more parts of the brain. You could say it learns to rewire associated with self-paced itself. Another possibility could be that as the brain heals, less finger tapping in chronic activation is required, and that’s a real form of recovery. The alcohol-dependent answers rest with understanding not the tapping itself, but the patients. mechanisms behind the tapping.” Alcoholism: Clinical and Experimental Research, 27(4), 704-712. HOW ALCOHOL GIVES AND THEN TAKES AWAY • Alcohol may be particularly damaging to key components of the “brain reward system.” • Alcohol sensitizes dopamine and serotonin neurons to toxic excessive excitation or “excitotoxicity.” • A brain growth hormone called BDNF can protect neurons against excitotoxicity. • BDNF may have important implications for treating alcoholics going through withdrawal. Mental diseases, including addiction and alcohol dependence, may indeed be “all in your head.” But not in the way you might think. Researchers have learned that alcohol may be particularly damaging to the brain’s reward pathways, specifically dopamine and serotonin neurons. This damage – a sensitization of the neurons to a process called excessive excitation or “excitotoxicity” of the N-methyl-D-aspartate (NMDA) glutamate receptor – could be an important component in transitioning from experimentation to addiction. However, researchers may have also discovered that a brain growth hormone called Brain Derived Neurotrophic Factor (BDNF) may be able to protect neurons against this excitotoxicity. “If dopamine and serotonin neurons are damaged,” said Fulton T. Crews, director of the Center for Alcohol Studies at the University of North Carolina, “this would disrupt reward processes in ways that could contribute to addiction.” Crews, lead author of a study recently published in the November edition of Alcoholism: Clinical and Experimental Research (ACER), explained that his findings are related to what is called a “reward deficiency hypothesis” of addiction. The “reward deficiency syndrome” links addictive, compulsive or impulsive disorders – such as alcoholism, substance abuse, smoking, compulsive overeating and obesity, Attention deficit disorder, Tourette’s syndrome and pathological gambling – with a “chemical imbalance” in the brain. Researchers knew that pleasure, to various degrees, is a distinct neurological function that is linked to a complex reward and reinforcement system. In particular, dopamine appears to be a primary neurotransmitter of reward in the nucleus accumbens and hippocampus areas of the brain. Serotonin is believed to have an additive or synergistic effect on dopamine. Alcohol is known to initially lead to an increase in dopamine release, which supposedly enhances reward/pleasure. However, chronic and/or high levels of alcohol will eventually lead to a decrease in dopamine release. This disruption of intercellular interactions or “chemical imbalance” can result in negative feelings such as anxiety, anger or in a craving for a substance, such as alcohol, that can alleviate the negative feelings. Yet because chronic drinking releases a continuously reduced amount of dopamine, more and more alcohol is needed to feel “normal.” “Science has come to the realization that what alcohol may be doing,” said Boris Tabakoff, chairman of the Department of Pharmacology at the University of Colorado School of Medicine, “is what I call ‘downregulating’ dopamine systems. This study shows that downregulation may actually be a result of neuronal damage. Alcohol leads to a sensitization to glutamate, the glutamate produces the damage, and the damage results in a lower function of the dopamine system.” continued ~ 39 40 40 HOW ALCOHOL GIVES AND THEN TAKES AWAY “This is important,” added Tabakoff, “because it provides an explanation for why individuals may not be able to control their drinking because of biological factors. If the neurons are damaged, they can keep trying to use alcohol to attain some level of pleasure, but they’ll never be able to do it.” Although there is no such thing as a specific gene for alcoholism, there does seem to be a “genetic predisposition” to the development of alcoholism. Tabakoff spoke of one study in which 20 to 28 percent of individuals with at least one alcoholic parent went on to develop alcoholism themselves. Normally, among those who have no familial history of alcoholism, around eight to 10 percent develop alcoholism. In short, those with a family history of alcoholism seem to have a two to three time’s greater chance of developing the disease. Although the exact role of biology in alcoholism has not yet been determined, research findings support both discovery as well as optimism. “This is one of the first studies to show a relationship between excitotoxicity, which likely occurs during ethanol withdrawal, and NMDA receptors,” said Richard A. Morrisett, associate professor of Pharmacology at the University of Texas at Austin. “But it is the first to show that BDNF can actually protect against this. The rescue or prevention of cell death is probably one of the most important aspects of this study.” “Clearly the future direction of this area of study is medication development and an understanding of protective factors,” said Tabakoff. “If you have an individual who is drinking a lot but decides to