No single substance abuse treatment approach is effective for everyone. The appropriateness of a given intervention depends on a number of variables including the types of substances used, severity of substance issues, the setting in which treatment is delivered, presence of co-occurring physical or mental disorders, time or funding limitations, and other unique needs or issues. As the literature on different substance abuse interventions continues to expand, it is important to understand which approaches are being implemented in the field across different populations and treatment settings.
The 2009 National Survey on Substance Abuse Treatment Services (N-SSATS) collects information on the frequency with which specific clinical or therapeutic approaches (hereafter referred to as “therapeutic approaches”) are used by treatment facilities. The specific therapeutic approaches addressed in N-SSATS were selected based on their representation of widely recognized evidence-based practices in substance abuse treatment. Surveyed treatment facilities were asked to indicate how often they used each of the following 12 practices: substance abuse counseling, relapse prevention, cognitive-behavioral therapy, motivational interviewing, 12-step facilitation, anger management, brief intervention, trauma-related counseling, contingency management/motivational incentives, rational emotive behavioral therapy, Matrix Model, and community reinforcement plus vouchers.
Not all therapeutic approaches are designed to apply to all substance abuse treatment clients; some variation is expected across different facilities depending on the populations served. Further, the N-SSATS questionnaire does not include detailed questions about the ways in which the approaches are implemented, but is intended instead to provide a general indication of their adoption by substance abuse treatment providers. This report describes each therapeutic approach and presents the frequency with which facilities reported using them (always or often, sometimes, rarely or never, or were not familiar with the approach) (Figure 1). The following descriptions of the therapeutic approaches were provided to N-SSATS respondents on the survey Web site; some information was also obtained from the Substance Abuse and Mental Health Services Administration (SAMHSA) National Registry of Evidence-based Programs and Practices (NREPP). Readers who would like more information on these therapeutic approaches can visit NREPP (at http://www.nrepp.samhsa.gov/) as well as SAMHSA ™ Treatment Improvement Protocols.
Study Finds Significant Mental Deficits in Toddlers Exposed to Cocaine Before Birth
Research Findings
Vol. 17, No. 5 (January 2003)
By Robert Mathias, NIDA NOTES Staff Writer
Since the mid-1980s, up to 1 million children born in the United States are estimated to have been exposed to cocaine in the womb. Determining cocaine’s impact on these children’s development has been difficult because there often are other possible explanations for physical and mental problems the children may have, such as the mother’s use of other substances during pregnancy and poor prenatal care. Now, a NIDA-supported study that was able to separate the effects of cocaine from those of many other such factors has found that children born to poor, urban women who used cocaine throughout pregnancy were nearly twice as likely as children with similar backgrounds but no prenatal cocaine exposure to have significant cognitive deficits during their first 2 years of life.
Mental Development Scores For Prenatally Cocaine-Exposed and Unexposed High-Risk Children
Tests of mental development at 6.5, 12, and 24 months showed average scores of cocaine-exposed and unexposed children from comparable backgrounds were below the normative score of 100 for children in the general population. At age 2, cocaine-exposed children did significantly poorer in mental development than children in the comparison group.
The study, led by Dr. Lynn Singer of Case Western Reserve University in Cleveland, Ohio, is the first to show a clear association between prenatal cocaine exposure and cognitive impairment in 2-year-olds. “Since cognitive performance at this age is indicative of later performance, these children may continue to have learning difficulties that need to be addressed when they reach school age,” Dr. Singer says.
“The findings of this well-controlled study make an important contribution to a growing body of knowledge about the effects of prenatal cocaine exposure that may help us to identify those exposed children who are at increased risk of developmental harm,” says Dr. Vince Smeriglio of NIDA’s Center on AIDS and Other Medical Consequences of Drug Abuse. Previous findings from other NIDA-supported studies that have been following cocaine-exposed children from birth have produced conflicting results about cocaine’s impact on developmental outcomes at this age, he notes. “Comparing and contrasting the circumstances in this study with those found in other studies of cocaine-exposed children may enable us to identify specific biological and environmental factors that increase or reduce the developmental risk from cocaine exposure,” Dr. Smeriglio says.
The study followed a group of 415 infants born at a large urban teaching hospital from 1994 through 1996 to mothers from low socio-economic backgrounds who had been identified by the hospital staff as being at high risk of drug abuse. Women who participated in the study were given urine tests for drug use immediately before or after delivery and interviewed shortly after they gave birth to produce estimates of the type, frequency, and amounts of drugs they had used during pregnancy. Each baby’s first stool, known as meconium, also was analyzed for the presence of cocaine and its metabolites to help establish the level of drug exposure. Of the 415 babies in the study, 218 had been exposed to cocaine and 197 had not. Both groups of infants also had been exposed to tobacco, alcohol, and marijuana during pregnancy.
Researchers measured the children’s developmental progress at 6.5, 12, and 24 months of age with the Bayley Scales of Infant Mental and Motor Development. Motor tests assessed the infants’ ability to control and coordinate their movements. Mental tests assessed language, memory, and ability to solve problems at 12 and 24 months. For example, children were asked to describe objects in pictures, remember where an object had been hidden, and put shaped objects into the correct spaces cut out on form boards.
To isolate cocaine’s effect, researchers adjusted test results for the effect of other risk factors, such as other drugs used during pregnancy; characteristics of biological mothers and alternative caregivers; the infants’ head size, weight, length, and gestational age at birth; and the quality of their postnatal home environments. The analysis showed that while prenatal cocaine exposure had not affected the infants’ motor development, it was clearly linked to significant deficits in their cognitive performance at age 2. Cocaine-exposed children scored 6 points lower on the Mental Development Index (MDI), averaging 82.7 percent compared to 88.7 percent for unexposed children and an average general population score of 100. Other findings include the following:
From 6.5 to 24 months, MDI scores declined for both groups, but cocaine-exposed children had a greater decline — 14 points compared to a 9-point decline for unexposed children.
Almost 14 percent (13.7 percent) of cocaine-exposed children had scores in the mental retardation range, below 70 on the MDI, nearly twice the 7.1-percent rate found in the unexposed children and almost five times the rate (about 2.8 percent) expected in the general population.
Nearly 38 percent (37.8 percent) of cocaine-exposed children had developmental delays requiring remedial intervention, nearly double the 20.9 percent rate for unexposed children.
The study found that other influences, including the mother’s intelligence scores and educational level, exposure to other substances, and the quality of the postnatal home environment, also played significant roles in poor outcomes for cocaine-exposed children. “However, after controlling for these factors in our analysis, we found that cocaine still has a harmful effect on cognitive performance,” Dr. Singer says. Additional support for this conclusion comes from mothers’ self-reports and biological data from mothers and infants that established a direct link between cocaine dose and toddlers’ cognitive performance. These data showed that children of mothers who used more cocaine and used it more frequently during pregnancy performed worse on the MDI than children of mothers who used less of the drug.
“The only risk factor we couldn’t completely control for is the effect of other drugs used during pregnancy,” Dr. Singer says, “because it is nearly impossible to find children who have been exposed only to cocaine.” The study partially adjusted for this influence by including children who had been heavily exposed to alcohol, tobacco, and marijuana in both groups. “Animal studies suggest there are possible synergistic effects of these drugs in combination, and the study may not have been large enough to control for these effects,” she notes.
“We believe that cocaine exposure is a neurologic risk factor that may take a poor child who has a lower IQ potential because of maternal and other risk factors and push him or her over the edge to mental retardation,” Dr. Singer says. For example, average IQ scores for both cocaine-exposed and unexposed toddlers in the study were well below the average score for the general population. “In effect, cocaine lowered the range of IQ scores and that means more children may require early stimulation and educational programs,” she says.
“While many children in this study may require special educational services when they enter school, it is important not to assume that the findings from a single study, with its unique characteristics, necessarily apply to all cocaine-exposed children,” cautions NIDA’s Dr. Smeriglio. Ultimately, NIDA’s extensive portfolio of research on groups of cocaine-exposed children being raised in a variety of settings should provide detailed information about mother, child, environment, and drug-use characteristics that can be used to develop interventions that reduce risk of harm and guide clinical care for cocaine-exposed children.
Source
Singer, L.T., et al. Cognitive and motor outcomes of cocaine-exposed infants. JAMA287(15):1952-1960, 2002. [Abstract]
From : National Institute on Alcohol Abuse and Alcoholism (NIAAA)
It is important to understand that these answers are not meant to provide specific medical advice, but to provide information to better understand the health consequences of alcohol abuse and dependence (alcoholism). Please consult your physician or other health care provider if you or a loved one has an alcohol problem.
Alcoholism, also known as alcohol dependence, is a disease that includes the following four symptoms:
Craving–A strong need, or urge, to drink.
Loss of control–Not being able to stop drinking once drinking has begun.
Physical dependence–Withdrawal symptoms, such as nausea, sweating, shakiness, and anxiety after stopping drinking.
Tolerance–The need to drink greater amounts of alcohol to get “high.”
For clinical and research purposes, formal diagnostic criteria for alcoholism also have been developed. Such criteria are included in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, published by the American Psychiatric Association, as well as in the International Classification Diseases, published by the World Health Organization. (See also “Publications,” Alcohol Alert No. 30: Diagnostic Criteria for Alcohol Abuse and Dependence.)
2. Is alcoholism a disease?
Yes, alcoholism is a disease. The craving that an alcoholic feels for alcohol can be as strong as the need for food or water. An alcoholic will continue to drink despite serious family, health, or legal problems.
Like many other diseases, alcoholism is chronic, meaning that it lasts a person’s lifetime; it usually follows a predictable course; and it has symptoms. The risk for developing alcoholism is influenced both by a person’s genes and by his or her lifestyle. (See also “Publications,” Alcohol Alert No. 30: Diagnostic Criteria for Alcohol Abuse and Dependence.)
3. Is alcoholism inherited?
Research shows that the risk for developing alcoholism does indeed run in families. The genes a person inherits partially explain this pattern, but lifestyle is also a factor. Currently, researchers are working to discover the actual genes that put people at risk for alcoholism. Your friends, the amount of stress in your life, and how readily available alcohol is also are factors that may increase your risk for alcoholism.
