research on drinking age

Age 21 Minimum Legal Drinking Age

A minimum legal drinking age (mlda) of 21 saves lives and protects health.

Minimum Legal Drinking Age (MLDA) laws specify the legal age when an individual can purchase alcoholic beverages. The MLDA in the United States is 21 years.  However, prior to the enactment of the National Minimum Drinking Age Act of 1984, the legal age when alcohol could be purchased varied from state to state. 1

An age 21 MLDA is recommended by the:

• American Academy of Pediatrics 2 • Community Preventive Services Task Force 4 • Mothers Against Drunk Driving 5 • National Highway Traffic Safety Administration 1 • National Prevention Council 8 • National Academy of Sciences (National Research Council and Institute of Medicine) 9

The age 21 MLDA saves lives and improves health. 3

Fewer motor vehicle crashes

• States that increased the legal drinking age to 21 saw a 16% median decline in motor vehicle crashes. 6

Decreased drinking

• After all states adopted an age 21 MLDA, drinking during the previous month among persons aged 18 to 20 years declined from 59% in 1985 to 40% in 1991. 7
• Drinking among people aged 21 to 25 also declined significantly when states adopted the age 21 MLDA, from 70% in 1985 to 56% in 1991. 7

Other outcomes

• There is also evidence that the age 21 MLDA protects drinkers from alcohol and other drug dependence, adverse birth outcomes, and suicide and homicide. 4

Drinking by those under the age 21 is a public health problem.

• Excessive drinking contributes to about 4,000 deaths among people below the age of 21 in the U.S. each year. 10
• Underage drinking cost the U.S. economy $24 billion in 2010. 11

Drinking by those below the age of 21 is also strongly linked with 9,12,13 :

• Death from alcohol poisoning.
• Unintentional injuries, such as car crashes,  falls, burns, and drowning.
• Suicide and violence, such as fighting and sexual assault.
• Changes in brain development.
• School performance problems, such as higher absenteeism and poor or failing grades.
• Alcohol dependence later in life.
• Other risk behaviors such as smoking, drug misuse, and risky sexual behaviors.

Alcohol-impaired driving

Drinking by those below the age of 21 is strongly associated with alcohol-impaired driving. The 2021 Youth Risk Behavior Survey 14  found that among high school students, during the past 30 days

• 5% drove after drinking alcohol.
• 14% rode with a driver who had been drinking alcohol.

Rates of drinking and binge drinking among those under 21

The 2021 Youth Risk Behavior Surveillance System found that among high school students, 23% drank alcohol and 11% binge drank during the past 30 days. 14

In 2021, the Monitoring the Future Survey reported that 6% of 8th graders and 28% of 12th graders drank alcohol during the past 30 days, and 2% of 8th graders and 13% of 12th graders binge drank during the past 2 weeks. 15

In 2014, the New York City Department of Health and Mental Hygiene and the New York State Liquor Authority found that more than half (58%) of the licensed alcohol retailers in the City sold alcohol to underage decoys. 17

Enforcing the age 21 MLDA

Communities can enhance the effectiveness of age 21 MLDA laws by actively enforcing them.

• A Community Guide review found that enhanced enforcement of laws prohibiting alcohol sales to minors reduced the ability of youthful-looking decoys to purchase alcoholic beverages by a median of 42%. 16
• Alcohol sales to minors are still a common problem in communities.

More information on underage drinking

• National Highway Traffic Safety Administration.  Determine Why There Are Fewer Young Alcohol Impaired Drivers External . Washington, DC. 2001.
• Committee on Substance Abuse, Kokotailo PK.  Alcohol use by youth and adolescents: a pediatric concern External .  Pediatrics . 2010;125(5):1078-1087.
• DeJong W, Blanchette J.  Case closed: research evidence on the positive public health impact of the age 21 minimum legal drinking age in the United States External .  J Stud Alcohol Drugs . 2014;75 Suppl 17:108-115.
• Task Force on Community Preventive Services.  Recommendations to reduce injuries to motor vehicle occupants: increasing child safety seat use, increasing safety belt use, and reducing alcohol-impaired driving Cdc-pdf External  [PDF-78 KB].  Am J Prev Med . 2001;21(4 Suppl):16-22.
• Mothers Against Drunk Driving (MADD). Why 21? 2018;  https://www.madd.org/the-solution/teen-drinking-prevention/why-21/ External . Accessed May 3, 2018.
• Shults RA, Elder RW, Sleet DA, et al.  Reviews of evidence regarding interventions to reduce alcohol-impaired driving Cdc-pdf External  [PDF-2 MB].  Am J Prev Med . 2001;21(4 Suppl):66-88.
• Serdula MK, Brewer RD, Gillespie C, Denny CH, Mokdad A.  Trends in alcohol use and binge drinking, 1985-1999: results of a multi-state survey External .  Am J Prev Med . 2004;26(4):294-298
• National Prevention Council. National Prevention Strategy: Preventing Drug Abuse and Excessive Alcohol Use  [PDF-4.7MB]. Washington, DC: US Department of Health and Human Services, Office of the Surgeon General; 2011.
• Bonnie RJ and O’Connell ME, editors. National Research Council and Institute of Medicine.  Reducing Underage Drinking: A Collective Responsibility External . Committee on Developing a Strategy to Reduce and Prevent Underage Drinking. Division of Behavioral and Social Sciences and Education. Washington, DC: The National Academies Press; 2004.
• Centers for Disease Control and Prevention (CDC). Alcohol-Related Disease Impact (ARDI) Application website . Accessed February 29, 2024.
• Sacks JJ, Gonzales KR, Bouchery EE, Tomedi LE, Brewer RD.  2010 national and state costs of excessive alcohol consumption External .  Am J Prev Med . 2015;49(5):e73-79.
• Miller JW, Naimi TS, Brewer RD, Jones SE.  Binge drinking and associated health risk behaviors among high school students External .  Pediatrics . 2007;119(1):76-85.
• Department of Health and Human Services. The Surgeon General’s call to action to prevent and reduce underage drinking External . Department of Health and Human Services, Office of the Surgeon General;2007.
• Centers for Disease Control and Prevention. 2021 Youth Risk Behavior Survey Data . Accessed on September 13, 2023.
• Johnston LD, Miech RA, O’Malley PM, Bachman JG, Schulenberg JE, Patrick ME. Monitoring the Future national survey results on drug use, 1975-2021: Overview, key findings on adolescent drug use external icon . Ann Arbor: Institute for Social Research, The University of Michigan; 2023.
• Elder R, Lawrence B, Janes G, et al.  Enhanced enforcement of laws prohibiting sale of alcohol to minors: systematic review of effectiveness for reducing sales and underage drinking External  [PDF-4MB].  Transportation Research E-Circular . 2007;E-C123:181-188.
• The New York City Department of Health and Mental Hygiene. Alcohol & Health website . Accessed October 18, 2016.

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Legal Drinking Age Of 21 Saves Lives, Even Though It's Flouted

Maanvi Singh

Students drink outside the Rose Bowl during the NCAA BCS national championship game in January. Gregory Bull/AP hide caption

Eighty percent of college students say they drink, despite laws making it illegal for anyone under 21 to drink alcohol. Critics of that drinking age say that lowering it would reduce binge drinking and alcohol-related deaths.

But that might be wishful thinking, a study says. Researchers from Boston University reviewed scientific literature published since 2006 and concluded keeping the legal drinking age at 21 reduces rates of drunk driving and crashes, and reduces rates of underage drinking.

The paper, published Monday in the Journal of Studies on Alcohol and Drugs , even goes so far as to say "case closed" — the minimum drinking age saves lives.

"If we choose to decrease the legal drinking age, there will be consequences," says William DeJong , the study's lead author and a professor of community health sciences at the Boston University School of Public Health.

People may find it difficult to justify a law that is mostly ignored, DeJong tells Shots, but "The weight of the evidence suggests that even though t the law is widely disobeyed, it does have a protective effect."

The review also looked at drinking habits in other countries, paying special attention to New Zealand, which lowered its drinking age from 20 to 18 in 1999. Several studies found a spike in alcohol-related car crashes and increased drinking there among still-underage 16- and 17-year -olds.

Shots - Health News

15-plus drinks a night: teenagers binge at dangerous heights.

The conclusion of this latest study isn't too surprising, according to Dr. Donald Vereen , director of the University of Michigan's Substance Abuse Research Center. "Magic bullets do not work for any problem or issue involving human beings," he tells Shots. And lowering the drinking age isn't going to stop underage drinking, he says.

The national minimum drinking age was established in 1984, when Congress passed a law penalizing states that allowed anyone younger than 21 to buy alcohol. Several studies included in this review compared binge drinking and drunk driving accidents before and after states increased the drinking age in the 1980s.

French Lessons: Why Letting Kids Drink At Home Isn't 'Tres Bien'

In 2004, a group of over 100 college presidents and chancellors formed an initiative to have the minimum drinking age reduced, saying that if undergraduates could legally drink, colleges would be able to better oversee their drinking and help them rein in the habit.

Many advocates of lowering the drinking age point to the European model of legal drinking at age 18 or below. But Vereen says the comparison is misguided. "In Germany, beer is just a part of the meal," he says. "It's not in the American culture to do that." The Boston University review also points to research that European teens aren't immune to the appeal of binge drinking.

"These kids are not interested in single malt scotches," Vereen adds. Teaching kids how to drink responsibly is a big process, he says, and should start at a young age. But lowering the drinking age won't do much to help.

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Why the drinking age should be lowered

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Alcohol Research and Health History

Why the drinking age should be lowered: an opinion based upon research.

Engs, Ruth C. (1997, 2014). “Why the drinking age should be lowered: An opinion based upon research. Indiana University: Bloomington, IN. Adapted from: IUScholarWorks Repository:  http://hdl.handle.net/2022/17594

The legal drinking age should be lowered to about 18 or 19 and young adults allowed to drink in controlled environments such as restaurants, taverns, pubs and official school and university functions. In these situations responsible drinking could be taught through role modeling and educational programs. Mature and sensible drinking behavior would be expected. This opinion is based upon research that I have been involved in for over thirty years concerning college age youth and the history of drinking in the United States and other cultures.

Although the legal purchase age is 21 years of age, a majority of college students under this age consume alcohol but in an irresponsible manner. This is because drinking by these youth is seen as an enticing "forbidden fruit," a "badge of rebellion against authority" and a symbol of "adulthood." As a nation we have tried prohibition legislation twice in the past for controlling irresponsible drinking problems. This was during National Prohibition in the 1920s and state prohibition during the 1850s. These laws were finally repealed because they were unenforceable and because the backlash towards them caused other social problems. Today we are repeating history and making the same mistakes that occurred in the past. Prohibition did not work then and prohibition for young people under the age of 21 is not working now.

The flaunting of the current laws is readily seen among university students. Those under the age of 21 are more likely to be heavy -- sometimes called "binge" -- drinkers (consuming over 5 drinks at least once a week). For example, 22% of all students under 21 compared to 18% over 21 years of age are heavy drinkers. Among drinkers only, 32% of under-age compared to 24% of legal age are heavy drinkers.

Research from the early 1980s until the present has shown a continuous decrease, and then leveling off, in drinking and driving related variables which has parallel the nation's, and also university students, decrease in per capita consumption. However, these declines started in 1980 before the national 1987 law which mandated states to have 21 year old alcohol purchase laws.

The decrease in drinking and driving problems are the result of many factors and not just the rise in purchase age or the decreased per capita consumption. These include: education concerning drunk driving, designated driver programs, increased seat belt and air bag usage, safer automobiles, lower speed limits, free taxi services from drinking establishments, etc.