stop, you need to treat that person with something more than moral support. The Article is based very process of withdrawal could damage the person’s neurons.” on the following Tabakoff spoke of developing drugs that will protect the neu-published research: rons, returning the individual’s pleasure systems to normal while Crews, F.T., Waage, H.G., avoiding irrevocable damage. Wilkie, M.B., & Lauder, J.M. Morrisett indicated there is a need for future studies that look at (November 1999). the effects of lower levels of alcohol on excitotoxicity. “The levels Ethanol pretreatment used in this study, 100 mM, are five times the legal levels of in- enhances NMDA toxication,” he said. “I would like to see what occurs at 20mM, excitotoxicity in biogenic because that’s more related to when we start to drink, when we amino neurons: may start to become dependent.” When a person starts to drink Protection by brain and is experiencing the reinforcing aspects, he said, that’s when derived neurotrophic “we’re having a little engine misfire.” At the point of full-blown factor. alcoholism, he said, “we’re addicted, we’re dependent, we’re Alcoholism: Clinical drinking fifths of whiskey a day, the car is wrecked.” and Experimental Research, 23(11), 1834. HOW SENSITIVE IS YOUR BRAIN TO ALCOHOL-INDUCED DAMAGE? • Alcohol’s neurotoxic effects can cause brain injury. • Alcohol-related brain injury may, in turn, place someone at greater risk of developing alcoholism. • Exercising the brain’s frontal cortex during treatment may help the recovery process. • Thiamin supplements may also improve recovery of the brain and response to treatment. Symposium findings from the June 2000 Research Society on Alcoholism meeting in Denver suggest that alcohol-induced brain injury may be the medium for the progression of alcoholism. The summary, published in the February issue of Alcoholism: Clinical and Experimental Research (ACER), may change the way researchers think about the influence of alcohol-related brain injury on how people develop addictions, respond to treatment and ultimately recover. “What these researchers are saying is that injury to the brain resulting from alcohol consumption is sum and parcel of the progression of the illness,” said Peter R. Martin, professor of psychiatry and pharmacology and director of the Vanderbilt Addiction Center at the Vanderbilt University School of Medicine. “It’s a different perspective on how alcoholism may progress. In the past 20 years, the emphasis of research has been on what makes some people respond to alcohol, regardless of whether their brain is damaged. What they’re saying here is that by drinking, you modify the brain, and the brain can be modified differentially in people. The neurotoxicity of alcohol ‘feeds back’ and determines, modulates or modifies the course of the alcoholism.” Symposium proceedings included four studies that addressed both preclinical (before the onset of the disease) and clinical (related to the symptoms and course of a disease) findings. According to Fulton T. Crews, director of the Center for Alcohol Studies at the University of North Carolina and one of the presenters, the symposium’s common ground was the relation of alcohol-induced deficits in central nervous function to addiction and recovery. “Data indicates that risk factors for alcoholism include heavy binge drinking, genetics and adolescent drinking,” said Crews. “These may also be risk factors for increased brain damage.” That’s the bad news; that simply drinking alcohol can injure someone’s brain, its neurotoxic effects depending on the individual’s genetic makeup, age, metabolism and even gender. The good news is that because of the close ‘working relationship’ between alcohol and the brain, recovery seems possible with the right kind of treatment. “Preclinical studies have suggested that brain damage is a component of the progression from casual drinking to addiction,” said Crews. “We know that alcoholics have decreased brain size. Clinical studies have suggested that ‘exercising the brain’ likely improves brain regrowth as well as recovery from the addiction. Regrowth of the frontal cortex in particular could be 41 continued ~ 42 42 HOW SENSITIVE IS YOUR BRAIN TO ALCOHOL-INDUCED DAMAGE? essential for a successful recovery. Including certain activities in therapy – activities that require the use of the frontal cortex, the site of executive function, impulse inhibition and goal setting – have been shown to improve recovery and increase retention in the treatment program. Also, thiamin therapy seems to increase treatment effects, likely by restoring aspects of central nervous system function.” In short, therapies that exercise certain areas of the brain can improve its function. This can, in turn, help improve an individual’s chances of recovery from alcoholism. The decrease in brain size that seems to accompany alcoholism appears to reverse during the recovery process. In addition, thiamin supplementation may help recovering alcoholics regain their capacity to remember. “The main point to be made here for the reader is that drinking alcohol can cause brain injury,” said Martin. “Maybe what determines why some people become alcoholics is not so much how they respond to the pharmacological actions of alcohol, but how sensitive their brain is to being