But remember: Risk is not destiny. Just because alcoholism tends to run in families doesn’t mean that a child of an alcoholic parent will automatically become an alcoholic too. Some people develop alcoholism even though no one in their family has a drinking problem. By the same token, not all children of alcoholic families get into trouble with alcohol. Knowing you are at risk is important, though, because then you can take steps to protect yourself from developing problems with alcohol. (See also “Publications,” A Family History of Alcoholism – Are You at Risk?; Alcohol Alert No. 18: The Genetics of Alcoholism.)
4. Can alcoholism be cured?
No, alcoholism cannot be cured at this time. Even if an alcoholic hasn’t been drinking for a long time, he or she can still suffer a relapse. Not drinking is the safest course for most people with alcoholism.
5. Can alcoholism be treated?
Yes, alcoholism can be treated. Alcoholism treatment programs use both counseling and medications to help a person stop drinking. Treatment has helped many people stop drinking and rebuild their lives. (See also “Publication,” Alcohol Alert No. 49: New Advances in Alcoholism Treatment.)
6. Which medications treat alcoholism?
Three oral medications–disulfiram (Antabuse®), naltrexone (Depade®, ReVia®), and acamprosate (Campral®)–are currently approved to treat alcohol dependence. In addition, an injectable, long-acting form of naltrexone (Vivitrol®) is available. These medications have been shown to help people with dependence reduce their drinking, avoid relapse to heavy drinking, and achieve and maintain abstinence. Naltrexone acts in the brain to reduce craving for alcohol after someone has stopped drinking. Acamprosate is thought to work by reducing symptoms that follow lengthy abstinence, such as anxiety and insomnia. Disulfiram discourages drinking by making the person taking it feel sick after drinking alcohol.
Other types of drugs are available to help manage symptoms of withdrawal (such as shakiness, nausea, and sweating) if they occur after someone with alcohol dependence stops drinking.
Although medications are available to help treat alcoholism, there is no “magic bullet.” In other words, no single medication is available that works in every case and/or in every person. Developing new and more effective medications to treat alcoholism remains a high priority for researchers. (See also “News Releases,” Jan. 17, 1995: Naltrexone Approved for Alcoholism Treatment and “Publication,” Alcohol Alert No. 61: Neuroscience Research and Therapeutic Targets.)
7. Does alcoholism treatment work?
Alcoholism treatment works for many people. But like other chronic illnesses, such as diabetes, high blood pressure, and asthma, there are varying levels of success when it comes to treatment. Some people stop drinking and remain sober. Others have long periods of sobriety with bouts of relapse. And still others cannot stop drinking for any length of time. With treatment, one thing is clear, however: the longer a person abstains from alcohol, the more likely he or she will be able to stay sober.
8. Do you have to be an alcoholic to experience problems?
No. Alcoholism is only one type of an alcohol problem. Alcohol abuse can be just as harmful. A person can abuse alcohol without actually being an alcoholic–that is, he or she may drink too much and too often but still not be dependent on alcohol. Some of the problems linked to alcohol abuse include not being able to meet work, school, or family responsibilities; drunk-driving arrests and car crashes; and drinking-related medical conditions. Under some circumstances, even social or moderate drinking is dangerous–for example, when driving, during pregnancy, or when taking certain medications.
9. Are specific groups of people more likely to have problems?
Alcohol abuse and alcoholism cut across gender, race, and nationality. In the United States, 17.6 million people–about l in every 12 adults–abuse alcohol or are alcohol dependent. In general, more men than women are alcohol dependent or have alcohol problems. And alcohol problems are highest among young adults ages 18-29 and lowest among adults ages 65 and older. We also know that people who start drinking at an early age–for example, at age 14 or younger–are at much higher risk of developing alcohol problems at some point in their lives compared to someone who starts drinking at age 21 or after. (See also “News Releases,” June 10, 2004 “ Alcohol Abuse Increases, Dependence Declines Across Decade: Young Adult Minorities Emerge As High-Risk Subgroups” and July 3, 2006 “ Early Drinking Linked to Higher Lifetime Alcoholism Risk. See also Alcohol Alert No. 55: Alcohol and Minorities: An Update.)
10. How can you tell if someone has a problem?
Answering the following four questions can help you find out if you or a loved one has a drinking problem:
Have you ever felt you should cut down on your drinking?
Have people annoyed you by criticizing your drinking?
Have you ever felt bad or guilty about your drinking?
Have you ever had a drink first thing in the morning to steady your nerves or to get rid of a hangover?
One “yes” answer suggests a possible alcohol problem. More than one “yes” answer means it is highly likely that a problem exists. If you think that you or someone you know might have an alcohol problem, it is important to see a doctor or other health care provider right away. They can help you determine if a drinking problem exists and plan the best course of action.
11. Can a problem drinker simply cut down?
It depends. If that person has been diagnosed as an alcoholic, the answer is “no.” Alcoholics who try to cut down on drinking rarely succeed. Cutting out alcohol–that is, abstaining–is usually the best course for recovery. People who are not alcohol dependent but who have experienced alcohol-related problems may be able to limit the amount they drink. If they can’t stay within those limits, they need to stop drinking altogether. (See the question 13, “What is a safe level of drinking?”) (See also “Publications/Pamphlets and Brochures,” How to Cut Down on Your Drinking.)
12. If an alcoholic is unwilling to get help, what can you do about it?
This can be a challenge. An alcoholic can’t be forced to get help except under certain circumstances, such as a traffic violation dor arrest that results in court-ordered treatment. But you don’t have to wait for someone to “hit rock bottom” to act. Many alcoholism treatment specialists suggest the following steps to help an alcoholic get treatment:
Stop all “cover ups.” Family members often make excuses to others or try to protect the alcoholic from the results of his or her drinking. It is important to stop covering for the alcoholic so that he or she experiences the full consequences of drinking.
Time your intervention. The best time to talk to the drinker is shortly after an alcohol-related problem has occurred–like a serious family argument or an accident. Choose a time when he or she is sober, both of you are fairly calm, and you have a chance to talk in private.
Be specific. Tell the family member that you are worried about his or her drinking. Use examples of the ways in which the drinking has caused problems, including the most recent incident.
State the results. Explain to the drinker what you will do if he or she doesn’t go for help–not to punish the drinker, but to protect yourself from his or her problems. What you say may range from refusing to go with the person to any social activity where alcohol will be served, to moving out of the house. Do not make any threats you are not prepared to carry out.
Get help. Gather information in advance about treatment options in your community. If the person is willing to get help, call immediately for an appointment with a treatment counselor. Offer to go with the family member on the first visit to a treatment program and/or an Alcoholics Anonymous meeting.
Call on a friend. If the family member still refuses to get help, ask a friend to talk with him or her using the steps just described. A friend who is a recovering alcoholic may be particularly persuasive, but any person who is caring and nonjudgmental may help. The intervention of more than one person, more than one time, is often necessary to coax an alcoholic to seek help.
Find strength in numbers. With the help of a health care professional, some families join with other relatives and friends to confront an alcoholic as a group. This approach should only be tried under the guidance of a health care professional who is experienced in this kind of group intervention.
Get support. It is important to remember that you are not alone. Support groups offered in most communities include Al-Anon, which holds regular meetings for spouses and other significant adults in an alcoholic’s life, and Alateen, which is geared to children of alcoholics. These groups help family members understand that they are not responsible for an alcoholic’s drinking and that they need to take steps to take care of themselves, regardless of whether the alcoholic family member chooses to get help. (See the question 19, “How can a person get help for an alcohol problem” for referral to support groups.)
You can call the National Drug and Alcohol Treatment Referral Routing Service ( Center for Substance Abuse Treatment) at 1-800-662-HELP (4357) for information about treatment programs in your local community and to speak to someone about an alcohol problem.
13. What is a safe level of drinking?
For most adults, moderate alcohol use–up to two drinks per day for men and one drink per day for women and older people–causes few if any problems. (One drink equals one 12-ounce bottle of beer or wine cooler, one 5-ounce glass of wine, or 1.5 ounces of 80-proof distilled spirits.)
Certain people should not drink at all, however:
Women who are pregnant or trying to become pregnant
People who plan to drive or engage in other activities that require alertness and skill (such as driving a car)
People taking certain over-the-counter or prescription medications
People with medical conditions that can be made worse by drinking
No, alcohol can harm the baby of a mother who drinks during pregnancy. Although the highest risk is to babies whose mothers drink heavily, it is not clear yet whether there is any completely safe level of alcohol during pregnancy. For this reason, the U.S. Surgeon General released advisories in 1981 and again in 2005 urging women who are pregnant or may become pregnant to abstain from alcohol ( http://www.lhvpn.net/hhspress.html). The damage caused by prenatal alcohol includes a range of physical, behavioral, and learning problems in babies Babies most severely affected have what is called Fetal Alcohol Syndrome (FAS). These babies may have abnormal facial features and severe learning disabilities. Babies can also be born with mild disabilities without the facial changes typical of FAS.
Alcohol’s effects do vary with age. Slower reaction times, problems with hearing and seeing, and a lower tolerance to alcohol’s effects put older people at higher risk for falls, car crashes, and other types of injuries that may result from drinking.
Older people also tend to take more medicines than younger people. Mixing alcohol with over-the-counter or prescription medications can be very dangerous, even fatal. (See the question 18, ”When taking medications, must you stop drinking?” for more information.) In addition, alcohol can make many of the medical conditions common in older people, including high blood pressure and ulcers, more serious. Physical changes associated with aging can make older people feel “high” even after drinking only small amounts of alcohol. So even if there is no medical reason to avoid alcohol, older men and women should limit themselves to one drink per day. (See also “Publications/Pamphlets and Brochures” Age Page: Alcohol Use and Abuse.)
16. Does alcohol affect women differently?
Yes, alcohol affects women differently than men. Women become more impaired than men do after drinking the same amount of alcohol, even when differences in body weight are taken into account. This is because women’s bodies have less water than men’s bodies. Because alcohol mixes with body water, a given amount of alcohol becomes more highly concentrated in a woman’s body than in a man’s. In other words, it would be like dropping the same amount of alcohol into a much smaller pail of water. That is why the recommended drinking limit for women is lower than for men. (See the question13, “What is a safe level of drinking?” for recommended limits.)