While there has been a decrease in per capita consumption and motor vehicle crashes, unfortunately, during this same time period there was an INCREASE in other problems related to heavy and irresponsible drinking among college age youth. Most of these reported behaviors showed little change until AFTER the 21 year old law in 1987. For example from 1982 until 1987 about 46% of students reported "vomiting after drinking." This jumped to over 50% after the law change. Significant increase were also found for other variables: "cutting class after drinking" jumped from 9% to almost 12%; "missing class because of hangover" went from 26% to 28%; "getting lower grade because of drinking" rose from 5% to 7%; and "been in a fight after drinking" increased from 12% to 17%. All of these behaviors are indices of irresponsible drinking. This increase in abusive drinking behavior is due to "underground drinking" outside of adult supervision in student rooms, houses, and apartments where same age individuals congregate. The irresponsible behavior is exhibited because of lack of knowledge of responsible drinking behaviors, reactance motivation (rebellion against the law), or student sub-culture norms.

Beginning in the first decade of the 21st century, distilled spirits [hard liquor] began to be the beverage of choice rather than beer among collegians. Previously beer had been the beverage of choice among students. A 2013 study of nursing students, for example, revealed that they consumed an average of 4.3 shots of liquor compared to 2.6 glasses of beer on a weekly basis.

This change in beverage choice along with irresponsible drinking patterns among young collegians has led to increased incidences of alcohol toxicity - in some cases leading to death from alcohol poisoning. However, the percent of students who consume alcohol or are heavy or binge drinkers has been relatively stable for the past 30 years.

Based upon the fact that our current prohibition laws are not working, the need for alternative approaches from the experience of other, and more ancient cultures, who do not have these problems need to be tried. Groups such as Italians, Greeks, Chinese and Jews, who have few drinking related problems, tend to share some common characteristics. Alcohol is neither seen as a poison or a magic potent, there is little or no social pressure to drink, irresponsible behavior is never tolerated, young people learn at home from their parents and from other adults how to handle alcohol in a responsible manner, there is societal consensus on what constitutes responsible drinking. Because the 21 year old drinking age law is not working, and is counterproductive, it behooves us as a nation to change our current prohibition law and to teach responsible drinking techniques for those who chose to consume alcoholic beverages.

Research articles that support this opinion are found in the Indiana University Repository at: https://scholarworks.iu.edu/dspace/handle/2022/17133/browse?type=title

and https://scholarworks.iu.edu/dspace/handle/2022/17130/browse?type=title

Some material here also used in: Engs, Ruth C. "Should the drinking age be lowered to 18 or 19." In Karen Scrivo, "Drinking on Campus," CQ Researcher 8 (March 20,1998):257.

Alcohol Research and Health History resources

(c) Copyright, 1975-2024. Ruth C. Engs, Indiana University, Bloomington, IN 47405

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• Systematic Review
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• Published: 25 August 2022

Age-related differences in the effect of chronic alcohol on cognition and the brain: a systematic review

• Lauren Kuhns   ORCID: orcid.org/0000-0002-3156-8905 1 , 2 ,
• Emese Kroon   ORCID: orcid.org/0000-0003-1803-9336 1 , 2 ,
• Heidi Lesscher 3 ,
• Gabry Mies 1 &
• Janna Cousijn 1 , 2 , 4  

Translational Psychiatry volume  12 , Article number:  345 ( 2022 ) Cite this article

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• Human behaviour

Adolescence is an important developmental period associated with increased risk for excessive alcohol use, but also high rates of recovery from alcohol use-related problems, suggesting potential resilience to long-term effects compared to adults. The aim of this systematic review is to evaluate the current evidence for a moderating role of age on the impact of chronic alcohol exposure on the brain and cognition. We searched Medline, PsycInfo, and Cochrane Library databases up to February 3, 2021. All human and animal studies that directly tested whether the relationship between chronic alcohol exposure and neurocognitive outcomes differs between adolescents and adults were included. Study characteristics and results of age-related analyses were extracted into reference tables and results were separately narratively synthesized for each cognitive and brain-related outcome. The evidence strength for age-related differences varies across outcomes. Human evidence is largely missing, but animal research provides limited but consistent evidence of heightened adolescent sensitivity to chronic alcohol’s effects on several outcomes, including conditioned aversion, dopaminergic transmission in reward-related regions, neurodegeneration, and neurogenesis. At the same time, there is limited evidence for adolescent resilience to chronic alcohol-induced impairments in the domain of cognitive flexibility, warranting future studies investigating the potential mechanisms underlying adolescent risk and resilience to the effects of alcohol. The available evidence from mostly animal studies indicates adolescents are both more vulnerable and potentially more resilient to chronic alcohol effects on specific brain and cognitive outcomes. More human research directly comparing adolescents and adults is needed despite the methodological constraints. Parallel translational animal models can aid in the causal interpretation of observed effects. To improve their translational value, future animal studies should aim to use voluntary self-administration paradigms and incorporate individual differences and environmental context to better model human drinking behavior.

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Introduction

Alcohol use disorder (AUD) is the most prevalent substance use disorder worldwide [ 1 ]. Most AUDs remain untreated [ 2 ] and for those seeking treatment, relapse rates are high [ 3 ]. Adolescence marks a rapid increase in AUD and an earlier onset of AUD is associated with worse long-term outcomes, including greater problem severity and more relapses [ 4 , 5 ]. Loss of control over alcohol use is a core aspect of AUD [ 6 ] and the developmentally normative difficulty to control motivational urges in tempting and arousing situations is thought to put adolescents at risk for developing addictive behaviors [ 7 ]. Moreover, neurotoxic consequences of alcohol use may be more severe for a developing brain [ 8 ]. Paradoxically, adolescence is also a period of remarkable behavioral flexibility and neural plasticity [ 9 , 10 , 11 ], allowing adolescents to adapt their goals and behavior to changing situations [ 12 ] and to recover from brain trauma more easily than adults [ 10 ]. In line with this, the transition from adolescence to adulthood is associated with high rates of AUD recovery without formal intervention [ 13 ]. While the adolescent brain may be a vulnerability for the development of addiction, it may also be more resilient to long-term effects compared to adults. Increased neural plasticity during this period could help protect adolescents from longer-term alcohol use-related cognitive impairments across multiple domains, from learning and memory to decision-making and cognitive flexibility. Therefore, the goal of this systematic review was to examine the evidence of age-related differences in the effect of alcohol on the brain and cognitive outcomes, evaluating evidence from both human and animal studies.

In humans, the salience and reinforcement learning network as well as the central executive network are involved in the development and maintenance of AUD [ 7 , 14 ]. The central executive network encompasses fronto-parietal regions and is the main network involved in cognitive control [ 15 ]. The salience network encompasses fronto-limbic regions crucial for emotion regulation, salience attribution, and integration of affective information into decision-making [ 15 , 16 ], which overlaps with fronto-limbic areas of the reinforcement learning network (Fig. 1 ). Relatively early maturation of salience and reinforcement learning networks compared to the central executive network is believed to put adolescents at heightened risk for escalation of alcohol use compared to adults [ 7 ]. Rodent models are regularly used for AUD research and allow in-depth neurobehavioral analyses of the effects of ethanol exposure during different developmental periods while controlling for experimental conditions such as cumulative ethanol exposure in a way that is not possible using human subjects because exposure is inherently confounded with age. For example, animal models allow for detailed neurobiological investigation of the effects of alcohol exposure in a specific age range on neural activation, protein expression, gene expression, epigenetic changes, and neurotransmission in brain regions that are homologous to those that have been implicated in AUD in humans.

A visual representation of the translational model of the executive control and salience networks in humans and rodents. The executive control and salience are key networks believed to play a part in adolescent vulnerability to alcohol-related problems.

While most of our knowledge on the effects of alcohol on the brain and cognitive outcomes is based on research in adults, several recent reviews have examined the effects of alcohol on the brain and cognition in adolescents and young adults specifically [ 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 ]. Heavy or binge drinking has been associated with reduced gray and white matter. Also, altered task-related brain activity [ 20 ], structural abnormalities [ 25 ], and overlapping behavioral impairment in executive functioning have been identified in adolescent and young adult alcohol users [ 19 ]. While some of the observed neurocognitive differences between drinkers and non-drinkers may be predisposing factors, they may be further exacerbated by heavy and binge drinking [ 21 , 23 ]. Furthermore, reviews of longitudinal studies concluded that adolescent alcohol use is associated with neural and cognitive alterations in a dose-dependent manner [ 17 , 22 ].

Although previous reviews underscore the potential negative consequences of heavy alcohol use on the brain and cognition in adolescence, they do not typically address the question of whether adolescents are differentially vulnerable compared to adults to the effects of alcohol on these outcomes. Explicit comparisons between adolescents and adults are crucial to identify potential risk and resilience factors. In the current review, we aimed to extend previous work by systematically examining this critical question: does the relationship between chronic alcohol use and neurocognitive outcomes differ between adolescents and adults? To address this question, we systematically reviewed human and animal studies that included both age groups and used a factorial design that would allow for the comparison of the effects of chronic alcohol use on cognitive and brain-related outcomes across age groups. We specifically highlight outcomes from voluntary self-administration paradigms when available and discuss the translational quality of the animal evidence base. We conclude with a discussion of prominent knowledge gaps, future research directions, and clinical implications.

Study inclusion criteria and search strategy

We followed the PRISMA guidelines for the current systematic review (The PRIMSA Group, 2009). An initial MedLine, Cochrane Library, and PsycInfo search was conducted during September of 2018 with terms related to alcohol, cognition, adolescence/adulthood, and study type (see Appendix for full search strategy and syntax). Two search updates using the same search strategy were conducted on 31 March 2020 and 3 February 2021. For all searches, the identified citations were split into batches and at least two of the following assessors (GM, LK, JC, or CG) conducted a blinded review to determine whether articles met the inclusion criteria. In the first phase of screening, only titles and abstracts were screened and articles that clearly did not meet the inclusion criteria were excluded. In the second phase, the remaining articles received a full-text review and those that did not meet all inclusion criteria were excluded. The first inclusion criterion that was not adhered to was recorded as the reason for excluding. If there was a discrepancy between authors after initial and full-text screening process, the reviewing authors discussed the article and a consensus was reached.

The inclusion criteria were: (1) Human samples including both adolescents younger than 18 and adults older than 18 and animal samples including adolescent (Post Natal Day (PND) 25–42 for rodents) and adult [ 8 ] animals (greater than PND 65 for rodents); (2) Exploration of alcohol as the independent variable and cognitive, reward-related, or brain outcomes as the dependent variables; (3) Alcohol and cognitive outcomes must meet our operationalization defined below; (4) Study design comparing adults and adolescents on outcome measures; (5) Administering or measuring alcohol use during adolescence or adulthood, not retrospectively (e.g., no age of onset work in humans using retrospective self-reports of alcohol consumption); (6) Primary quantitative data collection (no case studies, or review papers); (7) Solely looking at alcohol-related factors as the independent variables (e.g., cannot explore alcohol-related factors in individuals with psychosis); (8) Written in English; (9) Published in a peer-reviewed journal before February 3, 2021 (see Fig. 2 for a detailed screening process).

The definitions for adolescence are variable, hampering the direct comparison of human and rodent research. In rodents, the end of early-mid adolescence is considered to be approximately PND 42 when rats reach sexual puberty. By contrast, the boundaries for the onset of early adolescence are less clear. Based on the notion that most age-typical physiological changes that are characteristic of adolescence emerge from PND 28 [ 26 ], the conservative boundary for adolescence has been set at PND 28 (e.g., seminal review on adolescence [ 27 ]). The preceding week (PND 21-PND 28) has been described as the juvenile period (e.g., [ 28 , 29 ]) but these same reports consider PND 21-PND 23 as the lower boundary for early adolescence [ 28 , 29 ], further emphasizing that the boundary of PND28 may be too conservative. Indeed, multiple studies (e.g., [ 30 , 31 ]), have chosen to take PND25 as the boundary for early adolescence. Hence, we have decided to also follow this less conservative approach and include all studies where alcohol was administered between PND 25 and PND 42.