damaged by alcohol, which modifies their brain, thereby modifying the pharmacological actions of alcohol.” Martin added that future research should be directed at recovery. “We need to remember that even when an alcoholic stops drinking, there have been changes in the brain. We need to spend more time trying to understand how the brain recovers after people stop drinking, because that’s going to determine how well they ultimately do.” Article is based on the following published research: Bowden, S.C., Crews, F.T., Bates, M.E., Fals-Stewart, W., & Ambrose, M.L. (February 2001). Neurotoxicity and neurocognitive impairments with alcohol and drug use disorders: Potential roles in addiction and recovery. Alcoholism: Clinical and Experimental Research, 25(2), 317-321. THE BRAIN RISKS OF BINGE DRINKING THE BRAIN RISKS OF BINGE DRINKING • Neurodegeneration has been commonly thought to occur during alcohol withdrawal. • A new study has confirmed that neuronal damage can occur during a binge pattern of drinking. • Damage to the olfactory bulb, responsible for smell, occurred after just two days of binge drinking. • Damage to other regions of the brain occurred after just four days of binge drinking. Scientists agree that alcohol is toxic and that chronic alcohol abuse can damage all organs – including the brain – to various degrees. There is less agreement, however, on whether or how much neurodegeneration is triggered by alcohol’s toxicity during alcohol consumption or by the hyperexcitability caused by withdrawal from alcohol. A study in the April issue of Alcoholism: Clinical and Experimental Research (ACER) uses rodents to examine what effects just a few days of the equivalent of binge drinking can have on neuronal function. “Most studies of alcohol-induced brain damage have looked at humans who have been alcoholic for decades or rats treated with alcohol for six to 18 months,” said Fulton T. Crews, director of the Center for Alcohol Studies at the University of North Carolina and corresponding author for the study. “Our study shows significant damage in several regions of the brain after only four days, that it occurs during intoxication, and that the process is similar to a dark- cell degeneration that is primarily necrotic.” Necrosis refers to the pathologic death of cells or a portion of tissue or organ due to irreversible damage. Male Sprague-Dawley rats (n=120) were surgically implanted with intragastric catheters. Experimental rats (n= 80) were given alcohol at a rate equivalent to binge drinking, every eight hours for four consecutive days. Doses were based on their estimated blood alcohol levels. Control rats (n=40) were given an alcohol-free yet calorie-equivalent diet at the same rate. Several histological methods – such as amino cupric silver staining, fluoro-Jade B staining, hematoxylin and eosin staining, and transmission electron microscopy – were used to track the course, time points, and specific changes that occurred in conjunction with the alcohol intake. Some rats were sacrificed at two days, some at four days, and some after four days of alcohol and three days of withdrawal. “This study shows significant damage in the olfactory bulb after just 2 days of heavy drinking,” said Crews, “which is a short period of time relative to the decades of drinking that alcoholics do, and may be an important early process in the progression from experimentation with alcohol to addiction. In addition, the major current hypothesis regarding alcohol-induced brain damage suggests that damage occurs during withdrawal. All of these studies, however, were done in vitro (in an artificial environment). Our findings, which are in vivo (in the living body), indicate that alcohol-induced brain damage occurs during intoxication.” 43 continued ~ THE BRAIN RISKS OF BINGE DRINKING 44 “In the rat,” explained Michael A. Collins, professor of biochemistry at Loyola University Chicago, “which on one level is a ‘walking nose,’ the overall damage to the olfactory pathway is quite significant. The olfactory neurons in the bulb are some of the few neurons that are always turning over, dying and regenerating. One guess is that the repetitively elevated alcohol levels are pushing more of these neurons ‘over the edge,’ but apparently in a necrotic fashion.” Collins said that drinking patterns may specify the nature of neuropathology that occurs and the brain regions and neurons where it occurs. “The short-term binge pattern in these studies,” he said, “which affords periodically high blood and brain alcohol levels, seems to damage the olfactory cortical regions quite selectively. In other models in which lower alcohol levels are sustained for several months – more akin to the primary type of alcohol abuse in countries like France and Spain – rodents show significant loss of brain neurons in regions evidently not affected in the brief binge-drinking model used here, for example, the cerebellum and the frontal cortex.” Collins added that even though chronic alcohol abuse damages all organs to greater or lesser degrees, most attention has been paid to liver damage, largely because it is easier for doctors to detect and measure, and can eventually lead to liver-failure death. However, he added, “a study of relatively young alcoholics published some time ago in the British journal