In addition, chronic alcohol abuse takes a heavier physical toll on women than on men. Alcohol dependence and related medical problems, such as brain, heart, and liver damage, progress more rapidly in women than in men. (See also “Publications,” Alcohol Alert No. 62: Alcohol-An Important Women’s Health Issue.)
17. Is alcohol good for your heart?
Studies have shown that moderate drinkers are less likely to die from one form of heart disease than are people who do not drink any alcohol or who drink more.
If you are a nondrinker, however, you should not start drinking solely to benefit your heart. You can guard against heart disease by exercising and eating foods that are low in fat. And if you are pregnant, planning to become pregnant, have been diagnosed as alcoholic, or have another medical condition that could make alcohol use harmful, you should not drink.
If you can safely drink alcohol and you choose to drink, do so in moderation. Heavy drinking can actually increase the risk of heart failure, stroke, and high blood pressure, as well as cause many other medical problems, such as liver cirrhosis. (See also “Publications,” Alcohol Alert No. 16: Moderate Drinking and Alcohol Alert No. 45: Alcohol Coronary Heart Disease.)
18. When taking medications, must you stop drinking?
Possibly. More than 150 medications interact harmfully with alcohol. These interactions may result in increased risk of illness, injury, and even death. Alcohol’s effects are heightened by medicines that depress the central nervous system, such as sleeping pills, antihistamines, antidepressants, anti-anxiety drugs, and some painkillers. In addition, medicines for certain disorders, including diabetes, high blood pressure, and heart disease, can have harmful interactions with alcohol. If you are taking any over-the-counter or prescription medications, ask your doctor or pharmacist if you can safely drink alcohol. (See also “Publications,” Harmful Interactions; Mixing Alcohol with Medicines; Alcohol Alert No. 27 : Alcohol-Medication Interactions.)
19. How can a person get help for an alcohol problem?
There are many national and local resources that can help. The National Drug and Alcohol Treatment Referral Routing Service provides a toll-free telephone number, 1-800-662-HELP (4357), offering various resource information. Through this service you can speak directly to a representative concerning substance abuse treatment, request printed material on alcohol or other drugs, or obtain local substance abuse treatment referral information in your State ( see Treatment Referral Information).
Many people also find support groups a helpful aid to recovery. The following list includes a variety of resources:
Alcoholism (alcohol dependence) and alcohol abuse are two different forms of problem drinking. Alcoholism occurs when a person shows signs of physical addiction to alcohol (for …
The National Institute on Alcohol Abuse and Alcoholism (NIAAA) routinely receives a variety of questions about alcohol. We would like to share the following frequently asked …
Supports and conducts biomedical and behavioral research on the causes, consequences, treatment, and prevention of alcoholism and alcohol-related problems.
Alcoholism in the Workplace: A Handbook for Supervisors, including information on managing performance problems, leave issues, Employee Assistance, and followup.
For most adults, moderate alcohol use is not harmful. However, nearly 17.6 million adults in the United States are alcoholics or have alcohol problems.
Dr. Enoch Gordis, former Director of the National Institute on Alcohol Abuse and Alcoholism (NIAAA), has written, “Although alcohol is sometimes referred to as a …
If you are among the millions of people in this country who have a parent, grandparent, or other close relative with alcoholism, you may have wondered what your family’s …
Reviewed June 2010. Alcoholism and Recovery. According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA), nearly 17.6 million Americans—or 1 in 12 adults …
Low-Cost Incentives Improve Outcomes in Stimulant Abuse Treatment
Last Updated on Thursday, 06 January 2011 01:03
Thursday, 06 January 2011 01:02
Low-Cost Incentives Improve Outcomes in Stimulant Abuse Treatment
In community-based treatment programs, the intervention added $2.42 per patient per day to counseling
costs.
By Lori Whitten, NIDA Notes Staff Writer
The opportunity to win rewards worth as little as $1 for abstinence can help motivate outpatients to stay in behavioral therapy and remain drug-free, according to a NIDA Clinical Trials Network (CTN) study. At eight community-based addiction treatment programs across the United States, stimulant abusers who could earn a chance to win a prize by providing drug-free urine samples were four times as likely as peers who were not offered this incentive to attain 12 weeks of continuous abstinence. Prizes for the
incentive intervention cost the programs about $200, or
$2.42 a day per participant.
Many addiction treatment clinics face the challenge of high patient dropout rates. Reinforcing abstinence helps keep patients interested in attending treatment for longer periods, which can facilitate behavioral changes to keep them off drugs for the long haul,” says Dr. Nancy Petry of the University of Connecticut School of Medicine, coleader of the study. Prior research has found that, no matter how it is achieved, duration of abstinence during treatment is one of the best predictors of abstinence 1 year later. “More patients achieve this therapeutic milestone with a boost from incentive programs,” says the study’s other coleader, Dr. Maxine Stitzer of The Johns Hopkins University School of Medicine.
The CTN investigators randomly assigned 415 treatment-seeking stimulant abusers (see chart) to one of two conditions: usual care or usual care plus abstinence-based incentives for 12 weeks. Usual care typically consisted of group counseling, although some patients received individual and family therapy. Patients gave urine and breath samples twice weekly. Research assistants tested the urine samples for stimulants, opiates, and marijuana, and tested the breath samples for alcohol.
Each participant in the incentive condition received immediate feedback on his or her samples. After submitting stimulant-and alcohol-negative samples, the patient
could draw from an opaque container with 500 chips,
each with words of encouragement or an assigned value:
Half of the chips simply said, “good job;” 209 could be traded for $1 prizes, 40 for $20 prizes, and 1 for a $100
prize. Prizes were conferred immediately and included many options, ranging from toiletries, snacks, and bus tokens to kitchen items, telephones, and retail store certificates for televisions, music players, and DVD players. The number of draws earned increased by one each week in
which all the patient’s samples were stimulant-and alcohol-negative, but fell back to one following a positive sample or an unexcused absence. When a participant first achieved two consecutive weeks of abstinence, he or she received a $20 prize. Participants who submitted stimulant-and alcohol-negative samples could earn two bonus draws a week if their urine samples were also opioid-and marijuana-negative.
More patients in the incentive program (49 percent) than
in usual care (35 percent) completed 12 weeks of counseling. Patients in the incentive group achieved an average duration of sustained abstinence of 4.4 consecutive weeks, compared with only 2.6 weeks among counseling-only patients. Nineteen percent of patients receiving the incentive intervention attained 12 weeks of continuous abstinence compared with 5 percent of those in usual care. Intervention patients also attended more counseling
sessions (19 versus 16) and submitted more stimulant-
negative urine samples during treatment than patients in
usual care (48 versus 36 percent).
Incentives Accentuate The Positive
“Incentive programs, including low-cost ones, add excitement and additional reasons to attend substance abuse treatment. Many substance abusers are ambivalent about treatment, and rewards may help them stay involved in counseling,” says Dr. Petry. Extending retention in treatment may prolong abstinence, in part, because it gives counselors more time to help patients re-engage in a drug-free lifestyle, says Dr. Stitzer. Helping patients sustain abstinence once they leave therapy is a challenge for all treatments, including incentive programs.
Some previous clinical trials of voucher-based incentive programs showed benefits of the treatment persisting for 1 to 2 years, but others found no added value over the long term compared with usual care. Further research will focus on followup with patients to determine the conditions under which incentive interventions, particularly as applied by community-based treatment programs, support extended abstinence.
Other relatively small, often single-site NIDA-funded clinical trials over the past 15 years have demonstrated that motivational incentives are an effective adjunct to standard therapy for opiate-, marijuana-, alcohol-, and cocaine-addicted patients. Patients in most of those early studies always received vouchers exchangeable for goods or services, rather than chances
to win prizes, for positive behaviors; costs typically ran to about $1,000 per
patient over 3 months, with the result that few community programs adopted the motivational incentive approach. Dr. Petry developed her prize-drawing system to make incentives affordable for community programs. She has tested it successfully in several Connecticut treatment programs, and now its effectiveness is confirmed by the CTN trial. NIDA is collaborating with the Substance Abuse and Mental Health Services Administration’s Addiction Technology Transfer Center to promote awareness of the low-cost motivational incentive technique (see textbox).
The CTN researchers note that some community-based treatment providers resist the idea of motivational incentives based on a belief that clinicians should not reward patients for behaviors “that they are supposed to do anyway.” In response, the researchers point out that groups and individuals often use external incentives to motivate others—from employees’ bonuses
to children’s allowances for household
chores. Dr. Stitzer advocates a shift in perspective from punishing lapses to celebrating successes. She observes that counselors have often changed their views when they have seen incentives help revolving-door patients stay in therapy. “Incentive programs—the idea of catching people being good and rewarding the behavior— can infuse addiction treatment with a positive outlook and reinvigorate patients and counselors,” says Dr. Stitzer.
Source
• Petry, N.M., et al. Effect of prize-based incentives on
outcomes in stimulant abusers in outpatient psychosocial treatment programs: A National Drug Abuse Treatment Clinical Trials Network Study. Archives of General Psychiatry 62(10):1148-1156, 2005.
National Institute on Alcohol Abuse and Alcoholism No. 18 PH 357 July 1992
The Genetics of Alcoholism
The idea that alcoholism runs in families is an ancient one. In recent decades, science has advanced this idea from the status of folk-observation to systematic investigation (1-3). In the 1970s, studies documented that alcoholism does run in families (4,5). But does alcoholism run in families because a child learns to become an alcoholic from parents and the home environment, or because a child inherits genes that create an underlying predisposition for alcoholism? Or both? The studies did not resolve these questions.
Why do we do genetic research? The discovery of a specific genetic effect on the development of alcoholism would be beneficial for at least three reasons. First, it would lead to the identification of some people at risk, who could act to avoid developing alcohol-related problems (6,7). Second, it may help us to understand the role of environmental factors that are critical in the development of alcoholism (8). Third, it may lead to better treatments, based on new understandings of the physiological mechanisms of alcoholism (9-11).