The exact boundaries of human adolescence are similarly nebulous. From a neurodevelopmental perspective, adolescence is now often thought of as continuing until approximately age 25 because of the continuing maturation of the brain [ 32 ]. However, the delineation of adolescence and adulthood is also dependent on societal norms, and is commonly defined as the transitional period between puberty and legal adulthood and independence which typically begins around age eighteen. In light of this, we chose a relatively liberal inclusion criteria for the human studies; studies needed to include at least some adolescents below eighteen, the age at which drinking typically begins, as well as ‘adult’ participants over the age of eighteen. We are careful to interpret the results of human studies within the neurodevelopmental framework of adolescence, such that 18–25-year-olds are considered late adolescents to young adults who are still undergoing cognitive and brain maturation.

Notably, we excluded studies that assessed alcohol exposure retrospectively (primarily early onset alcohol studies) because age of onset variables are often inaccurate, with reported age of alcohol onset increasing with both historical age [ 33 ] and current alcohol use patterns [ 34 ]. In addition, we excluded work that has not undergone peer-review to ensure high-quality papers.

In humans, we defined cognition as any construct that typically falls within the umbrella of neuropsychological testing, as well as brain-based studies. We also included more distal constructs of cognition, like craving and impulsivity, because they play a prominent role in addictive behaviors [ 35 , 36 ]. In rodents, we defined cognition as attention, learning, and memory in line with a seminal review paper [ 37 ]. Given the importance of social cognition in patterns of alcohol use particularly in adolescence [ 38 ] and its proposed role in adolescent risk and resilience to addiction [ 39 ], we included social behavior as an outcome. Furthermore, because many rodent studies assessed anxiety-related behaviors and the high degree of comorbidity between anxiety disorders and alcohol addiction [ 40 ], we also included anxiety as a secondary outcome. On the other hand, locomotor activity was excluded as an outcome because even though behavioral sensitization is considered to reflect neurobiological changes that may underlie certain aspects of addictive behavior [ 36 ], the translational relevance for addictive behavior and human addiction in particular remains unclear [ 41 , 42 ]. Across both rodents and humans, general alcohol metabolization and ethanol withdrawal studies were not included except if they included brain-related outcomes. The relevant reported findings (i.e., the results of an analysis of comparing age groups on the effect of alcohol on an included outcome) were extracted by a one reviewer and then confirmed by at least one other reviewer. In addition, the characteristics of the sample, details of alcohol exposure, and study design were extracted by a single reviewer and then confirmed by at least one other reviewer. No automation tools were used for extraction. Within the included studies, peripheral findings that did not relate to cognition were excluded from review and not extracted. The protocol for this systematic review was not registered and no review protocol can be accessed.

Study search

Our searches identified 7229 studies once duplicates were removed. A total of 6791 studies were excluded after initial review of abstracts. Then, 434 studies received a full-text review and 371 were excluded for failing to meet all inclusion criteria. See Fig. 2 for a flow diagram of the full screening process. At the end of the inclusion process, 59 rodent studies and 4 human studies were included. The characteristics and findings of the final studies are detailed in Table 1 (rodents) and Table 2 (humans). Due to the heterogeneity of outcomes, meta-regression was not suitable for synthesizing results. Results are narratively synthesized and grouped based on forced or voluntary ethanol exposure and by outcome within the tables and by outcome only in text. Two authors independently rated the quality of evidence for human studies (Table 2 ) based on criteria used in a similar systematic review [ 43 ]: (1) strong level of causality: longitudinal design comparing adolescent and adults while adjusting for relevant covariates; (2) moderate level of causality: longitudinal design comparing adolescents and adults without adjusting for relevant covariates or cross-sectional designs with matched groups that considered relevant covariates; (3) weak level of causality: cross-sectional design without matched adolescent and adult groups and/or did not adjust for relevant covariates. A methodological quality assessment was not conducted for the animal studies due to a lack of empirically validated risk of bias tools and lack of standardized reporting requirements in the animal literature.

PRIMSA flow diagram detailing the screening process.

Animal studies

Cognitive outcomes, learning and memory.

Human evidence clearly suggests that alcohol is related to learning and memory impairments, both during intoxication [ 44 ] and after sustained heavy use and dependence [ 45 , 46 ]. Paradigms that assess learning and memory provide insight into the negative consequences of alcohol consumption on brain functioning, as well as the processes underlying the development and maintenance of learned addictive behaviors.

Conditioned alcohol aversion or preference: Lower sensitivity to alcohol’s aversive effects (e.g., nausea, drowsiness, motor incoordination) but higher sensitivity to alcohol’s rewarding effects has been hypothesized to underlie the higher levels of alcohol use, especially binge-like behavior, in adolescents compared to adults [ 47 ]. Several conditioning paradigms have been developed to assess the aversive and motivational effects of alcohol exposure.

The conditioned taste aversion (CTA) paradigm is widely used to measure perceived aversiveness of alcohol in animals. Repeated high-dose ethanol injections are paired with a conditioned stimulus (CS, e.g., a saccharin or NaCL solution). The reduction in CS consumption after conditioning is used as an index of alcohol aversion. Two studies examined CTA in mice [ 48 , 49 ] and two in rats [ 50 , 51 ]. Three of the four studies found age-related differences. In all three studies using a standard CTA paradigm, adolescents required a higher ethanol dosage to develop aversion compared to adults [ 48 , 49 , 50 ]. Using a similar second-order conditioning (SOC) paradigm pairing high doses of ethanol (3.0 g/kg) with sucrose (CS), both adolescent and adult rats developed equal aversion to the testing compartment paired with ethanol [ 51 ].

Overall, three studies found support for lower sensitivity to alcohol’s aversive effects in adolescents, whereas one observed no differences. Future research should employ intragastric as opposed intraperitoneal exposure to better mimic human binge-like drinking in order to increase the translational value of the findings.

To measure differences in alcohol’s motivational value, conditioned place preference (CPP) paradigms have been used. This involves repeated pairings of ethanol injections with one compartment and saline injections with another compartment of the testing apparatus. On test days, CPP is assessed by measuring how long the animal stays in the compartment paired with ethanol relative to saline injections. Four studies examined CPP, with two studies observing age-related differences [ 52 , 53 , 54 , 55 ]. In the only mouse study, history of chronic ethanol exposure during adolescence (2.0 g/kg for 15 days) but not adulthood [ 52 ] led to increased CPP after brief abstinence (5 days) before the conditioning procedure (2.0 g/kg, four doses over 8 days). This suggests that early ethanol exposure increases alcohol’s rewarding properties later on. However, two rat studies did not observe either preference or aversion in either age when using lower ethanol doses and a shorter exposure period (0.5 and 1.0 g/kg for 8 days) [ 53 ], nor when using higher doses and intermittent exposure (3.0 g/kg, 2 days on, 2 days off schedule) [ 55 ]. Next to species and exposure-specific factors, environmental factors also play a role [ 54 ], with adolescents raised in environmentally enriched conditions demonstrating CPP (2 g/kg) while adolescents raised in standard conditions did not. In contrast, CPP was insensitive to rearing conditions in adults with both enriched and standard-housed rats showing similar levels of CPP.

Overall, there is inconsistent evidence for age-related differences in the motivational value of ethanol. One study found support for increased sensitivity to the rewarding effects of ethanol in adolescents, whereas one found support for adults being more sensitive and two observed no differences.

Fear conditioning and retention: Pavlovian fear conditioning paradigms are used to investigate associative learning and memory in animals. These paradigms are relevant for addiction because fear and drug-seeking behavior are considered conditioned responses with overlapping neural mechanisms [ 56 ]. Rodents are administered an unconditioned stimulus (US; e.g., foot shock) in the presence of a conditioned stimulus (CS; unique context or cue). Conditioned responses (CR; e.g., freezing behavior) are then measured in the presence of the CS without the US as a measure of fear retention. Contextual fear conditioning is linked to hippocampus and amygdala functioning and discrete cue-based (e.g., tone) fear is linked to amygdala functioning. [ 57 , 58 , 59 ], and fear extinction involves medial PFC functioning [ 60 ]. Five studies investigated fear conditioning, four in rats [ 61 , 62 , 63 , 64 ] and one in mice [ 65 ].

Only one of the four studies observed age-related differences in tone fear conditioning. Bergstrom et al. [ 61 ] found evidence for impaired tone fear conditioning in male and female alcohol-exposed (18d) adolescent compared to adult rats after extended abstinence (30d). However, adolescent rats consumed more ethanol during the one-hour access period than adults, which may explain the observed age differences in fear tone conditioning. Small but significant sex differences in consumption also emerged in the adolescent group, with males showing more persistent impairment across the test sessions compared to females, despite adolescent females consuming more ethanol than males. In contrast, three studies found no evidence of impaired tone fear conditioning in either age group after chronic alcohol exposure (4 g/kg, every other day for 20d) and extended abstinence [ 62 , 63 ] (22d), [ 64 ].

Two of the three studies observed age-related differences in contextual fear conditioning [ 62 , 63 , 64 ]. In two studies with similar exposure paradigms, only adolescents exposed to chronic high dosages of ethanol (4 g/kg) showed disrupted contextual fear conditioning after extended abstinence (22d) [ 62 , 63 ]. Importantly, differences disappeared when the context was also paired with a tone, which is suggestive of a potential disruption in hippocampal-linked contextual fear conditioning specifically [ 64 ]. Furthermore, there may be distinct vulnerability periods during adolescence as contextual fear retention was disrupted after chronic alcohol exposure (4 g/kg, every other day for 20d) during early-mid adolescence but not late adolescence [ 62 ]. In the only study to combine chronic exposure and acute ethanol challenges, contextual conditioning was impaired by the acute challenge (1 g/kg) but there was no effect of pre-exposure history in either age group (4 g/kg, every other day for 20d) [ 63 ].

Only one study examined fear extinction, and found no effect of ethanol exposure (4/kg, every other day for 20d) on extinction after tone conditioning. However, adults had higher levels of contextual fear extinction compared to mid-adolescents while late adolescents performed similar to adults [ 62 ]. Moreover, looking at binge-like exposure in mice (three binges, 3d abstinence), Lacaille et al. [ 65 ] showed comparable impairments in long-term fear memory in adolescents and adults during a passive avoidance task in which one compartment of the testing apparatus was paired with a foot shock once and avoidance of this chamber after a 24 h delay was measured.

In sum, there is limited but fairly consistent evidence for adolescent-specific impairments in hippocampal-linked contextual fear conditioning across two rat studies, while no age differences emerged in context-based fear retention in one study of mice. In contrast, only one of the four studies found evidence of impaired tone fear conditioning in adolescents (that also consumed more alcohol), with most finding no effect of alcohol on tone fear conditioning regardless of age. With only one study examining medial PFC-linked fear extinction, no strong conclusions can be drawn, but initial evidence suggests context-based fear extinction may be diminished in mid-adolescents compared to adults and late adolescents. Research on age-related differences on the effect of alcohol on longer-term fear memory is largely missing.

Spatial learning and memory: The Morris Water Maze (MWM) is commonly used to test spatial learning and memory in rodents. Across trials, time to find the hidden platform in a round swimming pool is used as a measure of spatial learning. Spatial memory can be tested by removing the platform and measuring the time the animal spends in the quadrant where the escape used to be. The sand box maze (SBM) is a similar paradigm in which animals need to locate a buried appetitive reinforcer.