Lancet showed that indicators of relatively permanent cognitive damage, measured by neuropsychological tests, actually showed up earlier than clinical signs of liver damage. Sadly, when the brain – the limbic cortex and dentate gyrus of the hippocampus, in this case – loses its excitable cells, for all practical purposes they are gone for good. In the day-to-day life of an alcoholic, this means a decreased ability to learn, to recall, to make decisions, and perhaps to sense and appreciate life in its fullest.” According to some estimates, said Collins, alcohol abuse in the Article is based United States is perhaps the third or fourth most common cause on the following of brain damage, and may be even higher in other countries. published research: “Given this,” he said, “it is surprising that the mechanisms of Obernier, J.A., brain neuronal degeneration due to a widely abused Bouldin, T.W., neurotoxicant are so understudied and therefore still somewhat & Crews, F.T. obscure. Certainly this has implications for a college student con( April 2002). templating a weekend of binge drinking. Seriously, though, it is Binge ethanol possible that neuronal degeneration after a couple of days of exposure in adult heavy intoxication in the rat might translate to the human drinker rats causes necrotic who is not even a chronic alcohol abuser. There is no firm proof cell death. of this at present, and we would need brain imaging to deter-Alcoholism: Clinical mine whether acute short-term binge drinking in people could and Experimental be permanently deleterious to olfactory or other neurons.” Research, 26(4). ABSTINENCE MAY MAKE THE BRAIN GROW STRONGER ABSTINENCE MAY MAKE THE BRAIN GROW STRONGER • Chronic alcohol abuse leads to structural brain damage. • The damage includes loss of gray matter in the cortex and loss of white matter throughout the brain. • The greatest tissue loss occurs in the frontal lobe and cerebellum. • Prolonged abstinence from alcohol appears to allow some reversal of structural brain damage. Substantial research has demonstrated that chronic alcohol abuse leads to structural brain damage, especially to white matter, and primarily in the frontal lobes and cerebellum. Researchers have wanted to know for quite some time to what extent these effects may be reversible with abstinence from alcohol. A study in the November issue of Alcoholism: Clinical and Experimental Research (ACER) uses quantitative neuroimaging to reveal that prolonged abstinence may lead to partial reversal of structural brain damage, which suggests that brain function can improve with abstinence. “We wanted to know if abstinence from alcohol reverses the kind of structural and metabolic abnormalities that have been demonstrated by previous studies,” said Dieter J. Meyerhoff, associate professor of radiology at the University of California - San Francisco School of Medicine and lead author of the study. “We also wanted to know in what specific brain regions and tissue types (gray or white matter) damage would be reversed with prolonged abstinence.” Meyerhoff and his colleagues compared two groups. One group comprised alcoholics (with an average age of 46 years) who had already undergone treatment for their alcoholism and had been abstinent for an average of two years at the time of study. The second group comprised individuals who were heavy drinkers at the time of study and had never been treated for their drinking. The current drinkers were matched in drinking severity (average monthly alcohol use over lifetime and duration of alcohol use) to the prior drinking patterns of the abstinent alcoholics. A healthy control group was not included because the study’s intent was to measure the effects of abstinence from chronic drinking on alcohol-induced injury. All participants underwent magnetic resonance imaging (MRI) and proton magnetic resonance (MR) spectroscopic imaging of the brain. “These are non-invasive methods,” explained Meyerhoff, “which allow taking a ‘snapshot’ of the structural and metabolic integrity of all parts of the brain. As opposed to computed tomography scans, MRI can distinguish between gray and white matter tissue, which is important when we want to talk about the functional significance of brain damage in alcoholism. In addition, we used a localization approach that allowed us to investigate structural and metabolic brain changes in relatively small, yet anatomically well-defined brain regions.” They found that the abstinent alcoholics had a greater volume of white matter in their frontal lobes than currently heavy drinkers did, but not in other parts of the brain. White matter 45 continued ~ 46 46 ABSTINENCE MAY MAKE THE BRAIN GROW STRONGER volume was greatest in those alcoholics who had been abstinent for the longest time. In addition, the amount of white matter lesions in the abstinent alcoholics was smaller than in the current drinkers in most of the brain regions investigated. Finally, the volume of gray matter in the abstinent alcoholics was greater in some but not all regions of the frontal lobes. “These results suggest reversal of structural abnormalities in some brain regions of abstinent alcoholics,” said Meyerhoff, “and persistent structural damage in other brain regions. We still need to learn, however, what this means for the individual’s