Although investigations of the inheritance of a vulnerability to alcoholism are discussed here, a separate and distinct issue, not addressed here, is the possibility that a vulnerability to organ damage by alcohol is under some genetic control (12).
Researchers investigate possible genetic components of alcoholism by studying populations and families as well as genetic, biochemical, and neurobehavioral markers and characteristics (13,14). Two major methods of investigating the inheritance of alcoholism are studies of twins and of adoptees (15). Twin studies compare the incidence of alcoholism in identical twins with the incidence of alcoholism in fraternal twins (16,17). If there is a genetic component in the risk for alcoholism, then identical twins, who have identical genes, would be expected to exhibit similar histories of developing alcoholism (or not developing alcoholism). Fraternal twins, who are genetically different individuals born at the same time, would be more likely to differ in their tendencies to develop alcoholism. In general, researchers using the twin method have found these expectations to be true.
For example, Pickens and co-workers (18) studied 169 same-sex pairs of twins, both males and females, at least one of which had sought treatment for alcoholism. The researchers found greater concordance of alcohol dependence in identical twins than in fraternal twins. They also found greater concordance of alcohol abuse (defined by DSM-III–Diagnostic and Statistical Manual of Mental Disorders, Third Edition, of the American Psychiatric Association) in identical male twins but not in identical female twins. Other twin studies have produced more detailed information; for example, Partanen and co-workers (19), in studying 902 male Finnish twins, found that less severe drinking patterns were less heritable, and more severe drinking patterns were more heritable.
Among the difficulties in designing twin studies is accounting for unequal environmental conditions. Early studies assumed that the environments of two fraternal twins were as similar to each other as were the environments of two identical twins. Later studies showed that the environments of identical twins are more alike than are the environments of fraternal twins, and recent twin studies have taken this difference into account (14). The results of twin studies are useful and have suggested the possibility of a genetic component in inheritance (20); however, because focuses of the studies have varied, the results are difficult to interpret.
Adoption studies may employ a number of techniques. One is to compare the histories of children of alcoholics who are adopted by nonalcoholics and grow up in a nondrinking environment with the histories of children of nonalcoholics similarly raised in a nondrinking environment (21-23). If genetic factors play a role, then the adopted children of alcoholics should preferentially develop alcoholism as adults.
Problems in designing and interpreting adoption studies result from, among other things, the lack of detailed data on parents who give up children for adoption, and environmental biases (as in the predominance of a certain type of adopting family) (24).
In a pioneering study of adopted Danish children, Goodwin and co-workers found some evidence for the expected trends (4,21). Cloninger and co-workers subsequently performed a series of much larger studies of adoptees, which also revealed these trends (8,25).
Cloninger and co-workers (23) hypothesized that so-called type II alcoholics–characterized as having an early onset of drinking problems, usually being male, and displaying personality disorders such as antisocial behavior–had a more heritable form of alcoholism (26). However, other researchers have argued that the scenario of inheritance is more complex, and what is inherited is a mix of personality traits, such as those related to antisocial behavior, rather than alcoholism itself (27). Genes might play a direct role in the development of alcoholism, as in affecting the body’s metabolism of alcohol; or they might play a less direct role, influencing a person’s temperament or personality in such a way that the person becomes vulnerable to alcoholism.
Different models for the way in which alcoholism runs in families have been suggested by a limited number of family studies. Interpretation of these studies has been complicated by the likelihood that alcoholism is a heterogeneous condition, that is, a collection of different conditions that look similar, but whose mechanisms and modes of inheritance may differ. Additional studies are needed to sort out the mechanisms of transmission (28,29).
Population and family studies such as those cited above attempt to establish the presence of a broad genetic influence on alcoholism. To investigate specific genes, researchers have employed genetic marker studies. If specific human genes are related to alcoholism, then genes lying close to them on the same chromosome–and the traits they determine–may be inherited at the same time that the risk of alcoholism is inherited. This phenomenon is called linkage. An assortment of genes hypothesized to be linked to alcoholism has been examined (30), but none has passed a rigorous test for linkage (31).
Still being studied is a marker referred to as the dopamine D2 receptor, which Blum and co-workers (32) found to be present more often in alcoholics than in nonalcoholics (also see 33). In animal studies, the dopamine D2 receptor had been associated with brain functions relating to reward, reinforcement, and motivation. However, a number of researchers have been unable to duplicate the results of Blum’s study (34,35). Some researchers believe dopamine D2 might modulate the severity of alcoholism, rather than serve as a primary cause. The dopamine D2 association continues to be interesting, but it does not seem to be transmitted in families in such a way that it is responsible for alcoholism; its role, if any, has yet to be determined (36).
To search the human genome for specific genes related to alcoholism, researchers employ two experimental techniques. The first, the candidate gene approach, involves hypothesizing that particular genes are related to the physiology of alcoholism and then individually testing these genes for linkage (37). The second approach, scanning of the human genome, involves characterizing, piece by piece, the entire length of DNA and finding ge nes that relate to alcoholism, without proposing candidate genes.
Additionally, researchers use animal models to study the genetics of alcoholism. These models have several advantages over human subjects. Using animals, researchers can study larger numbers and more generations of subjects, can arrange informative matings, can better manipulate the environment, and can make measurements that would not be possible on humans. The main limitation of using animals to study alcoholism is that there is no animal model of alcoholism that encompasses the whole spectrum of alcoholic behaviors in humans.
Researchers nevertheless have studied alcohol-related behaviors in animals that are believed to resemble aspects of human alcoholism. These include consumption of and preference for alcohol, sedation induced by alcohol, locomotor activation by alcohol (thought by some investigators to model the euphoric effects of alcohol in humans), motor discoordination and hypothermia induced by alcohol, withdrawal from alcohol, and tolerance to various effects of alcohol (38). Researchers have succeeded in breeding lines of rodents with high or low measures of most of these traits; this success demonstrates that the traits are substantially genetically determined in rodents.
Researchers, using animals, have yet to identify a single gene responsible for any alcohol-related behavior. They have established that all of the above-mentioned traits are determined by multiple genes, and that the individual traits are, for the most part, determined independently of each other. One useful distinction revealed by studies using animals is that genes determining the tendency to become tolerant to certain effects of alcohol are different from genes determining the severity of withdrawal symptoms (even though in a clinical setting these reactions are often seen together) (38). Using the powerful genetic methods available in animals, investigators are beginning to map genes responsible for some of the animals’ alcohol-related behaviors. The recent development of a scheme that makes it possible to predict the location on the human genome of a similar gene mapped in a mouse will provide an additional source of candidate genes for linkage studies in humans (39). This approach also will help to distinguish those animal behaviors now under study that will be most valuable for understanding human alcohol-related behavior.
The Genetics of Alcoholism–A Commentary by
NIAAA Director Enoch Gordis, M.D.
Progress has been made in understanding genetic vulnerability to alcoholism. We know, for instance, that more than one gene is likely to be responsible for this vulnerability. We now must determine what these genes are and whether they are specific for alcohol or define something more general, such as differences in temperament or personality that increase an individual’s vulnerability to alcoholism. We must also determine how genes and the environment interact to influence vulnerability to alcoholism. Based on our current understanding, it is probable that environmental influences will be at least as important, and possibly more important, than genetic influences. Success in uncovering the genes involved in a vulnerability to alcoholism will help us to recognize the potential for alcoholism in high-risk individuals, to intervene at an early stage, and to develop new treatments for alcohol-related problems. This is a productive area of research that will continue to yield important answers to the basic questions of what causes alcoholism and how we can prevent and treat it.
