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 Volume 14, Number 10
December 2001 

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Previous Issue
Psychological Scientists in the Private Sector

Adolescents and Alcohol Abuse:
New Knowledge, New Challenges

For the past several years, the National Institute on Alcohol Abuse and Alcoholism (NIAAA) has co-sponsored with the American Psychological Society, a pre-conference symposium at the APS Annual Convention. The focus of these programs is on the behavioral dimensions of alcohol abuse and addiction. Topics in the past have included behavioral genetics, college-age drinking, and alcohol use and mental disorders. In 2001, the NIAAA-APS symposium was titled Adolescents and Alcohol Abuse: New Knowledge, New Challenges.

In addition to the many researchers presenting at the symposium, the NIAAA was represented by Ellen Witt of the Cognitive and Clinical Neuroscience Program in the Division of Basic Research, and Cherry Lowman of the Treatment Research Branch in the Division on Clinical and Prevention Research. NIAAA funds more 90 percent of the alcohol-related research in the United States. The Institute has set a number of priorities for adolescent alcohol-related research, and is interested in supporting that research from the perspectives of neuroscience, genetics, cognitive science, epidemiology, prevention, treatment, and health services research. For more information on alcohol-related adolescent research, please visit the National Institute on Alcohol Abuse and Alcoholism web site at www.niaaa.nih.gov.

Contributors to this article: Michael Carolan, ROW Logicon; Fred Donodeo, NIAAA; Cherry Lowman, NIAAA; Amy Matush, NIAAA; Joan Romaine, NIAAA; Ellen Witt, NIAAA

Alcohol is the drug most abused by adolescents. Adolescents have a high rate of alcohol use in general and an epidemic rate at the college level. In view of recent findings that early initiation of drinking is associated with a dramatically increased risk of becoming alcohol-dependent at some point in life, efforts are underway to protect our nation's youth from the severe consequences of alcohol abuse and dependence. Many researchers are putting science-based information into the hands of those who can positively affect the consequences of adolescent drinking.

Scientists presenting at the symposium, which was held in conjunction with the APS Annual Convention in Toronto, described current research on the effects of alcohol on the adolescent brain, the neurocognitive and biological effects of alcohol use, and the development of effective prevention and treatment interventions for adolescent alcohol problems.

Throughout the symposium, emphasis was placed on bringing "bench science" to scientifically-based interventions that can reduce alcohol use by the nation's youth. "This is very exciting state-of-the-art research that has tremendous implications," said symposium chair Sandra A. Brown. Brown, an APS Charter Member, is an expert on adolescent treatment and secondary prevention interventions from the University of California-San Diego. She said that by looking at the implications of fundamental research findings for interventions aimed at alcohol use by adolescents, the symposium epitomizes NIAAA's research-to-practice priorities.


While there is a great deal known about adolescent drinking behaviors, much less is known about alcohol's effects on the adolescent brain. However, presenters at the symposium offered convincing evidence that adolescence represents a period of unique sensitivity to many of the effects of alcohol.

Areas known as the limbic system (the inner rim of the brain) actively develop during adolescence. Some of the functions of the inner rim of the brain include learning, memory, affect regulation, and goal-directed behavior. Recent studies in both animals and humans indicate that the limbic system may be particularly vulnerable to the effects of alcohol during adolescence. Current research on adolescent rats conducted by Duke University researcher Aaron M. White demonstrates that alcohol has a profound effect on the developing hippocampus. This area of the brain plays a major role in memory formation, particularly the storage and recall of facts, names, and events. According to White, alcohol "wreaks havoc" in the hippocampus, and impaired hippocampal function appears to be directly related to impaired memory formation.

Studies suggest that alcohol effects on the hippocampus vary with age. At the neurobiological level, adolescent rats show much greater vulnerability to the effects of alcohol than adult rats. At the behavioral level, adolescent rats administered alcohol are more impaired than adult rats in the ability to learn new spatial tasks.

Results of another study also provide evidence that the adolescent hippocampus in humans may be particularly susceptible to the effects of alcohol. Michael D. DeBellis of the University of Pittsburgh used magnetic resonance imaging technology to assess alcohol's effects on the brains of adolescents and young adults with adolescent-onset alcohol use disorders (AUD). The only evidence of possible toxic effects is a significant decrease in size of both the right and left hippocampi in AUD subjects with adolescent-onset drinking as compared with non-AUD matched controls.

Investigators believe that the longer AUD subjects met criteria for diagnosis, and the younger they were at the onset of AUD, the smaller the hippocampus. This suggests that an alcohol-related mechanism may account for this effect on the hippocampus. DeBellis concludes that age-related vulnerability may be due to the developmentally sensitive mechanisms of specific brain receptors.