brain function.” “We know that alcohol abuse can cause extensive damage to the brain,” said Edith Sullivan, associate professor of psychiatry at Stanford University Schoool of Medicine. “This can include volume deficits in cortical gray matter, which are neural cell bodies, as well as in white matter, which are the fibers that are extensions of the cell bodies and that connect cells. The regions most clearly affected are the frontal lobes. Additional brain structures affected are the corpus callosum (the large band of white matter fibers that connect the two cerebral hemispheres), the anterior aspect of the hippocampus and the mammillary bodies (brain structures that engage in consolidation of new memories) and the cerebellum (the ‘little brain’ that is critical to postural stability, motor timing and motor learning as well as certain components of cognitive functioning). The UCSF study suggests that the recovering alcoholic group, despite their older age, can experience a significant reversal of white matter abnormality with prolonged abstinence.” Sullivan said that future research needs to focus on longitudinal studies, using different modalities of brain imaging that follow alcoholics from early detoxification through periods of Article is based sobriety and relapse. She added that these studies need to take on the following into account nutritional factors, withdrawal symptoms and func-published research: tional outcomes in alcoholic men and women of all ages. O’Neill, J., Cardenas, V.A., This is in fact what Meyerhoff and his colleagues have in the & Meyerhoff, D.J. works: longitudinal studies of alcoholics who undergo treat (November 2001). ment for their drinking problem. “These studies are ongoing Effects of abstinence and include structural and metabolic MR studies integrated on the brain: with careful assessment of neuropsychological functioning. Quantitative MRI and Both abstainers and relapsers are examined to assess postu-MR spectroscopic lated improvement with abstinence and postulated status quo imaging in chronic or further deterioration with relapse.” Although more data alcohol abuse. have yet to be collected and analyzed, said Meyerhoff, “it Alcoholism: Clinical appears that even after many years of heavy drinking, the brain and Experimental has the capacity to repair at least some of the structural dam-Research, age that has occurred.” 25(11), 1673-1682. COGNITIVE NEUROSCIENCE TAKES ON ALCOHOL COGNITIVE NEUROSCIENCE TAKES ON ALCOHOL • Alcohol is known to impair an individual’s ability to control his/her behavior. • Impaired behavioral control is known to be a factor in accidents, antisocial acts and binge drinking. • Psychologists are jointly investigating the effects of alcohol on brain activity that is associated with behavioral control. • Findings show that specific cognitive processes, certain individual characteristics, and some environmental conditions can all influence alcohol’s effects on behavioral control. A study in the January issue of Alcoholism: Clinical and Experimental Research (ACER) examines how alcohol – through its effects on underlying cognitive processes – may effect someone’s self-control in different ways. “Drinkers can sometimes display foolish, inappropriate or harmful behavior that they would not exhibit when sober,” said Muriel Vogel-Sprott, professor of psychology at the University of Waterloo and first author of the paper. “This is commonly attributed to the effects of alcohol, for example, explaining away the behavior by saying ‘I couldn’t stop myself’ or ‘I didn’t mean it.’” Vogel-Sprott’s paper was based on research presented at a symposium during the June 2000 Research Society on Alcoholism meeting in Denver. Researchers tested the effects of a moderate dose of alcohol (approximately two or three beers) on social drinkers’ performance of a task. The objective was to assess specific cognitive processes that govern behavior. “Some of the presentations showed that alcohol could diminish cognitive control of response inhibition,” said Vogel-Sprott, “and that vulnerability to this disinhibition varied among individuals. In addition, there are some personal attributes – such as impulsivity, symptoms of attention deficit disorder, and the capacity to keep in mind the relevant information needed to guide behavior – that are related to poorer inhibition under alcohol. Yet other research used event-related functional magnetic resonance imaging (MRIs or brain scans) to identify those brain areas and networks that are activated when cognitive inhibitory tasks are performed. This work showed that both successful and unsuccessful inhibition of behavior is distinguishable by different brain activity and, furthermore, these effects are altered by alcohol.” Vogel-Sprott’s own research examined intentional control of behavior, assessing the degree to which conscious (intentional) and unconscious (automatic) cognitive processes influence performance. She found that a moderate dose of alcohol selectively diminished intentional control when social drinkers’ behavior had no environmental consequence. However, when performance under alcohol had some ‘payoff’ (for example, money or verbal approval), intentional control was well retained. “Was the behavior due to alcohol,” mused Vogel-Sprott, “or was it intentional? This