Six rat studies examined spatial learning and memory using these paradigms. Three of the six studies observed age-related differences. Four examined the effects of repeated ethanol challenges 30 minutes prior to MWM training, showing mixed results [ 30 , 66 , 67 , 68 ]. While one found ethanol-induced spatial learning impairments in adolescents only (1.0 and 2.0 g/kg doses) [ 66 ], another found no age-related differences, with both age groups showing impairments after moderate doses (2.5 g/kg) and enhancements in learning after very low doses (0.5 g/kg) [ 67 ]. Sircar and Sircar [ 68 ] also found evidence of ethanol-induced spatial learning and memory impairments in both ages (2.0 g/kg). However, memory impairments recovered after extended abstinence (25d) in adults only. Importantly, MWM findings could be related to thigmotaxis, an anxiety-related tendency to stay close to the walls of the maze. Developmental differences in stress sensitivity may potentially confound ethanol-related age effects in these paradigms. Using the less stress-inducing SBM, adults showed greater impairments in spatial learning compared to adolescents after 1.5 g/kg ethanol doses 30 min prior to training [ 30 ].

Two studies examined the effects of chronic ethanol exposure prior to training with or without acute challenges [ 69 , 70 ]. Matthews et al. [ 70 ] looked at the effect of 20 days binge-like (every other day) pre-exposure and found no effect on spatial learning in either age following an extended abstinence period (i.e., 6–8 weeks). Swartzwelder et al. [ 69 ] examined effects of 5-day ethanol pre-exposure with and without ethanol challenges before MWM training. Ethanol challenges (2.0 g/kg) impaired learning in both age groups regardless of pre-exposure history. Thigmotaxis was also increased in both age groups after acute challenges while pre-exposure increased it in adults only.

In sum, evidence for impaired spatial learning and memory after acute challenges is mixed across six studies. Two studies found support for ethanol having a larger impact in adolescents compared to adults, whereas one study found the opposite and three studies did not observe any differences. Differences in ethanol doses stress responses may partially explain the discrepancies across studies. Importantly, given the sparsity of studies addressing the effects of long-term and voluntary ethanol exposure, no conclusion can be drawn about the impact of age on the relation between chronic alcohol exposure and spatial learning and memory.

Non-spatial learning and memory: Non-spatial learning can also be assessed in the MWM and SBM by marking the target location with a pole and moving it across trials, measuring time and distances traveled to locate the target. By assessing non-spatial learning as well, studies can determine whether learning is more generally impaired by ethanol or whether it is specific to hippocampal-dependent spatial learning processes. A total of six studies assessed facets of non-spatial learning and memory. Two of the six studies observed age-related differences.

In the four studies that examined non-spatial memory using the MWM or SBM in rats, none found an effect of alcohol regardless of dose, duration, or abstinence period in either age group [ 30 , 66 , 67 , 70 ]. Two other studies examined other facets of non-spatial memory in rats [ 65 , 71 ]. Galaj et al. [ 71 ] used an incentive learning paradigm to examine conditioned reward responses and approach behavior towards alcohol after chronic intermittent ethanol (CIE; 4 g/kg; 3d on, 2d off) exposure to mimic binge drinking. To examine reward-related learning and approach behavior, a CS (light) was paired with food pellets and approach behavior to CS only presentation and responses to a lever producing the CS were measured. In both adolescents and adults, the ethanol-exposed rats showed impaired reward-related learning after both short (2d) and extended (21d) abstinence. No effect of alcohol on conditioned approach behavior was observed in either age group during acute (2d) or extended (21d) abstinence. Using a novel object recognition test in mice, Lacaille et al. [ 65 ] assessed non-spatial recognition memory by replacing a familiar object with a novel object in the testing environment. Explorative behavior of the new object was used as an index of recognition. After chronic binge-like exposure (three injections daily at 2 h intervals) and limited abstinence (4d), only adolescents showed reduced object recognition.

Across facets of non-spatial memory, there is little evidence for age-related differences in the effect of chronic alcohol, with four of the six studies finding no age differences. For memory of visually cued target locations in the MWM and SBM paradigms, alcohol does not alter performance in either age. Also, both adolescents and adults appear similarly vulnerable to alcohol-induced impairments in reward-related learning based on the one study. Only in the domain of object memory did any age-related differences emerge, with adolescents and not adults showing reduced novel object recognition after binge-like alcohol exposure in one study. However, more research into object recognition memory and reward-related learning and memory is needed to draw strong conclusions in these domains.

Executive function and higher-order cognition

Executive functions are a domain of cognitive processes underlying higher-order cognitive functions such as goal-directed behavior. Executive functions can include but are not limited to working memory, attentional processes, cognitive flexibility, and impulse control or inhibition [ 72 ]. A core feature of AUD is the transition from goal-directed alcohol use to habitual, uncontrolled alcohol use. Impaired executive functioning, linked to PFC dysfunction [ 73 ], is assumed to be both a risk factor and consequence of chronic alcohol use. A meta-analysis of 62 studies highlighted widespread impairments in executive functioning in individuals with AUD that persisted even after 1-year of abstinence [ 46 ]. Thirteen studies examined facets of executive functioning and higher-order cognition, specifically in the domains of working memory, attentional processes, cognitive flexibility, impulsivity in decision-making, and goal-directed behavior [ 65 , 74 , 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 ].

Working memory: Working memory refers to the limited capacity system for temporarily storing and manipulating information, which is necessary for reasoning and decision-making [ 84 ]. In the Radial Arm Maze test (RAM) [ 85 ], some of the equally spaced arms (typically eight) around a circular platform contain a food reward for animals to find. Spatial working memory is measured by recording the number of revisits to previously visited arms (i.e., working memory error) and first entries into unbaited arms (i.e., reference memory). Alternatively, the hippocampus mediated [ 86 ] spontaneous tendency to alternate arms can be used as a measure of spatial working memory. In this case, revisiting an arm in back-to-back trials in close temporal succession is interpreted as a working memory error. Five studies examined the effects of chronic ethanol exposure on spatial working memory [ 65 , 75 , 79 , 80 , 83 ]. One of the five studies observed age-related differences.

Chronic binge-like alcohol exposure had no effects on spontaneous alterations after prolonged abstinence (2d on, 2d off; 3 weeks abstinence) [ 79 , 80 ] in rats or limited abstinence (three injections daily at 2 h intervals; 24 h abstinence) [ 65 ] in mice, nor on RAM performance in rats (2d on, 2d off) [ 75 , 83 ]. However, acute ethanol challenges (1.5 g/kg) after chronic binge-like exposure (2d on, 2d off) resulted in RAM test impairments in both age groups in rats [ 75 , 83 ], with some evidence for increased working memory errors in adolescents [ 83 ].

In sum, there is little evidence for impairments in working memory function in rats after chronic ethanol exposure, with four of the five studies observing no difference between age groups. While acute intoxication impairs working memory function in both ages, there is evidence from only one study that adolescents may make more working memory errors.

Attentional processes: Attentional processing refers to the selection of information that gains access to working memory [ 87 ]. PPI is a pre-attentional cognitive function which provides an index of sensorimotor gating and measures the ability of a lower intensity sensory stimulus to reduce the magnitude of response to a more intense stimulus presented closely afterward. Reduced sensorimotor gating (reduced PPI) can disrupt information processing and thereby impair cognitive function, while enhanced sensorimotor gating (enhanced PPI) may reflect behavioral inflexibility [ 88 ]. For example, lesions in the medial PFC produce both behavioral inflexibility and enhancements in PPI in rats. Two studies assessed attentional processes by measuring prepulse inhibition (PPI) in rats [ 82 , 89 ]. One study observed age-related differences and one did not.

Slawecki and Ehlers [ 82 ] observed age-related differences in sensorimotor gating following ethanol vapor exposure (2w) and brief abstinence (6d), with adolescents showing enhanced PPI at some decibels reflective of behavioral inflexibility, while adults did not exhibit PPI at any of the intensities tested. Slawecki et al. [ 89 ] did not observe any age-related differences in PPI during the acute phase of ethanol withdrawal (7–10 h abstinence) during a period of chronic ethanol exposure (14d).

In sum, there is limited and mixed evidence from two studies of age-related differences in the pre-attentional process of sensorimotor gating. Only one study found support for adolescent sensitivity to ethanol effects.

Cognitive flexibility: Cognitive flexibility refers to the ability to update information based on environmental factors r changing goals in order to adaptively guide decision-making and is linked to the inability to reduce or abstain from drinking [ 90 ]. Three studies examined facets of cognitive and behavioral flexibility [ 79 , 80 , 81 ]. Two of the three studies observed age-related differences.

In two rat studies, cognitive flexibility was assessed using reversal learning paradigms [ 79 , 80 ]. In the reversal learning paradigm, rats were trained on simple (e.g., visual cue) and more complex discriminations (e.g., visual + scent cue) between rewarded and non-rewarded bowls. After learning the discriminants, the rewards were reversed. Ethanol exposure reduced flexibility in both adolescents and adults for simple discriminations in both studies. Age-related differences emerged for the more complex discriminations in one study, with only adults showing reduced flexibility after prolonged abstinence (21d) following binge-like exposure (5 g/kg, 2d on, 2d off) [ 79 ]. In contrast, both age groups showed reduced flexibility for complex discrimination in the other study after prolonged abstinence (21d) despite adolescents consuming more ethanol orally than adults during the 28 week exposure [ 80 ].

In another study, Labots et al. [ 81 ] used a conditioned suppression of alcohol-seeking task after two months of voluntary ethanol consumption (2 months) in rats to examine flexibility around alcohol-seeking behavior. After stratifying the age groups based on levels of ethanol consumption, medium- and high-consuming, adolescents showed higher levels of conditioned suppression compared to similarly drinking adults, indicating greater behavioral flexibility and control over alcohol-seeking in adolescents after chronic voluntary exposure.

Overall, there is limited evidence for adolescent resilience to the effects of chronic alcohol on cognitive flexibility. Two studies found support for adolescent resilience to ethanol’s effect on behavioral flexibility, whereas another study found no differences between adolescents and adults.

Impulsivity: Impulsivity is a multi-faceted behavioral trait that encompasses impaired response inhibition, preference for an immediate reward over a larger but delayed reward, and premature expression of behaviors which may be maladaptive or in conflict with conscious goals. Impulsivity is a risk-factor for the development of addiction and may also be a consequence of sustained substance use [ 35 ]. Pharmacological evidence points towards overlapping neuronal mechanisms in impulsivity and addictive behavior, particularly within the mesolimbic dopamine system [ 91 ]. Two studies examined impulsive decision-making behavior in rats [ 74 , 78 ]. Both studies observed age-related differences.

One study examined impulsive behavior using a delay-discounting task in which choices are made between immediate small rewards and larger delayed rewards [ 78 ]. Regardless of age, chronic intermittent exposure (2d on, 2d off) had no effect on choice behavior in non-intoxicated rats. Following acute challenges, adolescents but not adults demonstrated a reduced preference for the large reward regardless of ethanol exposure history, reflecting a general adolescent-specific heightened impulsivity during intoxication. Another study examined decision-making under risk conditions using an instrumental training and probability-discounting task [ 74 ]. After prolonged abstinence (20d), rats were trained to press two levers for sucrose rewards and were concurrently trained to choose between two levers with different associated probabilities of reward and reward size, creating a choice between a certain, small reward and an uncertain, large reward (i.e., riskier choice). Ethanol consumption was voluntary and while adolescents initially consumed more ethanol than adults at the beginning of the exposure period, the total amount of consumption was similar by the end of the exposure period. Only adolescents showed increased risky and sub-optimal decision-making compared to age-matched controls, while adults performed similarly to controls.

In sum, both studies found support for ethanol having a larger impact on adolescent compared to adults on impulsive behavior.