References
(1) Roe, A. The adult adjustment of children of alcoholic parents raised in foster homes. Quarterly Journal of Studies on Alcohol 5:378-393, 1944. (2) Goodwin, D.W. The genetics of alcoholism: A state of the art review. Alcohol Health & Research World 2(3):2-12, 1978. (3) Goldman, D., & Linnoila, M. Genetic approaches to alcoholism. Progress in Neuro-Psychopharmacology and Biological Psychiatry 10:237-242, 1986. (4) Goodwin, D.W.; Schulsinger, F.; Moller, N.; Hermansen, L.; Winokur, G.; & Guze, S.B. Drinking problems in adopted and nonadopted sons of alcoholics. Archives of General Psychiatry 31:164-169, 1974. (5) Cotton, N.S. The familial incidence of alcoholism: A review. Journal of Studies on Alcohol 40:89-116, 1979. (6) Goodwin, D.W. Biological factors in alcohol use and abuse: Implications for recognizing and preventing alcohol problems in adolescence. International Review of Psychiatry 1:41-49, 1989. (7) Goodwin, D.W. Genetic determinants of reinforcement from alcohol. In: Cox, W.M., ed. Why People Drink: Parameters of Alcohol as a Reinforcer. New York: Gardner Press, 1990. pp. 37-50. (8) Cloninger, C.R.; Bohman, M.; & Sigvardsson, S. Inheritance of alcohol abuse: Cross-fostering analysis of adopted men. Archives of General Psychiatry 36:861-868, 1981. (9) Begleiter, H., & Porjesz, B. Potential biological markers in individuals at high risk for developing alcoholism. Alcoholism: Clinical and Experimental Research 12:488-493, 1988. (10) Goedde, H.W., & Agarwal, D.P., eds. Alcoholism: Biomedical and Genetic Aspects. New York: Pergamon Press, 1989. (11) Crabbe, J.C., & Harris, R.A., eds. The Genetic Basis of Alcohol and Drug Actions. New York: Plenum Press, 1991. (12) Annoni, G.; Weiner, F.R.; Colombo, M.; Czaja, M.J.; & Zern, M.A. Albumin and collagen gene regulation in alcohol- and virus-induced human liver disease. Gastroenterology98:197-202, 1990. (13) Cloninger, C.R., & Begleiter, H., eds. Genetics and Biology of Alcoholism: Banbury Report 33. New York: Cold Spring Harbor Laboratory Press, 1990. (14) McGue, M. ”Genes, Environment, and the Etiology of Alcoholism.” Paper presented at the Working Group on the Development of Alcohol-Related Problems in High-Risk Youth conference, Washington, DC, Nov. 14-16, 1991. (15) Pickens, R.W., & Svikis, D.S. Genetic influences in human substance abuse. Journal of Addictive Diseases 10:205-214, 1991. (16) Hrubec, Z., & Omenn, G.S. Evidence of genetic predisposition to alcoholic cirrhosis and psychosis: Twin concordances for alcoholism and its biological endpoints by zygosity among male veterans. Alcoholism: Clinical and Experimental Research 5:207-212, 1981. (17) Pickens, R.W., & Svikis, D.S. The twin method in the study of vulnerability to drug abuse. In: Pickens, R.W., and Svikis, D.S., eds. Biological Vulnerability to Drug Abuse. National Institute on Drug Abuse Research Monograph Series No. 89. DHHS Pub. No. (ADM)88-1590. Washington, DC: Supt. of Docs., U.S. Govt. Print. Off., 1988. pp. 41-51. (18) Pickens, R.W.; Svikis, D.S.; McGue, M.; Lykken, D.T.; Heston, L.L.; & Clayton, P.J. Heterogeneity in the inheritance of alcoholism. Archives of General Psychiatry 48:19-28, 1991. (19) Partanen, J.; Bruun, K.; & Markkanen, T. Inheritance of Drinking Behavior. Helsinki: Finnish Foundation for Alcohol Studies, 1966. (20) Kendler, K.S.; Heath, A.C.; Neale, M.C.; Kessler, R.C.; & Eaves, L.J. A population-based twin study of alcoholism in women. Journal of the American Medical Association 268(14): 1877-1882, 1992. (21) Goodwin, D.W.; Schulsinger, F.; Hermansen, L.; Guze, S.B.; & Winokur, G. Alcohol problems in adoptees raised apart from alcoholic biological parents. Archives of General Psychiatry 28:238-243, 1973. (22) Cadoret, R.J.; Cain, C.A.; & Grove, W.M. Development of alcoholism in adoptees raised apart from alcoholic biologic relatives. Archives of General Psychiatry 37:561-563, 1980. (23) Cloninger, C.R.; Bohman, M.; Sigvardsson, S.; & von-Knorring, A.L. Psychopathology in adopted-out children of alco holics: The Stockholm adoption study. In: Galanter, M., ed. Recent Developments in Alcoholism. Vol. 3. New York: Plenum Press, 1985. pp. 37-51. (24) Searles, J.S. The role of genetics in the pathogenesis of alcoholism. Journal of Abnormal Psychology 97(2):153-167, 1988. (25) Bohman, M.; Sigvardsson, S.; & Cloninger, C.R. Maternal inheritance of alcohol abuse: Cross-fostering analysis of adopted women. Archives of General Psychiatry 38:965-969, 1981. (26) Cloninger, C.R. Neurogenetic adaptive mechanisms in alcoholism. Science 236:410-416, 1987. (27) Schuckit, M.A. Biological vulnerability to alcoholism. Journal of Consulting and Clinical Psychology 55(3):301-309, 1987. (28) Hill, S.Y. Absence of paternal sociopathy in the etiology of severe alcoholism: Is there a type III alcoholism? Journal of Studies on Alcohol 53:161-169, 1992. (29) Gilligan, S.B.; Reich, T.; & Cloninger, C.R. Etiologic heterogeneity in alcoholism. Genetic Epidemiology 4:395-414, 1987. (30) Cook, C.C., & Gurling, H.M. Candidate genes and favored loci for alcoholism. In: Cloninger, C.R., and Begleiter, H., eds. Genetics and Biology of Alcoholism: Banbury Report 33. New York: Cold Spring Harbor Laboratory Press, 1990. pp. 227-236. (31) Goldman, D. Molecular markers for linkage of genetic loci contributing to alcoholism. In: Galanter, M., ed. Recent Developments in Alcoholism. Vol. 6. New York: Plenum Press, 1988. pp. 333-349. (32) Blum, K.; Noble, E.P.; Sheridan, P.J.; Montgomery, A.; Ritchie, T.; Jagadeeswaran, P.; Nogami, H.; Briggs, A.H.; & Cohn, J.B. Allelic association of human dopamine D2 receptor gene in alcoholism. Journal of the American Medical Association 263(15):2055-2060, 1990. (33) Comings, D.E.; Comings, B.G.; Muhleman, D.; Dietz, G.; Shahbahrami, B.; Tast, D.; Knell, E.; Kocsis, P.; Baumgarten, R.; Kovacs, B.W.; Levy, D.L.; Smith, M.; Borison, R.L.; Evans, D.D.; Klein, D.N.; MacMurray, J.; Tosk, J.M.; Sverd, J.; Gysin, R.; & Flanagan, S.D. The dopamine D2 receptor locus as a modifying gene in neuropsychiatric disorders. Journal of the American Medical Association 266(13):1793-1800, 1991.(34) Bolos, A.M.; Dean, M.; Lucas-Derse, S.; Ramsburg, M.; Brown, G.L.; & Goldman, D. Population and pedigree studies reveal a lack of association between the dopamine D2 receptor gene and alcoholism. Journal of the American Medical Association 264:3156-3160, 1990. (35) Turner, E.; Ewing, J.; Shilling, P.; Smith, T.L.; Irwin, M.; Schuckit, M.; & Kelsoe, J.R. Lack of association between an RFLP near the D2 dopamine receptor gene and severe alcoholism. Biological Psychiatry 31:285-290, 1992. (36) Karp, R.W. D2 or not D2?Alcoholism: Clinical and Experimental Research 16:786-787, 1992. (37) Goldman, D., & Haber, R. Genetic variation in serotonin and ALDH underlying alcoholism. In: Cloninger, C.R., and Begleiter, H., eds. Genetics and Biology of Alcoholism: Banbury Report 33. New York: Cold Spring Harbor Laboratory Press, 1990. pp. 237-252. (38) Phillips, T.J., & Crabbe, J.C. Behavioral studies of genetic differences in alcohol action. In: Crabbe, J.C., and Harris, R.A., eds. The Genetic Basis of Alcohol and Drug Actions. New York: Plenum Press, 1991. pp. 25-104. (39) Nadeau, J.H. Linkage and Synteny Homologies Between Mouse and Man. Bar Harbor, ME: Jackson Laboratory, 1990.
All material contained in the Alcohol Alert is in the public domain and may be used or reproduced without permission from NIAAA. Citation of the source is appreciated.
Copies of the Alcohol Alert are available free of charge from the Scientific Communications Branch, Office of Scientific Affairs, NIAAA, Willco Building, Suite 409, 6000 Executive Boulevard, Bethesda, MD 20892-7003. Telephone: 301-443-3860.
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
Public Health Service * National Institutes of Health
National Institute on Alcohol Abuse and Alcoholism No. 21 PH 345 July 1993
Alcohol and Cancer
Cancer kills an estimated 526,000 Americans yearly, second only to heart disease (1). Cancers of the lung, large bowel, and breast are the most common in the United States. Considerable evidence suggests a connection between heavy alcohol consumption and increased risk for cancer, with an estimated 2 to 4 percent of all cancer cases thought to be caused either directly or indirectly by alcohol (2).
A strong association exists between alcohol use and cancers of the esophagus, pharynx, and mouth, whereas a more controversial association links alcohol with liver, breast, and colorectal cancers. Together, these cancers kill more than 125,000 people annually in the United States (1). The following sections discuss alcohol’s role in these cancers.
What Is Cancer?
Cancer is a group of diseases characterized by cells that grow out of control; in many cases, they form masses of cells, or tumors, that infiltrate, crowd out, and destroy normal tissue. Although the body strictly regulates normal cells to grow within the confines of tissues, cancer cells reproduce independently, uninhibited by tissue boundaries. Cancer develops in three stages: initiation, promotion, and progression. Cancer-causing agents, known as carcinogens, can contribute to the first two stages.
Cancer initiation occurs when a cell’s DNA (the substance that genes are made of) is irreversibly changed so that, once triggered to divide, the cell will reproduce indefinitely. The “change” involves mutations to the cell’s genes that can occur spontaneously or can be induced by a carcinogen. In some cancers, it has been shown that the mutations occur in oncogenes, genes that normally promote cell division, or in suppressor genes, genes that normally suppress cell division. Thus, it is believed that cancer-causing mutations result in overpromotion or undersuppression of cell reproduction. During cancer promotion, the initiated cell is stimulated to divide. The stimulus can be natural, as when tissue damage requires proliferation of new cells, or it can be caused by a carcinogen. During cancer progression, tumors produced by the replicating mass of cells metastasize, or spread, from the initial or primary tumor to other parts of the body, forming secondary
cancers.
Alcohol’s Link to Cancer
Two types of research link alcohol and cancer. Epidemiologic research has shown a dose-dependent association between alcohol consumption and certain types of cancer; as alcohol consumption increases, so does risk of developing certain cancers. More tenuous results have come from research into the mechanism by which alcohol could contribute to cancer development.
Epidemiologic Research
The strongest link between alcohol and cancer involves cancers of the upper digestive tract, including the esophagus, the mouth, the pharynx, and the larynx (3). Less consistent data link alcohol consumption and cancers of the liver, breast, and colon (3).
Upper digestive tract. Chronic heavy drinkers have a higher incidence of esophageal cancer than does the general population. The risk appears to increase as alcohol consumption increases (4-6). An estimated 75 percent of esophageal cancers in the United States are attributable to chronic, excessive alcohol consumption (7).
Nearly 50 percent of cancers of the mouth, pharynx, and larynx are associated with heavy drinking (7). People who drink large quantities of alcohol over time have an increased risk of these cancers as compared with abstainers (8,9). If they drink and smok e, the increase in risk is even more dramatic (5,6).
Liver. Prolonged, heavy drinking has been associated in many cases with primary liver cancer. However, it is liver cirrhosis, whether caused by alcohol or another factor, that is thought to induce the cancer (10,11). In areas of Africa and Asia, liver cancer afflicts 50 or more people per 100,000 per year, usually associated with cirrhosis caused by hepatitis viruses. In the United States, liver cancer is relatively uncommon, afflicting approximately 2 people per 100,000, but excessive alcohol consumption is linked to as many as 36 percent of these cases by some investigators (2,12).