question is controversial, particularly in the courts, where the intentionality of an alcohol-related offence can affect the sentence. The research presented in this symposium indicates that the answer is 47 continued ~ 48 48 COGNITIVE NEUROSCIENCE TAKES ON ALCOHOL complex. On one hand, it appears that alcohol can impair cognitive processes controlling inhibition and intentional behavior. But, on the other hand, the intensity of impairment may also depend upon the characteristics of the drinker and the consequences of behavior in the drinking situation.” Mark Fillmore, assistant professor of psychology at the University of Kentucky, was another of the presenters during the symposium. His research examined how a drug such as alcohol can disturb a person’s ability to control behavior. His findings showed that alcohol-induced impairment of inhibitory control appears to have some commonalities with Attention Deficit Hyperactivity Disorder (ADHD). “It seems that alcohol reduces the ability to stop some actions,” he said. “This is important because we all have to sometimes stop what we are doing to reflect and plan more appropriate actions. Impulsiveness can lead to a host of problems in school, work and with peer relations. My work discovered that low to moderate doses of alcohol impair the ability to stop actions much in the same way that individuals with ADHD have difficulty stopping inappropriate actions, such as throwing a punch. The effects of alcohol are short-lived, lasting only about an hour or so. But these observations suggest that alcohol can produce a temporary mental state in some individuals that resembles impulsiveness, and perhaps, ADHD-like symptoms.” Fillmore’s work also found that stimulant drugs can block the impairing effects of alcohol so that the ability to stop actions while under the influence of alcohol is improved. This is similar to findings that stimulant drugs (such as Ritalin) can increase the ability to stop behaviors in in-Article is based dividuals with ADHD. on the following published research: “The fact that both ADHD and acute doses of alcohol can impair Nicolas, J.M., the ability to withhold inappropriate behavior,” he said, “raises Fernandez-Sola, J., the possibility that people with ADHD might suffer greater Fatjo, F., impairment from alcohol. The major challenge for alcohol Casamitjana, R., researchers has been to figure out why some people develop Bataller, R., problems, while others do not. The ability to identify a pre- Sacanella, Tobias, E., existing trait (such as ADHD) among some individuals that con- Badia, E., & Estruch, R. tributes to alcohol problems is a very important development.” (January 2001). Increased circulating The varied yet interconnected research presented at the sym-leptin levels in chronic posium demonstrates how scientists using research tools from alcoholism. cognitive science and neuropsychology are working together to Alcoholism: Clinical study how alcohol impairs behavioral control. “We didn’t find and Experimental an easy answer,” said Vogel-Sprott, “but we have a better ‘big Research, picture’ understanding of how alcohol impairs behavior.” 25(1), 83-88. JUST A SPOONFUL OF THIAMIN? JUST A SPOONFUL OF THIAMIN? • Two neurological disorders are linked through thiamin deficiency. • One disorder can be treated with thiamin supplements; the other may be incurable. • Heavy drinkers, anorexics and senior citizens are considered at risk. • Up to 10 percent of alcoholics in the U.S. may be affected. • Australian cases decreasing, but thiamin may yet be added to beer. Something as simple as thiamin (vitamin B1) may help, or hinder, your brain’s capacity to function and perhaps even survive. Alcoholics, anorexics and senior citizens may be especially vulnerable, according to recent studies of two neurological disorders called Wernicke’s Encephalopathy (WE) and Korsakoff’s Syndrome (KS). The two studies, published in the October issue of Alcoholism: Clinical and Experimental Research (ACER), jointly found that mammillary bodies in the brain may shrink as cognition and memory decrease. “These findings are significant because they point toward the importance of nutritional factors in the condition of the brain,” said Edith Sullivan, associate professor of psychiatry at Stanford University School of Medicine and lead author of one of the studies. Sullivan based her study on in vivo, or living patients. WE is a potentially fatal disorder caused by thiamin deficiency. WE usually occurs in people who have been drinking heavily and not eating, but can also occur after persistent vomiting or during hunger strikes. Recent studies have shown that young women suffering from anorexia nervosa may also develop WE due to severe nutritional deficiencies. Of increasing concern is the potentially large number of senior citizens who may be apathetic about the quality of their diet, may not be eating enough, or may forget to eat altogether. Heavy drinkers are those known to be most affected by WE. “Brain damage as a result of alcohol consumption is probably the second most common cause of dementia in the United States, behind Alzheimer’s Disease,” said Dr. Peter Martin of the Vanderbilt University School of Medicine. Heavy drinkers often eat improperly. Furthermore, alcohol impedes the digestive tract’s normal absorption of those few nutrients that may be consumed. Nerve, muscle and brain tissue are extremely sensitive to low levels of vitamins, nutrients and minerals, and can begin to deteriorate when deprived. Body stores of thiamin can be depleted within about three weeks. WE is characterized by double vision, mental confusion, muscle weakness and unsteady gait. Unlike other disease states caused by alcohol, WE may reverse through rapid treatment with thiamin. If left untreated, however, the person can go into a coma and die. In some cases, even if treated, they can develop permanent memory damage in the form of KS. KS is often associated with a previous episode of WE, but is distinguished by amnesia. KS is often recognized when the confusion associated with WE clears following thiamin treatment. 