Goal-directed behavior: Goal-directed behavior refers to when actions are sensitive to both the outcome value (goal) and contingency between the behavior and the outcome [ 92 ]. Two studies used a sign-tracking and omission contingency learning paradigm to examine goal-directed versus habitual behavior [ 76 , 77 ]. One study observed age-related differences and the other did not. Sign tracking refers to tasks where a cue predicts a reward, but no response is needed for the reward to be delivered. Despite this, after repeated pairings of the cue and reward, animals and humans may respond (e.g., via a lever) when the cue is presented anyway, and even when no reward is known to be available. Sign-directed behavior is considered habitual and has been proposed to underlie the lack of control of alcohol use in addiction [ 93 ]. In humans, sign-tracking behavior is difficult to differentiate from goal-directed behavior based on only the observable behavior, i.e., seeing a cue such as a favorite drink or bar and then having a drink [ 94 ]. In the context of alcohol use, reflexively having a drink when seeing an item that is often associated with the rewarding effects of alcohol (e.g., wine glass, bar, smell of alcohol) despite not consciously desiring the alcohol ‘reward’ is an example of how habitual behavior (possibly driven by sign-tracking) can initiate the behavior as opposed to an intentional goal [ 93 ]. Omission contingency refers to a 2nd phase after sign-tracking when the response is punished and the behavior must be inhibited to avoid punishment. After both forced and voluntary ethanol exposure (6w), no alterations to sign-tracking behavior were observed in adolescent and adult rats [ 76 , 77 ]. One study did observe an age-related difference in omission contingency learning, with adolescents performing better than adults after chronic voluntary ethanol exposure [ 77 ]. This preliminarily suggests that adolescents may be more capable of adapting their behavior to avoid punishment compared to adults after chronic use. However, before behavioral testing began, adolescent rats were abstinent for 17 days, while adults were only abstinence for 10 days which may have influenced the results.

In summary, one study found support for adolescents being less sensitive to ethanol effects on goal-directed behavior compared to adults, whereas one study found no effect of ethanol in either age group.

Across the domains of executive function, there is some evidence that adolescents may be more vulnerable to impairments in certain executive and higher-order cognitive functions following chronic alcohol exposure, with increased risky decision-making after prolonged abstinence [ 74 ], impulsivity during intoxication [ 78 ], and reduced working memory function during intoxication after chronic exposure. In contrast, animals exposed to alcohol during adolescence may better retain cognitive flexibility [ 77 , 79 ] and are better able to regain control over alcohol-seeking in adulthood [ 81 ].

Other behavioral outcomes

Anxiety : AUD is highly comorbid with anxiety disorders [ 95 ], especially in adolescence [ 96 ]. While anxiety is not strictly a cognitive outcome, it is related to altered cognitive functioning [ 97 , 98 ]. Many studies assessing the effects of ethanol on the rodent brain and cognition also include anxiety-related measures. Multiple paradigms have been developed to elicit behaviors thought to reflect anxiety in rodents (e.g., rearing, startle, avoidance, etc.). In the open field test (OFT), anxiety is indexed as the tendency to stay close to perimeter walls as animals have a natural aversion to brightly lit open spaces [ 99 ]. In the elevated plus maze paradigm, rodents are placed at the center of an elevated four-arm maze with two open arms two closed arms [ 100 ]. The open arms elicit unconditioned fear of heights/open spaces and the closed arms elicit the proclivity for enclosed, dark spaces. Anxiety is indexed as entries/duration of time in open vs. closed arms, as well as rearing, freezing, or other postural indices of anxiety. In startle paradigms, the startle response is a defensive mechanism reflecting anxiety which follows a sudden, unpredictable stimulus (e.g., tones, light) [ 101 ]. In light-dark box paradigms, anxiety is elicited using a testing apparatus with a light and dark compartment, relying on the conflict between natural aversions to well-lit spaces and the tendency to explore new areas. Percentage of time spent in the light compartment, latency to return to the dark compartment, movement between compartments (transitions), and rearing-behavior are measured as indices of anxiety [ 102 ]. Anxiety can also be assessed using a social interaction test with an unfamiliar partner, with approach and avoidance behaviors measured to index anxiety [ 103 ]. In the novel object test (NOT) [ 104 ], anxiety is elicited by the introduction of a new object in the rodent’s environment. The amount of contacts and time spent in contact with the object is used as an index of anxiety. Similarly, in the marble-burying test (MBT), novel marbles are placed in an environment and the amount of defensive burying of the objects is used as an index of anxiety [ 105 ].

Eleven studies examined anxiety-like behavior in rodents with mixed results across paradigms [ 70 , 78 , 82 , 83 , 89 , 106 , 107 , 108 , 109 , 110 , 111 ]. Overall, five of the eleven studies observed age-related differences.

Two studies used the OFT, finding no effects of voluntary (2w, 4 h/day access) or forced (12/day vapor) ethanol exposure on anxiety-like behavior in adolescents or adult rats during withdrawal (7–9 h) [ 110 ] or after a brief abstinence period (4 days) [ 107 ]. One study used both the MBT and NOT after voluntary ethanol consumption (2 h/d for 2 weeks; no abstinence) and observed higher anxiety in ethanol-exposed adults and reduced anxiety in ethanol-exposed adolescents compared to controls as indexed by marble burying [ 106 ]. However, no age effects were observed in response to a novel object, with reduced interaction with the novel object in both age groups after chronic exposure.

Four studies used the elevated maze paradigm with mixed results. Only one study observed age-related differences in mice after chronic exposure (8–10w vapor) [ 109 ]. Adolescents showed reduced anxiety compared to adults during the acute withdrawal period, but all mice were kept under chronic social isolation and unpredictable stress conditions, which may have affected the results. Two studies in rats found no effect of intermittent (1 g/kg) or binge-like (5 g/kg) exposure in either age group after short (24 h) [ 70 ] or sustained abstinence (20d) [ 83 ]. A third study observed heightened anxiety in both age groups after intermittent exposure (4 g/kg), with anxiety increasing with prolonged abstinence periods (24 h to 12d) [ 108 ].

Three rat studies used a startle paradigm to assess anxiety. Two observed reduced acoustic startle responses after ethanol exposure (12 h/d vapor) in both age groups during acute withdrawal periods (7–10 h) and following more sustained abstinence (6d) [ 82 , 89 ]. In the other study, light-potentiated startle was also reduced in both ages during days 1–10 of withdrawal after binge-like exposure (2d on, 2d off), but age-related differences emerged when the rats were re-exposed via a 4-day binge (1–4/kg). Then, only adults showed higher levels of light-potentiated startle compared to controls [ 78 ], suggesting that ethanol pre-exposure increases anxiety in adults but not adolescents when re-exposed to ethanol after withdrawal.

Two studies used the light-dark box paradigm with mixed results [ 89 , 111 ]. Only adult rats showed increased mild anxiety-like behaviors during early withdrawal (7–10 h) after chronic vapor exposure 12 h/d) [ 89 ]. In contrast, no age-related differences emerged after voluntary ethanol consumption (18 h/d access; 3d/w for 6 weeks), with male mice showing less anxiety-like behavior in both ages [ 111 ]. In contrast, the one study using the social interaction test observed reduced anxiety in adult mice compared to both adolescents and age-matched controls during early withdrawal (4–6 h) after chronic, unpredictable vapor exposure [ 109 ].

In summary, there is inconsistent evidence for age-related differences in the effect of chronic ethanol exposure on anxiety outcomes in rodents. The substantial differences across studies in how anxiety was elicited and measured make it challenging to draw strong conclusions. In the five studies that found age-related differences, adults tend to show higher levels of anxiety, particularly during early withdrawal; however, the opposite was found in the one study examining anxiety in social interactions. Six studies did not observe any age-related differences. Overall, adolescents may be less sensitive to the anxiety-inducing effects of chronic alcohol exposure.

Social behavior: Two studies were identified that examined the effects of chronic ethanol exposure on social behavior in rats [ 112 , 113 ], with both observing age-related differences. After chronic exposure (1 g/kg, 7d), followed by a brief abstinence period (24–48 h), one study found a decrease in social preference in adolescents only [ 112 ], while the other study found no ethanol-related effects on social behavior (2 g/kg, 10d) [ 113 ]. After acute challenges, age and treatment interactions emerged in both studies, but the directions of the results are inconsistent. In the first study, adolescents showed increased social preference, as indexed by the number of cross-overs between compartments toward and away from a peer, across multiple acute doses (0.5–1.0 g/kg) administered immediately before testing, while adults showed no changes in social preference [ 112 ]. In contrast, Morales et al. [ 113 ] found evidence for age-related temporal differences in social activity after acute challenge, with adults showing decreased social impairment five minutes post injection (1 g/kg) and adolescents (1.25 g/kg) after 25 min compared to age-matched controls.

The findings from these two studies paint a complicated and inconsistent picture of the effects of ethanol on social behavior in adults and adolescents warranting further research. One study found support for a larger effect of chronic ethanol on adolescent social behavior compared to adults, while the other did not observe effects of ethanol in either group. One study found support for a larger effect of chronic plus acute ethanol intoxication on social behavior, with the opposite observed in the other.

Brain outcomes

Neurotransmitter systems.

Glutamate is the brain’s main excitatory neurotransmitter and plays a crucial role in synaptic plasticity (i.e., experience-related strengthening or weakening of synaptic connections). Glutamatergic transmission plays an important role in the formation and maintenance of addictive behaviors and the nucleus accumbens (NAc) is considered an important hub in this, receiving glutamatergic input from cortical-limbic areas and dopaminergic input from the midbrain [ 114 ]. Seven studies investigated glutamate functioning in regions of the brain [ 106 , 107 , 108 , 109 , 115 , 116 , 117 , 118 ]. Four of the seven studies observed age-related differences.

Three studies investigated glutamate-related processes in the NAc [ 106 , 107 , 118 ]. Two weeks of voluntary binge drinking (4-h access, no abstinence) did not affect expression of calcium-dependent kinase II alpha (CaMKIIα) and the AMPA receptor GluA1 subunit in the NAc of mice [ 107 ]. In contrast, Lee et al. [ 106 ] showed that voluntary binge drinking (2-h access, no abstinence) increased mGlu1, mGlu5, and GluN2b expression in the shell of the NAc, as well as PKCε and CAMKII in the core of the NAc in adult mice only. In rats, Pascual et al. [ 118 ] showed reduced NR2B phosphorylation in the NAc of adolescents only after two weeks of chronic intermittent ethanol exposure; an effect that also lasted until 24 h after end of exposure. This indicates that adolescents might be less affected by the effects of ethanol on NAc-related glutamatergic neurotransmission than adults. This may in turn mediate decreased withdrawal symptoms and potentially facilitate increased drinking [ 106 ].

Two studies investigated glutamate-related processes in the (basolateral) amygdala [ 107 , 116 ]. In mice, Agoglia et al. [ 107 ] showed decreased CaMKIIα phosphorylation in adolescents, but increased GluA1 expression in adults after two weeks of voluntary binge drinking (4-h access, no abstinence). Also, drug-induced AMPAR activation resulted in increased binge drinking in adolescents but decreased binge drinking in adults, highlighting the potential importance of glutamatergic signaling in age-related differences in alcohol consumption. However, Falco et al. [ 116 ] reported no difference in NR2A mRNA levels in the basolateral amygdala for either age group after 60-day abstinence.

Alcohol’s effects on frontal cortex functioning is thought to be mediated by alterations in NMDA receptor subunit expression [ 119 , 120 ]. Two studies investigated glutamate-related processes in the frontal cortex of rats [ 115 , 118 ]. Pascual et al. [ 118 ] showed reduced NR2B phosphorylation after two weeks of forced intermittent ethanol exposure in adolescents only. Using a 2-week ethanol vapor paradigm, Pian et al. [ 115 ] found different patterns of NMDAR subunit expression. These patterns were highly dependent on abstinence duration (0 h, 24 h, 2w), however, they only statistically compared results within rather than between age groups. Ethanol exposure was associated with decreased NR1 receptor expression in both age groups, but only the adult group showed a decrease in NR2A and NR2B expression. The NR1 and NR2A expression returned to normal during withdrawal, but in adults NR2B expression increased after two weeks of abstinence.