The association between alcohol use and liver cancer is difficult to interpret, because liver cirrhosis and hepatitis B and C virus infections often confound data (13). Studies of the interactions between alcohol, hepatitis viruses, and cirrhosis will help clarify these associations with liver cancer (see below).
Breast. Chronic alcohol consumption has been associated with a small (averaging 10 percent) increase in a woman’s risk of breast cancer (14-17). According to these studies, the risk appears to increase as the quantity and duration of alcohol consumption increases. Other studies, however, have found no evidence of such a link (18-20).
The inconsistency and weakness of epidemiologic findings suggest that a third confounding factor, such as nutrition, may be responsible for the link between alcohol and breast
cancer (15). However, studies that adjusted for dietary factors such as fat intake found that the association between alcohol and breast cancer remained (14,21,22).
Recent studies suggest that alcohol may play an indirect role in the development of breast cancer. These studies indicate that alcohol increases estrogen levels in premenopausal women, which, in turn, may promote breast cancer (23).
Colon. Epidemiologic studies have found a small but consistent dose-dependent association between alcohol consumption and colorectal cancer (15,24), even when controlling for fiber and other dietary factors (15,25,26). Despite the large number of studies, however, causality cannot be determined from the available data.
Other cancers. A few studies have linked chronic heavy drinking with cancers of the stomach, pancreas, and lungs (3). However, the association is consistently weak and the majority of studies have found no association (3).
Mechanisms of Alcohol-Related Cancers
The epidemiologic data provide little insight into whether or how alcohol increases the risk for various cancers. For some cancers, such as mouth and esophageal, alcohol is thought to play a direct causal role. For others, such as liver and breast cancers, alcohol is thought to play an indirect role by enhancing mechanisms that may cause cancer. Studies looking at these direct and indirect mechanisms may shed light on alcohol’s role in developing cancers.
Oncogenes. Preliminary studies show that alcohol may affect cancer development at the genetic level by affecting oncogenes at the initiation and promotion stages of cancer. It has been suggested that acetaldehyde, a product of alcohol metabolism, impairs a cell’s natural ability to repair its DNA, resulting in a greater likelihood that mutations causing cancer initiation will occur (27). It has recently been suggested that alcohol exposure may result in overexpression of certain oncogenes in human cells and, thereby, trigger cancer promotion (28).
Alcohol as a cocarcinogen. Although there is no evidence that alcohol itself is a carcinogen, alcohol may act as a cocarcinogen by enhancing the carcinogenic effects of other chemicals. For example, studies indicate that alcohol enhances tobacco’s abil ity to stimulate tumor formation in rats (29). In humans, the risk for mouth, tracheal, and esophageal cancer is 35 times greater for people who both smoke and drink than for people who neither smoke nor drink (30), implying a cocarcinogenic interaction between alcohol and tobacco-related
carcinogens (29).
Alcohol’s cocarcinogenic effect may be explained by its interaction with certain enzymes. Some enzymes that normally help to detoxify substances that enter the body can also increase the toxicity of some carcinogens. One of these enzymes is called cytochrome P-450 (31,32). Dietary alcohol is able to induce cytochrome P-450 in the liver, lungs, esophagus, and intestines (29,33), where alcohol-associated cancers occur. Subsequently, carcinogens such as those from tobacco and diet can become more potent as they, too, pass through the esophagus, lungs, intestines, and liver and encounter the activated enzyme (29,33).
Nutrition. Chronic alcohol abuse may result in abnormalities in the way the body processes nutrients and may subsequently promote certain types of cancer. Reduced levels of iron, zinc, vitamin E, and some of the B vitamins, common in heavy drinkers, have been experimentally associated with some cancers (29). Also, levels of vitamin A, hypothesized to have anticancer properties (34), are severely depressed in the liver and esophagus of rats during chronic alcohol consumption (35-37).
A recent study indicates that as few as two drinks per day negates any beneficial effects of a “correct” diet on decreasing risk of colon cancer (38). Although the study suggests that a diet high in folic acid, a B vitamin found in fresh fruits and vegetables, decreases the risk for colon cancer, it also warns that alcohol consumption may counter this protective action and increase the risk for colon cancer by reducing folic acid levels.
Mechanisms of liver cancer. The possible role of alcohol in the development of liver cancer is incompletely understood. In Asia and Africa, hepatitis B virus infection is thought to cause most liver cancer; the association is less frequent in the United States. Eighty percent of patients with liver cancer also have cirrhosis (39), and between 27 and 80 percent test positive for hepatitis B or C infection (40). The chronic heavy drinking that causes liver cirrhosis might exacerbate cirrhosis caused independently by the hepatitis B or C viruses. Some studies indicate that alcohol consumption hastens the development of liver cancer in patients with hepatitis C infection (41), whereas others indicate that alcohol has no compounding effect in such patients (42).
Suppression of immune response. Alcoholism has been associated with suppression of the human immune system. Immune suppression makes chronic alcohol abusers more susceptible to various infectious diseases and, theoretically, to cancer (43).
Summary
Although epidemiologic studies have found a clear association between alcohol consumption and development of certain types of cancer, study findings are often inconsistent and may vary by country and by type of cancer. The key to understanding the association lies in research designed to decipher how alcohol may promote cancer. Such studies examine
alcohol’s metabolic effects at the cellular and genetic levels. Research examining the ways in which alcohol may induce cancers has found some potential mechanisms, the most promising of which implicates oncogenes.
Alcohol and Cancer–A Commentary by
NIAAA Director Enoch Gordis, M.D.
As can be seen from this Alcohol Alert, the evidence for alcohol’s role in promoting some cancers (e.g., cancers of the mouth and throat) is stronger than the evidence linking alcohol use to other cancers, such as breast cancer. Public health policy should reflect the str ength of the evidence of alcohol’s role in promoting various cancers. Convincing evidence of
alcohol’s effects on common cancers–even when these effects are minor–has important public health implications. However, it is equally important that the public not be subjected to undue alarm when evidence for an increased risk for cancer due to alcohol use is weak or inconclusive.
References
(1) American Cancer Society.Cancer Facts and Figures. Atlanta, GA: American Cancer Society, 1993. (2) Rothman, K.J. The proportion of cancer attributable to alcohol consumption. Preventive Medicine 9(2):174-179, 1980. (3) International Agency for Research on Cancer.IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Vol. 44. United Kingdom: World Health Organization, 1988. (4) Klygis, L.M.,and Barch, D.H. The role of ethanol in esophageal carcinoma. In: Watson, R.R., ed. Alcohol and Cancer. Boca Raton, FL: CRC Press, 1992. pp. 73-89. (5) Blot, W.J. Alcohol and cancer. Cancer Research (Suppl.) 52:2119s-2123s, 1992. (6) Franceschi, S.;Talamini, R.; Barra, S.; Barón, A.E.; Negri, E.; Bidoli, E.; Serraino, D.; and La Vecchia, C. Smoking and drinking in relation to cancers of the oral cavity, pharynx, larynx, and esophagus in Northern Italy. Cancer Research 50(20):6502-6507, 1990. (7) Stinson, F.S.,and DeBakey, S.F. Alcohol-related mortality in the United States, 1979-1988. British Journal of Addiction 87(5):777-783, 1992.(8) Franceschi, S.,and La Vecchia, C. Ethanol and risk of cancer of the oral cavity, pharynx, and esophagus. In: Watson, R.R., ed. Alcohol and Cancer. Boca Raton, FL: CRC Press, 1992. pp. 119-134. (9) Talamini, R.;Franceschi, S.; Barra, S.; and La Vecchia, C. The role of alcohol in oral and pharyngeal cancer in non-smokers, and of tobacco in non-drinkers. International Journal of Cancer 46(3):391-393, 1990. (10) Takada, A.;Takase, S.; and Tsutsumi, M. Alcohol and hepatic carcinogenesis. In: Yirmiya, R., and Taylor, A.N., eds. Alcohol, Immunity, and Cancer. Boca Raton, FL: CRC Press, 1993. pp. 187-209.