49 continued ~ 50 50 JUST A SPOONFUL OF THIAMIN? Although KS may sometimes respond to thiamin treatment, it is often permanent. Researchers agree that the nutritional deficiencies caused by heavy drinking can lead to WE, and if not treated, eventually KS. Exact numbers of those afflicted are difficult to find but Martin speculated that at least 10 percent of alcoholics have some degree of the two syndromes. Even though most alcoholics do not have the characteristics of an “extreme stage of brain damage” such as Wernicke’s or Korsakoff’s, “70 percent of alcoholics have some sort of brain damage,” he said. “At one point I calculated that there were about 10 million people in the U.S. who may have some sign of brain damage related to alcohol,” he said. In Australia, the two disorders are often referred to jointly as Wernicke-Korsakoff Syndrome (WKS), according to Clive Harper, professor of neuropathology at the University of Sydney and Royal Prince Alfred Hospital and lead author of the second study. During the 1980s, Australia had the ignoble distinction of having the highest recorded rates of WE in the world, mostly among the alcoholic population, as well as large numbers of people needing long-term care because of KS. Harper estimated the former at 500 cases per year, the latter at 2,000 per year. The problem was considered so acute that in 1991, the Australian government mandated that bread flour be enriched with thiamin. This same requirement has been mandatory for a number of years in the United Kingdom, Canada and Denmark. In the U.S., most bread flour is enriched, but enrichment is not mandatory. Since the 1991 enrichment of bread flour in Australia, WKS rates have significantly decreased but remain higher than those in most other Western countries – enough to prompt discussion of thiamin supplementation of alcoholic beverages, primarily beer (the preferred beverage of many WE patients). Harper said that “WE diagnosis is probably missed about 80 percent of the time worldwide. About one in every hundred people who have a coroner’s autopsy are found to have WE, even though it is very easy to treat, because the diagnosis can easily be missed.” People suffering from WE or KS or WKS, whatever name you prefer, he said, clearly make up “a big hidden group throughout the world that needs further study.” Article is based on the following published research: Sheedy, D., Lara, A., Garrick, T., & Harper, C. (October 1999). Size of mamillary bodies in health and disease: Useful measurements in neuroradiological diagnosis of Wernicke’s encephalopathy. Alcoholism: Clinical and Experimental Research, 23(12), 1624. Sullivan, E.V., Lane, B., Deshmukh, A., Rosenbloom, M.J., Desmond, J.E., Lim, K.O., & Pfefferbaum, A. (October 1999). In vivo mammillary body volume deficits in amnesic and nonamnesic alcoholics. Alcoholism: Clinical and Experimental Research, 23(12), 1629. ALCOHOL AND THIAMIN DEFICIENCY TOGETHER: A DANGEROUS ALCOHOL AND THIAMIN DEFICIENCY TOGETHER: A DANGEROUS COMBINATION? • Heavy alcohol use is associated with thiamin (Vitamin B1) deficiency. • Alcohol and thiamin deficiency together may have a more damaging impact on the brain. • Learning and reference memory appear to be the most sensitive to their synergistic effects. • The role of thiamin supplementation is examined. Researchers and clinicians know that chronic abuse of alcohol may lead to a deficiency in thiamin (also known as Vitamin B1). This deficiency can wreak havoc on the brain, causing a wide spectrum of deficits in cognition, behavior and motor coordination. What researchers now suspect, as noted in a recent study in Alcoholism: Clinical and Experimental Research (ACER), is that chronic alcohol consumption and thiamin deficiency combined may have a synergistic and even more devastating effect on the brain and mental capacities. “We were looking for an interaction between ethanol and thiamin deficiency,” explained Philip Langlais, professor of psychology at San Diego State University, professor of neurosciences at the University of California - San Diego, and lead author of the study. “We wanted to see if you took thiamin deficiency and combined it with chronic alcohol intake, would you then create a situation that would produce a more severe impairment of cognition and memory than you would with either thiamin deficiency alone, or exposure to chronic alcohol ingestion alone.” Using rat subjects, they did indeed find a synergistic effect, sometimes. Learning (for example, figuring out the rules of chess) and