Conrad and Winder [ 109 ] assessed long-term potentiation (LTP) in the bed nucleus stria terminalis (BNST), a major output pathway of the amygdala towards the hypothalamus and thalamus. Voluntary ethanol exposure resulted in blunted LTP responses in the dorsolateral BNST regardless of age. However, all mice were socially isolated during the experiments to induce anxiety, so it is unclear whether the effects were solely due to ethanol exposure.

Two studies looked at glutamate receptor subunit expression in the hippocampus [ 108 , 115 ]. Pian et al. [ 115 ] observed increased expression of NR1, NR2A, and NR2B in adults after 2 weeks of ethanol exposure. In adolescents, a reduction in NR2A expression was observed. After abstinence, adult levels returned to normal, while in adolescents, decreased NR1 and NR2A expression was seen after 24 h but an increased expression of these subunits was seen after 2 weeks of abstinence. These findings support regional specific effects of age group, with potentially increased sensitivity to the impact of alcohol on glutamatergic mediated hippocampal functioning in adolescents. Unlike expected, van Skike et al. [ 108 ] did not find effects of chronic intermittent ethanol exposure or withdrawal on NMDA receptor subunit expression in the hippocampus and cortex as a whole in adolescent and adult rats. The authors speculate that these null results might be associated with the exposure design (limited exposure and route of administration) and lack of withdrawal periods compared to Pian et al. [ 115 ].

In sum, there is limited and inconsistent evidence for age-related differences in glutamate function across seven studies. The direction of the observed age-related differences varies across regions, with evidence of both increased and decreased sensitivity to ethanol effects in adolescents compared to adults in the four studies that observed age-related differences.

GABA is the brain’s main inhibitory neurotransmitter. GABA A receptors are a primary mediator of alcohol’s pharmacological effects [ 121 ]. A total of four studies looked at GABAergic functioning [ 108 , 116 , 122 , 123 ]. Three of the four studies observed age-related differences.

One study investigated GABA-related processes in the (basolateral) amygdala, showing reduced GABA A α1 and GAD67 (enzyme that converts Glutamate to GABA) mRNA expression in adult rats only, 60 days after 18-days ethanol exposure [ 116 ].

Two studies looked at the rat cortex as a whole [ 108 , 122 ]. Van Skike et al. did not find effects of chronic intermittent ethanol exposure on GABA A receptor expression [ 108 ]. Grobin et al. [ 122 ] showed that, while basal GABA A receptor functioning was not affected by 1 month of chronic intermittent ethanol exposure, GABA A receptors were less sensitive to the neurosteroid THDOC in adolescents. This neuromodulatory effect was not found in adults and did not persist after 33 days of abstinence. However, these results indicate that neurosteroids may play an indirect role in age differences in the GABAA receptor’s response to alcohol.

Two studies focused on the rat hippocampus [ 108 , 124 ]. Fleming et al. [ 124 ] found age-specific effects of chronic intermittent ethanol exposure on hippocampal (dentate gyrus) GABA A receptor functioning. Adolescent rats showed decreased tonic inhibitory current amplitudes after ethanol exposure, which was not the case for young adult and adult rats. Also, only the adolescents showed greater sensitivity to (ex vivo) acute ethanol exposure induced enhanced GABAergic tonic currents. The specificity of these effects to adolescent exposure might indicate adolescent vulnerability to ethanol-induced effects on the hippocampus; however, Van Skike et al. [ 108 ] did not find any effects of chronic intermittent ethanol exposure on GABA A receptor expression in the hippocampus.

In sum, given the limited number of studies and lack of replicated effects, no clear conclusions can be drawn about the role of age on the effects of alcohol on GABAergic neurotransmission. Age-specific effects appear to be regionally distinct. The only available study found support for heightened adult sensitivity to ethanol in the amygdala. In contrast, one study found support for greater adolescent sensitivity in the hippocampus and whole cortex, whereas the other found no age-related differences.

The mesocorticolimbic dopamine system, with dopaminergic neurons in the ventral tegmental area (VTA) projecting to the NAc and prefrontal cortex, plays a key role in AUD, particularly through reward and motivational processes [ 14 ]. Only two studies investigated dopaminergic processes, focusing on the frontal cortex, NAc, and broader striatum [ 118 , 125 ]. Both studies observed age-related differences in certain dopamine outcomes.

Carrara-Nascimento et al. [ 125 ] investigated acute effects of ethanol in adolescent and adult mice 5 days after a 15-day treatment with either ethanol or saline. In the PFC, ethanol pretreated adolescents showed reduced dopamine levels (DA) and related metabolites (DOPAC and HVA) in response to an acute ethanol challenge compared to ethanol pretreated adults and adolescent saline controls. In the NAc, there were no differences between pretreated adolescents and adults, but analyses within each age group revealed that ethanol-pretreatment with an acute challenge decreased DOPAC within the adolescent group. Results from the dorsal striatum also showed no differences between adolescents and adults. However, within the adolescent group, ethanol pre-treatment increased DOPAC and, within the adult group, it increased HVA. Pascual et al. [ 118 ] found similar results looking at the expression of DRD1 and DRD2 dopamine receptors after two weeks of chronic intermittent ethanol exposure in rats. In the NAc and dorsal striatum, DRD2 expression was reduced in adolescent compared to adult exposed rats, while both DRD1 and DRD2 expression were reduced in the frontal cortex.

These results suggest reduced alcohol-induced dopamine reactivity in adolescents in the PFC and NAc based on the two available studies, but more studies are warranted for a more detailed understanding of the relationship between age and dopamine receptor expression following chronic ethanol exposure.

Acetylcholine

Acetylcholine is a known neuromodulator of reward and cognition-related processes [ 126 ]. The composition and expression of nicotinic and muscarinic acetylcholine receptors have been implicated in various alcohol use-related behaviors [ 127 , 128 ]. Only one study investigated cholinergic processes and observed age-related differences. Vetreno et al. [ 129 ] showed global reductions in choline acetyltransferase (ChAT; cholinergic cell marker) expression after adolescent onset, but not adult onset of forced intermittent binge-like exposure (20 days – every other day, 25 days abstinence).

Neuromodulatory processes

Neurodegeneration and neurodevelopment.

Chronic alcohol consumption is thought to lead to brain damage by influencing processes involved in neurodegeneration and neurogenesis. The formation of addictive behaviors is paralleled by the formation of new axons and dendrites, strengthening specific neuronal pathways [ 130 ]. While brain morphology is commonly investigated in humans, it is a proxy of the impact of alcohol on the brain and therefore rarely studied in rodents. Five studies investigated facets of neurodegeneration or development in rodents [ 55 , 65 , 131 , 132 , 133 ]. All five studies observed age-related differences.

Huang et al. [ 131 ] showed reduced cerebral cortex mass in adolescent mice, but shortening of the corpus collosum in adults after 45 days of ethanol injections, suggesting some age-specific regional effects. Using an amino cupric silver staining, significant brain damage was revealed for both adolescent and adult rats after 4 days of binge-like ethanol exposure [ 132 ]. However, adolescents showed more damage in the olfactory-frontal cortex, perirhinal cortex, and piriform cortex.

Looking at hippocampal neurogenesis, ethanol exposure has been shown to initially reduce hippocampal neurogenesis in adult rodents, recovering after 1-month abstinence [ 134 ]. Compared to adults, neurogenesis in the dentate gyrus of the hippocampus was found to be reduced in adolescent exposed mice (Bromodeoxyuridine levels) [ 65 ] and rats (doublecortin levels) [ 133 ]. Lacaille et al. [ 65 ] also measured the expression level of genes involved in oxidative mechanisms after binge-like alcohol exposure. In whole brain samples, they found increased expression of genes involved in brain protection (i.e., gpx3, srxn1) in adults, but increased expression of genes involved in cell death (i.e., casp3) combined with decreased expression of genes involved in brain protection (i.e., gpx7, nudt15) in adolescents. Casp3 protein levels were also higher in the whole brain of adolescent exposed mice [ 65 ] and the adolescent dentate gyrus [ 133 ], suggesting more neurodegeneration and less neurogenesis in adolescents versus adults following ethanol consumption.

Cyclin-dependent kinase 5 (CDK5) is involved in axon, dendrite, and synapse formation and regulation. CDK5 is overexpressed in the prefrontal cortex and the NAc following exposure to substances of abuse including alcohol [ 135 ]. Moreover, CDK5 inhibition has been shown to reduce operant self-administration of alcohol in alcohol-dependent rats [ 136 ]. One study reported higher H4 acetylation of the CDK5 promoter in the PFC of adult versus adolescent ethanol-exposed rats during acute withdrawal, however, CDK5 mRNA expression was control-like after 2 weeks of abstinence [ 55 ].

In sum, strong conclusions cannot be drawn due to the limited number of studies and lack of replicated effects. However, preliminary evidence points to adolescent vulnerability to damage in the cortex, reduced neurogenesis, and increased neurodegeneration in the hippocampus and the cortex as a whole based on four of the five studies. In contrast, one study found support for adult vulnerability to ethanol’s effects axon, dendrite, and synapse formation and regulation.

Growth factors

Brain-derived neurotrophic factor (BNDF) and nerve growth factor (NGF) are involved in brain homeostasis and neural recovery [ 137 , 138 ]. While ethanol exposure initially increases BDNF and NGF, chronic ethanol exposure seems to reduce BDNF and NGF levels and can thereby result in long-term brain damage and related cognitive problems [ 139 , 140 ]. Four studies investigated growth factor expression in the frontal cortex [ 54 , 55 , 79 , 80 ] and two studies also investigated the hippocampus [ 79 , 80 ]. All four studies of the frontal cortex observed age-related differences. Neither study of the hippocampus observed age-related differences.

In rats, 30 weeks of chronic ethanol exposure reduced prefrontal mBDNF and β-NGF regardless of age, despite adolescents consuming more ethanol [ 80 ]. Moreover, the reduction of mBDNF was correlated with higher blood alcohol levels and was persistent up to 6–8 weeks abstinence. Interestingly, during acute withdrawal (48 h) adolescents but not adults temporarily showed control-like mBDNF levels. This might indicate an attempt to counteract neurodegeneration as a result of ethanol exposure in adolescents. These results were partially replicated using a shorter intermittent exposure paradigm (13 doses, 2 days on/off) [ 79 ]. While intoxication after chronic ethanol exposure reduced prefrontal BDNF, levels recovered after 3-weeks abstinence regardless of age. However, during acute withdrawal (24 h), BDNF was still reduced in early-adolescent onset rats, increased in adult-onset rats, but control-like in mid-adolescent onset-rats, suggesting slower recovery in younger animals. Looking at BDNF gene regulation, a similar study (8 doses, 2 days on/off) reported higher H3 demethylation but lower H4 acetylation of the BDNF promoter in the PFC of adult versus adolescent ethanol-exposed rats during acute withdrawal [ 55 ]. However, prefrontal BDNF mRNA expression returned to control levels after 2 weeks of abstinence. Interestingly, social housing may be protective, as reduced prefrontal BDNF was no longer observed in alcohol-exposed adolescent mice housed in environmentally enriched relative to standard conditions [ 54 ]. Two studies investigated hippocampal BDNF expression but reported no significant interactions between alcohol exposure and age group [ 79 , 80 ].