(11) Villa, E.;Melegari, M.; and Manenti, F. Alcohol, viral hepatitis, and hepatocellular carcinoma. In: Watson, R.R., ed. Alcohol and Cancer. Boca Raton, FL: CRC Press, 1992. pp. 151-165. (12) Duffy, S.W., and Sharples, L.D. Alcohol and cancer risk. In: Duffy, J.L., ed. Alcohol and Illness: The Epidemiological Viewpoint. Edinburgh: Edinburgh University Press, 1992. pp. 64-127. (13) Mufti, S.I. Alcohol and cancers of the esophagus and liver. In: Yirmiya, R., and Taylor, A.N., eds. Alcohol, Immunity, and Cancer. Boca Raton, FL: CRC Press, 1993. pp. 159-186. (14) Friedenreich, C.M.; Howe, G.R.; Miller, A.B.; and Jain, M.G. A cohort study of alcohol consumption and risk of breast cancer. American Journal of Edidemiology 137(5):512-520, 1993. (15) Longnecker, M.P.Alcohol consumption in relation to risk of cancers of the breast and large bowel. Alcohol Health & Research World 16(3):223-229, 1992. (16) Longnecker, M.P.; Berlin, J.A.; Orza, M.J.; and Chalmers, T.C. A meta-analysis of alcohol consumption in relation to risk of breast cancer. Journal of the American Medical Association 260(5):652-656, 1988. (17) Nasca, P.C.; Baptiste, M.S.; Field, N.A.; Metzger, B.B.; Black, M.; Kwon, C.S.; and Jacobson, H. An epidemiological case-control study of breast cancer and alcohol consumption. International Journal of Epidemiology 19(3):532-538, 1990. (18) Chu, S.Y.; Lee, N.C.; Wingo, P.A.; and Webster, L.A. Alcohol consumption and the risk of breast cancer. American Journal of Epidemiology 130(5):867-877, 1989. (19) Schatzkin, A.; Piantadosi, S.; Miccozzi, M.; and Bartee, D. Alcohol consumption and breast cancer: A cross-national correlation study. International Journal of Epidemiology 18(1):28-31, 1989. (20) Webster, L.A.;Layde, P.M.; Wingo, P.A.; and Ory, H.W. Alcohol consumption and risk of breast cancer. Lancet2(8352):724-726, 1983. (21) Willett, W.C.; Stampfer, M.J.; Colditz, G.A.; Rosner, B.A.; Hennekens, C.H.; and Speizer, F.E. Moderate alcohol consumption and the risk of breast cancer. New England Journal of Medicine 316(19):1174-1180, 1987. (22) Schatzkin, A.;Jones, D.Y.; Hoover, R.N.; Taylor, P.R.; Brinton, L.A.; Ziegler, R.G.; Harvey, E.B.; Carter, C.L.; Licitra, L.M.; Dufour, M.C.; and Larson, D.B. Alcohol consumption and breast cancer in the Epidemiologic Follow-up Study of the First National Health and Nutrition Examination Survey. New England Journal of Medicine 316(19):1169-1173, 1987. (23) Reichman, M.E.;Judd, J.T.; Longcope, C.; Schatzkin, A.; Clevidence, B.A.; Nair, P.P.; Campbell, W.S.; and Taylor, P.R. Effects of alcohol consumption on plasma and urinary hormone concentrations in premenopausal women. Journal of the National Cancer Institute 85(9):722-727, 1993. (24) Longnecker, M.P.; Orza, M.J.; Adams, M.E.; Vioque, J.; and Chalmers, T.C. A meta-analysis of alcoholic beverage consumption in relation to risk of colorectal cancer. Cancer Causes and Control 1(1):59-68, 1990. (25) Kune, S.; Kune, G.A.; and Watson, L.F. Case-control study of alcoholic beverages as etiological factors: The Melbourne Colorectal Cancer Study. Nutrition and Cancer 9(1):43-56, 1987. (26) Potter, J.D., and McMichael, A.J. Diet and cancer of the colon and rectum: A case-control study. Journal of the National Cancer Institute 76(4):557-569, 1986. (27) Espina, N.;Lima, V.; Lieber, C.S.; and Garro, A.J. In vitro and in vivo inhibitory effect of ethanol and acetaldehyde on 06methylguanine transferase. Carcinogenesis 9(5):761-766, 1988. (28) Kharbanda, S.; Nakamura, T.; and Kufe, D. Induction of the c-jun proto-oncogene by a protein kinase C-dependent mechanism during exposure of human epidermal keratinocytes to ethanol.Biochemical Pharmacology 45(3):675-681, 1993. (29) Garro, A.J., and Lieber, C.S. Alcohol and cancer. Annual Review of Pharmacology and Toxicology30:219-249, 1990. (30) Blot, W.J.; McLaughlin, J.K.; Winn, D.M.; Austin, D.F.; Greenberg, R.S.; Preston-Martin, S.; Bernstein, L.; Schoenberg, J.B.; Stemhagen, A.; and Fraumeni, J.F. Smoking and drinking in relation to oral and pharyngeal cancer. Cancer Research 48(11):3282-3287, 1988. (31) Seitz, H.K., and Osswald, B. Effect of ethanol on procarcinogen activation. In: Watson, R.R., ed. Alcohol and Cancer. Boca Raton, FL: CRC Press, 1992. pp. 55-72. (32) Garro, A.J.; Espina, N.; and Lieber, C.S. Alcohol and cancer. Alcohol Health & Research World 16(1):81-86, 1992. (33) Farinati, F.; Lieber, C.S.; and Garro, A.J. Effects of chronic ethanol consumption on carcinogen activating and detoxifying systems in rat upper alimentary tract tissue. Alcoholism:Clinical and Experimental Research 13(3):357-360, 1989. (34) Leo, M.A.; Kim, C.; and Lieber, C.S. Increased vitamin A in esophagus and other extrahepatic tissues after chronic ethanol consumption in the rat. Alcoholism: Clinical and Experimental Research 10(5):487-492, 1986. (35) Mobarhan, S.; Layden, T.J.; Friedman, H.; Kunigk, A.; and Donahue, P. Depletion of liver and esophageal epithelium vitamin A after chronic moderate ethanol consumption in rats: Inverse relation to zinc nutriture. Hepatology 6(4):615-621, 1986. (36) Sato, M., and Lieber, C.S. Hepatic vitamin A depletion after chronic ethanol consumption in baboons and rats. Journal of Nutrition 111(11):2015-2023, 1991. (37) Ziegler, R.G. A review of epidemiologic evidence that carotenoids reduce the risk of cancer. Journal of Nutrition 119(1):116-122, 1989. (38) Giovannucci, E.; Stampfer, M.J.; Colditz, G.A .; Rimm, E.B.; Trichopoulos, D.; Rosner, B.A.; Speizer, F.E.; and Willett, W.C. Folate, methionine, and alcohol intake and risk of colorectal adenoma. Journal of the National Cancer Institute 85(11):875-884, 1993. (39) Simonetti, R.G.;Cammà, C.; Fiorello, F.; Politi, F.; D’Amico, G.; and Pagliaro, L. Hepatocellular carcinoma: A worldwide problem and the major risk factors. Digestive Diseases and Sciences 36(7):962-972, 1991. (40) Nalpas, B., and Brechot, C. The role of hepatitis viruses in the genesis of hepatocellular carcinoma in alcoholic cirrhotics. In: Watson, R.R., ed. Alcohol and Cancer. Boca Raton, FL: CRC Press, 1992. pp. 91-118. (41) Yamauchi, M.;Nakahara, M.; Maezawa, Y.; Satoh, S.; Nishikawa, F.; Ohata, M.; Mizuhara, Y.; Hirakawa, J.; Nakajima, H.; Fujisawa, K.; and Gotaro, T. Prevalence of hepatocellular carcinoma in patients with alcoholic cirrhosis and prior exposure to hepatitis C. American Journal of Gastroenterology 88(1):39-43, 1993. (42) Miyamura, T.; Saito, I.; Yoneyama, T.; Takeuchi, K.; Ohbayashi, A.; Watanabe, Y.; Choo, Q-L.; Houghton, M.; and Kuo, G. Role of hepatitis C virus in hepatocellular carcinoma. In: Hollinger, F.B.; Lemon, S.M.; and Margolis, H., eds. Viral Hepatitis and Liver Disease. Baltimore: Williams & Wilkins, 1991. pp. 559-562. (43) Roselle, G. Alcohol and the immune system. Alcohol Health & Research World 16(1):16-22, 1992.
All material contained in the Alcohol Alert is in the public domain and may be used or reproduced without permission from NIAAA. Citation of the source is appreciated.
National Institute on Alcohol Abuse and Alcoholism No. 31 PH 362 January 1996
Drinking and Driving
Driving involves multiple tasks, the demands of which can change continually. To drive safely, one must maintain alertness, make decisions based on ever-changing information present in the environment, and execute maneuvers based on these decisions. Drinking alcohol impairs a wide range of skills necessary for carrying out these tasks. This Alcohol Alert examines alcohol impairment of driving skills and describes some factors that increase motor vehicle crash risk.
Some Factors That Influence Crash Risk
Blood alcohol concentration. The proportion of alcohol to blood in the body is expressed as the blood alcohol concentration (BAC). In the field of traffic safety, BAC is expressed as the percentage of alcohol in deciliters of blood–for example, 0.10 percent (i.e., 0.10 grams per deciliter). A 160-pound man will have a BAC of approximately 0.04 percent 1 hour after consuming two 12-ounce beers or two other standard drinks on an empty stomach (1).
All State laws stipulate driver BAC limits, which now vary by State. According to these laws, operating a vehicle while having a BAC over the given limit is illegal (2). The BAC limit for drivers age 21 and older in most States is 0.10 percent, although some States have reduced the limit to 0.08 percent.
The many skills involved in driving are not all impaired at the same BAC’s (3). For example, a driver’s ability to divide attention between two or more sources of visual information can be impaired by BAC’s of 0.02 percent or lower (3-5). However, it is not until BAC’s of 0.05 percent or more are reached that impairment occurs consistently in eye movements, glare resistance, visual perception, reaction time, certain types of steering tasks, information processing, and other aspects of psychomotor performance (3,4,6,7).
Research has documented that the risk of a motor vehicle crash increases as BAC increases (3,4,8) and that the more demanding the driving task, the greater the impairment caused by low doses of alcohol (3). Compared with drivers who have not consumed alcohol, the risk of a single-vehicle fatal crash for drivers with BAC’s between 0.02 and 0.04 percent is estimated to be 1.4 times higher; for those with BAC’s between 0.05 and 0.09 percent, 11.1 times higher; for drivers with BAC’s between 0.10 and 0.14 percent, 48 times higher; and for those with BAC’s at or above 0.15 percent, the risk is estimated to be 380 times higher (8).
Youth. Youthful age has been cited as one of the most important variables related to crash risk (9). Young drivers are inexperienced not only in driving but in drinking and in combining the two activities (9). In 1994, almost 7,800 persons ages 16 through 20 were drivers in fatal motor vehicle crashes (10). Twenty-three percent of these drivers, for whom drinking any quantity of alcohol is illegal, had BAC’s of 0.01 percent or higher, compared with 26 percent of drivers age 21 and older (10).
According to Hingson and colleagues, each 0.02-percent increase in BAC above 0.00 percent places 16- to 20-year-old drivers at greater risk for a crash than older drivers (11). Roadside surveys indicate that young people are less likely than adults to drive after drinking; however, especially at low and moderate BAC’s, their crash rates are substantially higher than those of other groups (9).
Driving inexperience and immaturity are considered to be the main causes of motor vehicle crashes among drivers ages 16 to 20, even when alcohol is not involved (9). In one study, Hingson and colleagues concluded that drivers in th is age group have a greater risk than older drivers of being involved in a fatal crash even with a BAC of 0.00 percent (11). Young people’s lack of driving experience renders them less likely than more experienced drivers to cope successfully with hazardous situations (9). This, combined with a penchant for risk-taking driving behavior such as speeding–along with a tendency both to underestimate the dangerous consequences of such behaviors and to overestimate their driving skill–contributes to the high crash rate among young drivers (12,13).