reference memory (remembering and consistently applying the rules) appeared the most sensitive to the damaging, synergistic effects of alcohol and thiamin deficiency. Short-term working memory (incorporating the rules of chess into game strategies), on the other hand, was most affected by alcohol alone. Neurological symptoms were most associated with thiamin deficiency. Alcohol impedes the digestive tract from absorbing needed nutrients. Nerve, muscle and brain tissue are exquisitely sensitive to low levels of vitamins, nutrients and minerals such as thiamin, magnesium, potassium and phosphorus. When nutrients disappear, tissues slowly deteriorate. Thiamin deficiency contributes to two clinical conditions along the alcoholic’s path toward dementia. The first ‘phase’ is called Wernicke’s Encephalopathy (WE), in which people become extremely confused, develop abnormal eye movements, experience muscle weakness, and demonstrate gait disturbances. The second phase is called Wernicke-Korsakoff Syndrome (WKS). It is associated with a more severe amnesia and significant cognitive and reasoning impairments. The first two conditions may respond to, and possibly be reversed by, thiamin treatment. The final and – for all practical purposes, untreatable – phase is dementia. “This study significantly adds to the database in at least one respect,” said David V. Gauvin, psychopharmacologist and drug science specialist at the Drug Enforcement Administration. 51 continued ~ 52 52 ALCOHOL AND THIAMIN DEFICIENCY TOGETHER: A DANGEROUS COMBINATION? “It shows that there are unique interactions between alcohol and thiamin deficiency. We don’t see that one plus one equals two; rather, one plus one equals three.” Gauvin said that he would add a third component to the damaging equation: thiamin supplementation. “This unique synergism is not just about alcohol and thiamin deficiency,” he said, “it’s also about thiamin supplementation, and the whole issue of mega-dosing.” Gauvin mentioned a study in which he participated where researchers found that thiamin injections made the recipients even more sensitive to the effects of alcohol. He is concerned that the standard practice of giving alcoholics thiamin injections, in order to counteract the progression to symptoms of WE and WKS, may be more detrimental than helpful. “When you have a surplus of thiamin,” he explained, “you have the capacity to induce magnesium deficiencies, which have been linked to a number of alcohol’s negative effects.” He conjectured that thiamin-induced magnesium deficiency could be the root cause of a new sensitization to alcohol’s effects. Another way of counteracting thiamin deficiency – most often linked to poor nutrition among alcoholics, anorexics and senior citizens – is food supplementation. Both Langlais and Gauvin noted the Australia example (see Just a Spoonful of Thiamin? article). “When we gave our animals regular food that contained thiamin, they did not develop sensitization to alcohol,” said Gauvin. Article is based “The body can naturally absorb and process low-graded doses on the following of thiamin in the gut and the liver. It’s the whopping injections published research: that are problematic. Gauvin is less comfortable with the Ciccia, R.M., proposition of supplementing alcohol with thiamin. “If you & Langlais, P.J. supplement alcohol with mega-doses of Vitamin B, what you (May 2000). may actually be doing is inducing magnesium deficiencies.” An examination of the synergistic Conversely, Langlais believes that we nonetheless need to interaction of ethanol “re-examine the issue of fortifying alcoholic beverages and and thiamin perhaps other foods. We also need to seriously think about deficiency in the educating alcoholics with respect to their diet and nutrition.” development of neurological signs Gauvin had one final caution. “What does this say about vitamin and long-term supplementation? We have such a benign feeling about vitamins, cognitive and memory that we can mega-dose all we want to. Yet there is a physiologi-impairments. cal result from the overuse or abuse of vitamins. The bowel and Alcoholism: Clinical the whole digestive system have been developed in such a way to and Experimental allow for a very unique interaction between food and our needs. Research, Yet bigger is not better, more is not better.” 24(5), 622-634. CHRONIC DRINKING INCREASES CORTISOL DURING INTOXICATION CHRONIC DRINKING INCREASES CORTISOL DURING INTOXICATION AND WITHDRAWAL • Cortisol, a “stress hormone,” plays an important role in the regulation of emotion, cognition, reward, immune functioning and energy utilization. • New research has found that long-term chronic drinking produces an increase in cortisol both during intoxication and withdrawal. • Cortisol appears to increase significantly during the progression from chronic intoxication to withdrawal. • Health implications may include sleep disruption, cognitive deficits, diabetes and mood disturbances. Cortisol, known as a “stress hormone,” plays an important role in the regulation of emotion, cognition, reward, immune functioning and energy utilization. A study published in the September issue of Alcoholism: Clinical and Experimental Research (ACER) has found that long-term chronic drinking produces an increase in cortisol both during intoxicati