In sum, the results of the four available studies suggest lower prefrontal BDNF during chronic alcohol use that recovers after abstinence regardless of age. However, the rate of recovery may be influenced by age with slower recovery in adolescents. In the two available studies, no age-related differences were observed in BDNF expression in the hippocampus.

Transcription factors

The transcription factors cFos and FosB are transiently upregulated in response to substance use, and ΔFosB accumulates after chronic exposure, particularly in striatal and other reward-related areas [ 141 ]. Two studies investigated cFos and FosB [ 55 , 142 ] and one study ΔFosB related processes [ 111 ]. All three studies observed age-related differences.

After chronic ethanol exposure (8 doses, 2 days on/off), adolescent compared to adult rats showed increased prefrontal H3 and H4 acetylation of the cFos promotor region and increased H4 acetylation and H3 dimethylation of FosB promotor regions after acute abstinence [ 55 ]. Moreover, mRNA expression of FosB was elevated in adolescents but not adults after 2-weeks abstinence. The upregulating effects of an acute ethanol challenge on prefrontal cFos appears to reduce after chronic pre-treatment to a larger extent in adolescent than adult exposed mice [ 142 ]. This pattern of results was similar in the NAc, but desensitization to ethanol’s acute effects on cFos in the hippocampus was more pronounced in adults. Faria et al. [ 142 ] also looked at Egr-1 (transcription factor, indirect marker of neuronal activity and involved in neuroplasticity), showing a stronger reduction in Egr-1 expression in the PFC, NAc, and hippocampus of adolescent versus adults after repeated ethanol exposure. Regarding ∆FosB, Wille-Bille et al. [ 111 ] found increased ∆FosB in adolescent compared to adult rats in the prelimbic PFC, dorsomedial striatum, NAc core and shell, central amygdala nucleus capsular, and basolateral amygdala after 3 days per week 18 h ethanol exposure sessions for 6 weeks. In sum, the three available studies provide preliminary evidence for increased adolescent vulnerability to ethanol-induced long-term genetic (mRNA expression) and epigenetic (methylation) changes in mesocorticolimbic areas.

Immune factors

Ethanol is known to trigger immune responses in the brain (e.g., increase production of hemokines and cytokines), causing inflammation and oxidative stress [ 143 , 144 , 145 ]. Three studies examined immune factors [ 146 , 147 , 148 ]. Two of the three studies observed age-related differences.

Microglia remove damaged brain tissue and infectious agents and are key to the brain’s immune defense. Only one study investigated microglia levels [ 146 ]. Although direct comparisons between age groups were missing, both adolescent and adult rats showed less microglia in the hippocampus (CA and DG) and peri-entorhinal cortex, and more dysmorphic microglia in the hippocampus after 2 and 4 days of binge-like ethanol exposure [ 146 ]. Notably, age groups were matched on intoxication scores, with adolescents needing more ethanol to reach the same level of intoxication. An in silico transcriptome analysis of brain samples from mice after 4 days of 4 h/day drinking in the dark, suggest overexpression of neuroimmune pathways related to microglia action (toll-like receptor signaling, MAPK signaling, Jak-STAT signaling, T-cell signaling, and chemokine signaling) in adults that was not observed in adolescents, while adolescents consumed more ethanol [ 147 ]. Similarly, ethanol-exposed adult mice showed higher chemokine expression (CCL2/MCP-1) in the hippocampus, cerebral cortex, and cerebellum and higher cytokine expression (IL-6, but not TNF-α) in the cerebellum, while no chemokine or cytokine changes were observed in ethanol exposed adolescent mice [ 148 ]. Both adolescents and adults showed increased astrocyte levels in the hippocampus (CA1) and the cerebellum after ethanol exposure, but changes in astrocyte morphology were only observed in the adult hippocampus.

In sum, two of the studies found support for increased immune responses after ethanol exposure in adults compared to adolescents, whereas the one other study found no difference between the age groups.

HPA-axis functionality

Chronic stress and HPA-axis functionality have been associated with the maintenance of AUD (e.g., reinstatement drug seeking, withdrawal) [ 149 ]. Two studies investigated corticotropin-release factor (CRF) expression in rats [ 116 , 150 ]. One study observed age-related differences and the other did not.

Falco et al. [ 116 ] found decreased CRF mRNA expression in the adult but not adolescent basolateral amygdala 2 months after 18-day restricted ethanol exposure. In contrast, Slawecki et al. did not find any interaction between age and treatment on CRF levels in the amygdala, as well as the frontal lobe, hippocampus, hypothalamus, and caudate 7 weeks after 10-days of ethanol vapor exposure.

No conclusions can be drawn. One study observed found support for reduced effects of ethanol on HPA-axis functionality compared to adults, whereas the other observed no difference between the age groups. Future studies using different (voluntary) exposure paradigms are needed to further investigate the effects of alcohol on HPA activity in relation to age of alcohol exposure.

Neuropeptides

Neuropeptides are a diverse class of proteins that have a modulatory function in many different processes, including but not limited to neurotransmission, stress, immune responses, homeostasis, and pain [ 151 , 152 , 153 ]. Only one study investigated neuropeptides in rats and observed age-related differences [ 150 ].

Slawecki et al. [ 150 ] specifically investigated neuropeptide-Y, substance-P, and interleukine expression in the frontal lobe, hippocampus, hypothalamus, dorsal striatum, and amygdala 7 weeks after 10-days of ethanol vapor exposure in rats [ 150 ]. Interactions between age and treatment were found for the hippocampus and caudate only. Ethanol-induced reductions in hippocampal neuropeptide-Y and increases in caudate neurokinine were more pronounced in adults compared to adolescents suggesting long-lasting effects of ethanol in adults but not adolescents.

Ethanol metabolism

The first metabolite of ethanol is acetaldehyde, which has been theorized to mediate the effects of ethanol on both brain and behavior [ 154 ]. Only one study investigated ethanol metabolism in the brain and did not observe age-related differences [ 155 ].

Rhoads et al. showed that despite the fact that adolescent rats consumed more alcohol brain catalase levels after 3-weeks of ethanol exposure (no abstinence) did not differ between adolescents and adults [ 155 ]. Although the general role of catalase in ethanol metabolism is small, catalase can oxidize ethanol to acetaldehyde in the brain, affecting elimination of ethanol after consumption [ 156 , 157 ]. These findings may therefore imply that ethanol metabolism may not differ between adolescent and adult animals, which should be studied in a more direct manner.

Full proteome analysis

While the previously described studies focused on specific factors involved in neurotransmission, brain health, and plasticity, proteomics allows for the study of the full proteome in a specific region or tissue type. One study investigated the impact of age on ethanol-induced changes in the hippocampal proteome, observing age-related differences [ 158 ]. In this study, rats intermittently and voluntarily consumed beer for 1 month and the hippocampal proteome was analyzed after 2 weeks of abstinence. The results point to the involvement of many of the factors described above and imply age-specific effects of alcohol. Adult beer exposure increased citrate synthase (part of the citric acid, or Krebs, cycle) and fatty acid binding proteins (involved in membrane transport) compared to controls. Adolescent beer exposure increased cytoskeletal protein T-complex protein 1 subunit epsilon (TCP-1), involved in ATP-dependent protein folding, and reduced expression of a variety of other proteins involved in glycolysis, glutamate expression, aldehyde detoxification, protein degradation, and synaptogenesis, as well as neurotransmitter release. These more extensive changes suggest that the adolescent hippocampus might be more vulnerable to the effects of ethanol exposure, but more studies are needed to clarify and replicate these findings and extend the focus to different brain areas.

Neuronal activity and functioning

Ethanol-induced molecular changes may eventually change neuronal activity. Three studies investigated neuronal activity and functioning [ 89 , 159 , 160 ] using electrophysiological methods. All three studies observed age-related differences.

Galaj et al. [ 159 ] assessed firing patterns and the structure of pyramidal neurons in the L2 and L5 layers of the prelimbic cortex of the rat brain using ex vivo electrophysiological recordings and morphological staining. Following chronic intermittent ethanol exposure and brief abstinence (2 days), adolescents, but not adults, showed reduced amplitudes of spontaneous excitatory post-synaptic currents (sEPSCs) in L5 neurons compared to controls, indicating reductions in intrinsic excitability. In line with this, Dil staining showed increased thin spine ratios in the L5 layer in adolescents only. Age differences were more pronounced after prolonged abstinence (21 days), with adolescents showing reduced amplitude and frequency of sEPSCs in L5 neurons while adult’s L5 neurons showed augmented firing patterns (i.e., amplitude and frequency). Furthermore, adolescent rats showed decreased total spine density and non-thin spines, indicating less excitatory postsynaptic receptors in the L5 layer. In contrast, adults showed increases in spine density and non-thin spines.

Li et al. [ 160 ] examined the functioning of CA1 interneurons, which are important for learning and memory processes [ 161 ], in the rat hippocampus using ex vivo whole-cell recordings. After prolonged abstinence (20 days), voltage-gated A-type potassium channel ( I A ) conductance was measured. Differences emerged between age groups (although no statistical interaction effect was directly assessed): EtOH-exposed adolescents and adults both showed lower I A mean peak amplitude compared to the respective control groups. However, adolescents also showed reduced I A density and increased mean decay time, which decreased in adults. Furthermore, only adolescents showed increased depolarization required for activation compared to controls, which can result in higher interneuron firing rates in the CA1 region that could affect learning processes. Additional research is needed to connect these findings to behavioral measures of learning and memory.

Slawecki et al. [ 89 ] was the only study to use in vivo electroencephalogram (EEG) recordings with rats to examine function in the frontal and parietal cortex at different times during a 14-day vapor exposure period. During acute withdrawal (7–10 h abstinence period), following daily exposure no effects emerged in frontal cortical regions throughout the exposure period. In parietal regions, only adolescents showed increased high frequency (16–32 Hz and 32–50 Hz) power on days 8 and 12 compared to controls. Adolescent hyperexcitability during withdrawal may indicate increased arousal in adolescents compared to adults during withdrawal, but more studies linking brain activity to behavioral indices of withdrawal will allow for clearer interpretations.

Overall, strong conclusions cannot be drawn given the disparate paradigms and outcomes utilized. While adolescents and adults appear to differ in the effect of ethanol on neuronal firing, the meaning of these differences is not clear given the lack of connection between these findings and behavioral outcomes.

Human studies

Four studies examined age-related differences of the effect of alcohol on brain or cognition in humans [ 162 , 163 , 164 , 165 ].

Müller-Oehring et al. [ 162 ] examined the moderating role of age on resting state functional connectivity and synchrony in the default mode, central executive, salience, emotion, and reward networks of the brain in a sample of no/low and heavier drinkers aged 12–21 years old. While the study did not compare discrete groups of adolescents and adults, analyses investigating the interaction between continuous age and alcohol exposure history were conducted which provide insight into the effect of alcohol use on functional brain networks from early adolescence to emerging adulthood. Regardless of age, no differences were observed between matched subgroups of no/low drinkers and moderate/heavy drinkers in the default mode, salience, or reward networks. However, in the central executive network, connectivity between the superior frontal gyrus (SFG) and insula increased with age in the no/low drinkers but not in heavier drinkers. Age-related strengthening of this fronto-limbic connection correlated with better performance on a delay discounting task in boys, suggesting that adolescent alcohol use may interfere with typical development of higher-level cognitive functions. In the emotion network, amygdala-medial parietal functional synchrony was reduced in the heavier drinkers compared to the no/low drinkers and exploratory analyses suggested that weaker amygdala-precuneus/posterior cingulate connectivity related to later stages of pubertal development in the no/low drinking group only. Interestingly, in the default mode (posterior cingulate-right hippocampus/amygdala) and emotional networks (amygdala, cerebellum), connectivity in regions that exhibited age-related desynchronization was negatively correlated with episodic memory performance in the heavy drinkers. These results give preliminary evidence that alcohol might have age-dependent effects on resting state connectivity and synchronization in the central executive, emotion, and default mode networks that could potentially interfere with normative maturation of these networks during adolescence.