Another limbic system structure, the anterior cingulate cortex, is involved in affect regulation and motivation for goal-directed behavior. In a feasibility study using positron emission tomography, Duncan B. Clark examined an index of cingulate GABA (gamma-aminobutyric acid)-benzodiazepine receptor density in young adults with adolescent-onset AUDs and control subjects. Benzodiazepines are a class of drugs used to treat alcohol withdrawal, and scientists believe the GABA-benzodiazepine complex functions as a limbic system mediator of alcohol dependence.

Evidence from this University of Pittsburgh study found that chronic alcohol use may reduce GABA-benzodiazepine density and function in adolescents. Decreased GABA activity as a result of reduced receptor density could, to some extent, result in a loss of control over alcohol consumption and alcohol withdrawal.

Ralph Tarter, also from the University of Pittsburgh, found many of the studies' results alarming in terms of their implications for adolescent development. Among other things, he noted that the cognitive demands of today's technological society are critical. Although Americans drink less alcohol per capita today than during most of history, "what has changed is the rapid technology in society," said Tarter. "Therefore, even mild cognitive deficits, which would have been inconsequential a century ago, are extremely consequential today."


In early research on alcohol's effects in adolescents, investigators were unable to identify links between alcohol use, familial history of alcoholism, and neurocognitive functioning. To explain this unexpected finding, Marsha Bates at Rutgers University developed a hypothesis that compensatory cognitive mechanisms, in the face of brain dysfunction caused by alcohol or family history, stimulate other neurocircuits to adjust for the impaired ones.

A model called the "brain reserve theory," proposed by Bates, suggests that there are differences between individuals' brain structure and functioning that contribute to differing levels of neurocognitive vulnerability. When some insult such as heavy alcohol use bombards the brain, the resulting changes must exceed a certain threshold before any behavioral symptoms of dysfunction appear. Furthermore, individuals have different protective and risk factors that affect brain reserve capacity such as age, genetic endowment, education, etc.

One such factor that may pose a risk for brain changes is major depression at different points in the human life span. Bates indicates that the genetic transmission of neurocognitive components combines with a family history of depression to lower the (brain reserve capacity) threshold for measurable neuropsychological impairment.

A community sample study of youths from adolescence to early adulthood was tested over time (at 12, 15, and 18 years of age) and divided into three categories: a low risk group (low likelihood of family members diagnosed with alcoholism or depression); limited risk group (heightened likelihood due to maternal depression, paternal depression, and/or paternal alcoholism); and high risk group (extreme likelihood of sibling alcoholism and depression and substantial likelihood of paternal alcoholism).

The researchers found that the high-risk group was impaired relative to the other groups on four neuropsychological tests, and the likelihood of impairment increased between the ages of 12 to 18 years. Bates' research suggests that brain changes associated with familial alcoholism may combine with those associated with family histories of depression to cause or contribute to subtle differences in neurocognitive functioning. This association becomes stronger as individuals age past adolescence into adulthood.

Myelination and synaptic refinement render the adolescent brain more efficient, requiring less metabolism and blood flow. Experimentation with alcohol and other drugs during adolescence could potentially disrupt these kinds of neurodevelopments. Susan F. Tapert and Sandra Brown both of the University of California, San Diego, study brain functioning and response in adolescents. They hypothesize that persistent exposure to alcohol during adolescence will result in poor neurocognition and central nervous system functioning.

In particular, Tapert looks at the unique role of withdrawal in this process. A preliminary study of adolescents who used alcohol at least 100 times in their lifetime tested memory, visual spatial functioning, learning, and attention. Although the study did not uncover vast cognitive impairments in teens, Tapert indicates that for the 10 percent of highschoolers having drinking problems, the findings could be interpreted as the "difference between an A and a B in school or between a D and an F."

In a separate UC-SD study, Tapert and colleagues followed 115 youth in treatment centers over four years and found that post-treatment relapsers and nonrelapsers performed similarly while in treatment. Four years later, relapsers performed significantly worse on tests of attention. Those experiencing withdrawal symptoms or post-drinking effects since treatment performed more poorly on tests of visual spatial functioning. Further, neurocognition in females appears to be more affected by post-drinking effects than in males. Results suggest that women with a history of heavy drinking have less efficient brain functioning during a cognitive challenge.

Approaching the subject from a slightly different direction, University of Pittsburgh's Shirley Y. Hill began two ongoing pilot studies to look at three generations of relatives of male alcoholics (including families where there are two alcoholic brothers) and relatives of female alcoholics.

Among the groups studied, children from families with a high number of alcoholics generally begin drinking earlier than other children do. Hypotheses suggest that a dopaminergic circuit, considered a primary reward and pleasure pathway in the brain, may explain the findings. In addition, children between the ages of 8 and 18 have a developmental delay in reaching age-appropriate P300 levels, the cognitive brain wave marker associated with the ability to distinguish stimuli.