Gender. Twenty-nine percent of male drivers involved in fatal motor vehicle crashes had BAC’s of 0.01 percent or greater, compared with 15 percent of female drivers (10). However, studies indicate that at BAC’s ranging from 0.05 to 0.09 percent, crash risk may be greater for females than for males (8,14). Research shows that women metabolize alcohol differently from men, causing women to reach higher BAC’s at the same doses (4,15). However, laboratory studies of alcohol impairment of driving skills among women are rare and the results are inconclusive (6).
Combining medications with alcohol and driving.Combining certain medications with alcohol increases crash risk. Sedatives and tranquilizers alone can impair driving skills (16) and can impair them even more when combined with alcohol (17-20). For example, low doses of flurazepam, a sedative-hypnotic prescribed for the treatment of insomnia, alone can impair a driver’s ability to steer. The effect of this medication can be compounded with even a small dose of alcohol consumed the next morning (20). Driving skills can be impaired by other medications, such as codeine, as prescribed to treat moderately severe pain (20). When combined with alcohol, such medications’ adverse effects on driving skills are exacerbated, as are the effects of some antidepressants, most antihistamines, certain cardiovascular medications, and some antipsychotic medications (20).
Alcohol tolerance. The repeated performance of a particular task in association with alcohol consumption can lead to the development of a form of adaptation referred to as “learned” or “behavioral” tolerance (21). Learned tolerance can reduce the
alcohol-induced impairment that would ordinarily accompany the performance of that particular task (21). However, when conditions change or when something unexpected occurs, the tolerance acquired for that task can be negated (22).
These findings may be applicable to the performance of tasks involved in drinking and driving (21,23). A driver who has developed behavioral tolerance to driving a familiar car over a particular route under routine circumstances may drive without being involved in a crash, despite consumption of some alcohol (21,23). However, when encountering a novel environment–for example, a detour–or an unexpected situation, such as a bicycle darting in front of the car, this same driver would be at the same risk for a crash as a novice driver at the same BAC, due to lack of prior learning opportunities for these unexpected events.
Legal Sanctions for DUI Offenders
Legal sanctions, such as driver’s license suspension and court-ordered alcoholism treatment, are designed to deter drinking and driving (24). Driver’s license suspension and license revocation seem to be the most effective deterrents among the general driving population (24). However, a meta-analysis of deterrent strategies targeted to the drinking-and-driving population concluded that the most effective means for reducing rearrest for driving under the influence of alcohol (DUI) and crashes was a combination of license suspension and interventions such as education, psychotherapy/ counseling, and some followup (25).
Researchers contend that court-ordered treatment should be considered an adjunct, not an alternative, to license sanctions (24). According to Sadler and colleagues, a DUI conviction should serve to identify problem drinkers and guide or coerce them into alcohol treatment (26). Alcohol treatment for DUI offenders can range from short-term educational sessions to therapy programs lasting at least 1 year (24).
Treatment of convicted drinking drivers normally emphasizes modifying drinking behavior (24). The type and duration of treatment depend on factors such as the severity of the person’s drinking problem and DUI history (24,27). DUI offenders with less severe drinking problems benefit most from educational programs (24,27), although no known model is thought to be most effective (24) in reducing recidivism or alcohol-related crashes. For repeat offenders or those with more seve re drinking problems, therapy that lasts for at least 12 months (24) and that includes intensive programs focused on the individual appears to be most effective (27).
Prevention
The National Highway Traffic Safety Administration (NHTSA) credits State laws raising the legal drinking age to 21 with preventing almost 1,000 traffic deaths annually (11). Legislation to reduce the BAC limit to 0.02 percent or lower, referred to as the “zero tolerance law” for young drivers, has been passed by 29 States and the District of Columbia to reduce alcohol-related fatalities further (10,11). The National Highway Systems Act provides incentives for all States to reduce their BAC limits for drivers under 21 to 0.02 percent beginning October 1, 1998.
One study (11) examined the effectiveness of lowering BAC limits for young people in States where such laws have been in force for at least 1 year. The researchers found that after the BAC limits were lowered to 0.00 or 0.02 percent, the proportion of nighttime fatal crashes involving single vehicles in this age group dropped 16 percent.
Drinking and Driving–A Commentary by
NIAAA Director Enoch Gordis, M.D.
Progress has been made in reducing the consequences of drinking and driving; the percent of alcohol-related crash fatalities has declined from 43.6 percent of the total number of traffic crash fatalities in 1986 to 37.4 percent in 1992. Advances in technology (i.e., automobile engineering and road design), less public acceptance of drinking drivers, decreases in per capita consumption, and a growing willingness by the States to adopt public policies aimed at preventing alcohol-related injuries and deaths and enforce legal sanctions against drinking drivers may all be factors in this decline. Newer policies, such as the mandated “zero tolerance” for underage youth, have been shown to reduce crashes in this vulnerable age group. Additionally, increased attention to prevention programs that both impact on and affect adult behavior, such as server training, the designated driver concept, and intervention and education programs in secondary schools and colleges, have demonstrated some effectiveness in reducing alcohol-related driving fatalities.
While we have made progress, drinking and driving still claims about 15,000 lives annually. A variety of public policies, including law enforcement, prevention, and treatment efforts aimed at decreasing this unacceptably high rate, are being implemented by the States. Findings from research can provide information on which of these efforts, individually or in combination, are most effective in reducing drinking and driv-ing. For example, although license revocation combined with treatment has been shown to be effective in preventing repeat drinking and driving offenses, we do not yet know specifically which types of treatment are the most effective with which types of offenders.
References
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(6) Hindmarch, I.; Bhatti, J.Z.; Starmer, G.A.; Mascord, D.J.; Kerr, J.S.; & Sherwood, N. The effects of alcohol on the cognitive function of males and females and on skills relating to car driving. Human Psychopharmacology 7(2):105-114, 1992. (7) Finnigan, F., & Hammersley, R. The effects of alcohol on performance. In: Smith, A.P., & Jones, D.M., eds. Handbook of Human Performance: Vol. 2. Health and Performance. London, Academic Press, 1992. pp. 73-126. (8) Zador, P.L. Alcohol-related relative risk of fatal driver injuries in relation to driver age and sex. Journal of Studies on Alcohol 52(4):302-310, 1991.(9) Mayhew, D.R.; Donelson, A.C.; Beirness, D.J.; & Simpson, H.M. Youth, alcohol and relative risk of crash involvement. Accident Analysis and Prevention 18(4):273-287, 1986. (10) National Highway Traffic Safety Administration (NHTSA).Traffic Safety Facts 1994: A Compilation of Motor Vehicle Crash Data from the Fatal Accident Reporting System and the General Estimates System. Washington, DC: NHTSA, August 1995. (11) Hingson, R.; Heeren, T.; & Winter, M. Lower legal blood alcohol limits for young drivers. Public Health Reports 109(6):738-744, 1994. (12) Brown, I.D., & Groeger, J.A. Risk perception and decision taking during the transition between novice and experienced driver status. Ergonomics 31(4):585-597, 1988. (13) Jonah, B.A. Accident risk and risk-taking behaviour among young drivers. Accident Analysis and Prevention 18(4):255-271, 1986. (14) Waller, P.F., & Blow, F.C. Women, alcohol, and driving. In: Galanter, M., ed. Recent Developments in Alcoholism: Vol. 12. Alcoholism and Women. New York: Plenum Press, 1995. (15) Wells-Parker, E.;Popkin, C.L.; & Ashley, M. Drinking and driving among women: Gender trends, gender differences. In: Howard, J.; Martin, S.; Mail, P.; Hilton, M.; & Taylor, E., eds. Alcohol and Women: Issues for Prevention Research. National Institute on Alcohol Abuse and Alcoholism Research Monograph. Bethesda, MD: the Institute, in press. (16) O’Hanlon, J.F.; Vermeeren, A.; Uiterwijk, M.M.C.; van Veggel, L.M.A.; & Swijgman, H.F. Anxiolytics’ effects on the actual driving performance of patients and healthy volunteers in a standardized test.Neuropsychobiology 31(2):81-88, 1995. (17) Linnoila, M., & Mattila, M.J. Drug interaction on psychomotor skills related to driving: Diazepam and alcohol. Eur J Clin Pharmacol 5:186-194, 1973. (18) Hoyumpa, A.M., Jr. Alcohol interactions with benzodiazepines and cocaine. In: Kreek, M.J., & Stimmel, B., eds. Dual Addiction: Pharmacological Issues in the Treatment of Concomitant Alcoholism and Drug Abuse. New York: Haworth Press, 1984. pp. 21-34. (19) Chan, A.W.K. Effects of combined alcohol and benzodiazepine: A review.Drug and Alcohol Dependence 13(4):315-341, 1984. (20) Doria, J. Alcohol-drug interactions: Effects on driving performance. Alcohol Health & Research World 14(1):16-17, 1990. (21) Vogel-Sprott, M.Alcohol Tolerance and Social Drinking: Learning the Consequences. New York: Guilford Press, 1992. (22) Glencross, D.; Hansen, J.; & Piek, J. The effects of alcohol on preparation for expected and unexpected events. Drug and Alcohol Review 14(2):171-177, 1995. (23) Sdao-Jarvie, K., & Vogel-Sprott, M. Response expectancies affect the acquisition and display of behavioral tolerance to alcohol. Alcohol 8(6):491-498, 1991. (24) Nichols, J.L. Treatment versus deterrence. Alcohol Health & Research World 14(1):44-51, 1990. (25) Wells-Parker, E.; Bangert-Drowns, R.; McMillen, R.; & Williams, M. Final results from a meta-analysis of remedial in terventions with drink/drive offenders. Addiction 90(7):907-926, 1995. (26) Sadler, D.D.; Perrine, M.W.; & Peck, R.C. The long-term traffic safety impact of a pilot alcohol abuse treatment as an alternative to license suspensions. Accident Analysis and Prevention 23(4):203-224, 1991. (27) Wells-Parker, E.; Landrum, J.W.; & Topping, J.S. Matching the DWI offender to an effective intervention strategy: An emerging research agenda. In: Wilson, R.J., & Mann, R.E., eds. Drinking and Driving: Advances in Research and Prevention. New York: Guilford Press, 1990. pp. 267-289.
All material contained in the Alcohol Alert is in the public domain and may be used or reproduced without permission from NIAAA. Citation of the source is appreciated.