Hill proposes that adolescents from families with multigenerational alcohol dependence have morphological changes in their brains, making them more susceptible to alcohol abuse. It is important to emphasize that adolescents in this study are genetically at high risk, but are consuming very little alcohol. Brain-imaging techniques show children of alcoholics compared with children from families with no alcohol abuse have reductions in the size of the right amygdala, a structure in the brain that helps control basic emotions.

This work is the first to show that there are brain differences in kids with a genetically higher risk of developing alcohol dependence. According to Hill, the effect on the amygdala is significant because it is an important part of the reward circuit in the brain affecting addictive behavior, including cocaine use, gambling and now familial alcohol dependence.


Translating the concept of altered adolescent neurochemistry into scientifically-based interventions for adolescents with alcohol and alcohol-drug problems is a challenge that many researchers face.

According to Michael Dennis of Chestnut Health Systems, an Illinois-based behavioral health company, alcohol and marijuana are the leading substances found in arrests, emergency room admissions, autopsies, and treatment admissions. Prevention of substance abuse-related problems has been difficult: only 20 percent of adolescent prevention programs have been effective, according to Dennis. Although most adolescent treatment research focuses on adult models with little adaptation to adolescents, Dennis believes adolescent treatment has entered a renaissance over the last several years. The number of studies on adolescents and alcohol abuse has nearly tripled.

One such study, "Project Options," is an intervention program designed by Brown and her team of investigators from UC-SD. Even before the intervention was developed, data was gathered through biannual surveys at three high schools to determine preferred formats for alcohol education programs, strategies for confidentiality concerns of those participating, and incentives to improve youth participation.

"We used the developmental strategy-if they build it, they will come," said Brown, adding that if the youth are involved in the development of the program, it's more likely that the program will be seen as acceptable to them, resulting in fewer barriers to their participation.

Brown developed the intervention activities in three formats preferred by high school students: groups in a classroom setting (six sessions); individual in an office setting (four sessions); and an interactive web site. Material presented in each format was similar but tailored to the format.

Initial findings suggest that during the first and last year of the study, about 10 percent of students in the three high schools participated. One important finding was that many students attending the sessions were current drinkers, noted Brown. During the first year, more than half of the students who used the intervention were recent, i.e. past month, drinkers (approximately two-thirds of those using the web site, 40 percent of those in groups, and 30 percent of those in individual sessions). In addition, said Brown, "we found that we can alter perceptions of peer use, which is critical to youth decisions about continuing drinking or making changes in their drinking."

An intervention study, developed by Florida International University researcher Eric F. Wagner, the "Teen Intervention Project," is another example how treatment is beginning to focus on adolescent alcohol abuse. A community-based model, this program is a 10-session intervention with five to ten adolescents per group. Intervention topics cover education about alcohol and other drugs; their effects on adolescents; personal substance use patterns; self-monitoring; a cognitive behavioral approach to triggers; a motivational component; relapse prevention; and social support.

In addition, Wagner noted that there is a project called "Alcohol Treatment Targeting Adolescents in Need" (ATTAIN), an evaluation of the effectiveness of brief, community-based substance abuse treatment for Hispanic and African-American juvenile justice offenders in the Miami Dade Juvenile Justice System.

Howard A. Liddle of the University of Miami sees family therapy models has having potential applicability for adolescent substance abuse, indicating that many family therapy treatment models are built around the axiom that by changing the interaction you will change the person.

According to Liddle, there are multiple pathways in and multiple pathways out of substance abuse. "Methods need to be rendered to affect the multiple processes that create and perpetuate dysfunction," including, for example, processes involved in comorbid conditions, such as depression and anxiety disorders, he said.

Liddle said that another important element of family therapy models is the skill of the therapists themselves. Therapists work with the family, the adolescent individually, the social functioning within the family and peer groups, success in school, and juvenile justice problems. It is essentially a treatment approach that involves a lot of things at once, explains Liddle. "With that approach, you need therapists who are very skillful on variety of different fronts."

Peter Monti of Brown University says that researchers cannot depend on the adult treatment literature to discover how to treat adolescent substance abuse. The primary reasons are that adolescent use patterns are very different from those of adults and that developmental factors are very important to consider.

Nicotine addiction is an example of an area where a successful treatment in one population can spell failure in another, says Monti. Several newly funded studies of nicotine replacement therapy mixed with some variants of cognitive behavior therapy-a proven successful treatment of choice for adult nicotine dependence-are showing negative results with adolescents.

On the other hand, Monti suggests that researchers will increasingly have to grapple with psychopharmacology. "I am not advocating drugs for kids," said Monti. "I do, however, think there are some very promising approaches with psychopharmacological treatment in adults, and I think we would be remiss not to at least begin to address their potential when considering adolescent intervention research."

Copyright © 2001 American Psychological Society. All Rights Reserved.