Three studies examined age effects in alcohol-related implicit cognitions, specifically attentional bias [ 163 , 165 ], alcohol approach bias [ 165 ], and implicit memory associations and explicit outcome expectancies [ 164 ]. Attentional bias refers to the preferential automatic allocation or maintenance of attention to alcohol-related cues compared to neutral cues which is correlated with alcohol use severity and craving [ 166 ]. McAteer et al. [ 163 ] measured attentional bias with eye tracking during presentation of alcohol and neutral stimuli in heavy and light drinkers in early adolescents (12–13 yrs), late adolescents (16–17 yrs), and young adults (18–21 yrs). Regardless of age, heavy drinkers spent longer fixating on alcohol cues compared to light drinkers. Cousijn et al. [ 165 ] measured attentional bias with an Alcohol Stroop task [ 167 ], comparing the speed of naming the print color of alcohol-related and control words. Consistent with the findings of McAteer et al. [ 163 ], adults and adolescents matched on monthly alcohol consumption showed similar levels of alcohol attentional bias. In the same study, Cousijn et al. [ 165 ] did not find any evidence for an approach bias towards alcohol cues in any age group.

Rooke and Hine [ 164 ] found evidence for age-related differences in implicit and explicit alcohol cognitions and their relationship with binge drinking. Using a teen-parent dyad design, adolescents (13–19 yrs) showed stronger memory associations in an associative phrase completion task and more positive explicit alcohol expectancies than adults. Interestingly, both explicit positive alcohol expectancies and implicit memory associations were a stronger predictor of binge drinking in adolescents compared to adults. It is important to note that adolescents also had higher levels of binge drinking than adults in the study.

Cousijn et al. [ 165 ] also investigated impulsivity, drinking motives, risky decision-making, interference control, and working memory. No age differences emerged in the cognitive functioning measures including risky decision-making (Columbia Card Task – “hot” version), interference control (Classical Stroop Task), or working memory (Self-Ordered Pointing Task). However, adolescents were more impulsive (Barrett Impulsiveness Scale) than adults and reported more enhancement motives. Importantly, impulsivity as well as social, coping, and enhancement motives of alcohol use correlated with alcohol use in both ages. However, age only moderated the relationship between social drinking motives and alcohol use-related problems (as measured by the Alcohol Use Disorder Identification Test), with a stronger positive association in adolescents compared to adults. Importantly, the adolescent group had a different pattern of drinking, with less drinking days per month but more drinks per episode than the adult group.

In summary, human evidence is largely missing, with no studies comparing more severe and dependent levels of alcohol use between adolescents and adults. The preliminary evidence is too weak and heterogeneous to draw conclusions, warranting future studies investigating the impact of age.

The current systematic review assessed the evidence for the moderating role of age in the effects of chronic alcohol use on the brain and cognition. The identified 59 rodent studies (Table 1 ) and 4 human studies (Table 2 ) provide initial evidence for the presence of age-related differences. Rodents exposed to ethanol during adolescence show both increased risk and resilience to the effects of ethanol depending on the outcome parameter. However, due to the high variability in the outcomes studied and the limited number of studies per outcome, conclusions should be considered preliminary. Moreover, brain and behavioral outcomes were mostly studied separately, with studies focusing on either brain or behavioral outcomes. The behavioral consequences of changes in certain brain outcomes still need to be investigated. Table 3 provides a comprehensive overview of the strength of the evidence for age-related differences for all outcomes. Below, we will discuss the most consistent patterns of results, make connections between the behavioral and neurobiological findings when possible, highlight strengths and limitations of the evidence base, and identify the most prominent research gaps.

Patterns of results

Age-related differences in learning and memory-related processes appear to be highly domain specific. There is limited but fairly consistent evidence for adolescent-specific impairments in contextual fear conditioning, which could be related to hippocampal dysfunction. Results for other hippocampus-related memory processes such as spatial memory are mixed and largely based on forced exposure with acute challenge studies rather than voluntary long-term exposure to alcohol. The evidence base is currently insufficient to draw conclusions about the role of age in alcohol’s effects on non-spatial types of learning and memory. Alcohol generally did not impact performance in the non-spatial variants of the MWM and SBM paradigms or in reward-learning, but the results of the limited studies in the object-learning domain highlight potential impairments and the importance of age therein. For example, adolescents but not adults demonstrated impaired object memory in the only study using the novel object recognition task [ 65 ]. Acute challenges after chronic pre-exposure to alcohol also appear to impair performance in the working memory domain, with one study suggesting heightened adolescent sensitivity to working memory impairment [ 83 ]. Thus, although the domain-specific evidence is limited by the relative lack of research, overall patterns suggest that learning and memory functions that are primarily hippocampus-dependent may be differentially affected by adolescent compared to adult alcohol use. Studies focusing on neural hippocampal processes corroborate these findings, reporting more extensive changes in protein expression [ 158 ], less desensitization of cFos upregulation [ 142 ], larger changes in GABAa receptor subunit expression [ 124 ], longer lasting changes in NMDA receptor expression [ 115 ], and larger reductions in neurogenesis [ 65 , 133 ] in the hippocampus of adolescent compared to adult ethanol-exposed rodents. On the other hand, ethanol-induced changes in the hippocampus recovered more quickly in younger animals after abstinence [ 150 ] and adolescent mice showed less signs of ethanol-induced neuroinflammation compared to adults [ 148 ].

Higher rates of adolescent alcohol use, especially binge drinking, may be facilitated by a heightened sensitivity to the rewarding properties of alcohol in combination with a reduced sensitivity to the negative effects of high doses [ 47 ]. In line with this, there is limited but consistent evidence that adolescents show less CTA in response to chronic ethanol and consequently voluntarily consume more ethanol [ 50 ]. Importantly, distinct vulnerability periods within adolescence for altered CTA may exist [ 168 , 169 ], with early adolescents potentially being least sensitive to aversive effects. Future studies using chronic exposure paradigms comparing different stages of adolescence to adults are needed. In contrast to CTA, there is insufficient evidence of age-related differences in the motivational value of alcohol based on CPP paradigms, with only one of five studies reporting stronger CPP in adolescents than adults [ 52 ]. Adolescents may be more sensitive to the effects of environmental factors on the motivational value of alcohol than adults, as adolescents housed in enriched environments acquired CPP while those in standard housing did not, an effect that was not found in adults [ 54 ]. Evidence for environmentally enriched housing being protective against these changes in adolescents provides an important indication that environmental factors matter and are important factors to consider in future research on the motivational value of ethanol on both the behavioral and neural level. Complementary studies on the functioning of brain regions within the mesolimbic dopamine pathway and PFC, which play an important role in motivated behavior, indicate limited but consistent evidence for age-related differences. Adolescents showed less dopamine reactivity in the PFC and NAc compared to adults after chronic ethanol exposure. Furthermore, there is limited but consistent evidence that adolescents are more vulnerable to epigenetic changes in the frontal cortex and reward-related areas after chronic ethanol exposure. For instance, adolescents may be more sensitive to histone acetylation of transcription factors in motivational circuits underlying the rewarding effects of alcohol [ 55 ], which may contribute to addictive behaviors [ 170 , 171 ]. Chronic alcohol use is also associated with lower BDNF levels in the PFC and subsequent increases in alcohol consumption, implicating BDNF as an important regulator of alcohol intake [ 172 ]. While evidence is limited, chronic alcohol use consistently reduced prefrontal BDNF in both age groups. However, the rate of recovery of BDNF levels after abstinence appears to be slower in adolescents.

Regarding executive functioning, there is limited but fairly consistent evidence from animal studies that adolescents are more vulnerable to long-term effects of chronic exposure on decision-making and are more impulsive than adults during acute intoxication and after prolonged abstinence following chronic exposure. Impulsivity is associated with functional alterations of the limbic cortico-striatal systems [ 91 ], with involvement of both the dopaminergic and serotonergic neurotransmitter systems [ 173 ]. While no studies investigating serotonergic activity were identified, the consistent reduction in dopamine reactivity observed in the PFC and NAc in adolescents compared to adults parallel the behavioral findings. There is also limited but fairly consistent evidence that adolescents are more resilient to impairments in cognitive flexibility than adults following chronic exposure to alcohol, and that adolescents may more easily regain control over their alcohol-seeking behavior than adults. These behavioral findings provide preliminary support for the paradox of adolescent risk and resilience in which adolescents are at once more at risk to develop harmful patterns of drinking, but are also more resilient in that they may be more equipped to flexibly change behavior and with time regain control over alcohol consumption. However, studies assessing processes that might be related to brain recovery provide little conclusive evidence for potential underlying mechanisms of these behavioral findings. While adolescents appear more vulnerable to ethanol-induced brain damage [ 131 , 132 ], show reduced neurogenesis [ 65 , 133 ], and show less changes in gene expression associated with brain recovery [ 65 , 133 ], adults show relatively higher immune responses after repeated ethanol exposure [ 147 , 148 ]. The limited evidence for adolescent resilience to alcohol’s effects on cognitive flexibility diverge from the conclusions of recent reviews that focused mostly on adolescent-specific research. Spear et al. [ 18 ] concluded that adolescents are more sensitive to impairments in cognitive flexibility; however, this was based on adolescent-only animal studies. Similarly, the systematic review of Carbia et al. [ 19 ] on the neuropsychological effects of binge drinking in adolescents and young adults also revealed impairments in executive functions, particularly inhibitory control. However, as pointed out by the authors, the lack of consideration of confounding variables (e.g., other drug use, psychiatric comorbidities, etc.) in the individual studies and the lack of prospective longitudinal studies limit our ability to causally interpret these results. This further highlights the difficulty of conducting human studies which elucidate causal associations of the effects of alcohol, and the need for animal research that directly compares adolescents to adults to bolster interpretation of findings from human research.

Only a few studies have investigated age-related differences in cognitive functioning in humans. These studies focused on mostly non-dependent users and studied different outcomes, including cognitive biases and implicit and explicit alcohol-related cognitions. Overall, there was limited but consistent evidence that age does not affect alcohol attentional or approach biases, with heavy drinkers in both age groups allocating more attention to alcohol cues compared to controls [ 163 , 165 ]. In contrast, in line with a recent meta-analysis of the neurocognitive profile of binge-drinkers aged 10–24 [ 23 ], there is limited evidence that age affects alcohol associations. One study found age effects on implicit (memory associations) and explicit (expectancies) cognition in relation to alcohol use. Adolescents showed stronger memory associations and more positive expectancies than adults [ 164 ]. These expectancies were also predictive of higher binge drinking in adolescents but not adults, highlighting the importance of future research into age differences in alcohol-related cognitions and their consequences on alcohol consumption. However, the quality of the evidence was rated as weak based on the methodological design of the included studies.

Regarding anxiety-related outcomes, results are inconsistent across studies and paradigms. When age-differences are observed, adolescents often show reduced anxiety compared to adults during both acute withdrawal and sustained abstinence following chronic ethanol exposure. However, the direction of age-related effects of alcohol may also be anxiety-domain specific. In social settings, adults show reduced anxiety compared to adolescents. Research on the neurocircuitry of anxiety processes implicates the extended amygdala, especially the BNST, in anxiety behaviors with an emphasis on the role of GABAergic projections to the limbic, hindbrain, and cortical structures in rodents [ 174 ]. Despite adolescents showing less non-social anxiety than adults after ethanol exposure, no age-differences were observed for LTP in the BNST [ 109 ]. Also, GABA receptor expression in the hippocampus and whole cortex was not altered by ethanol exposure in either age group [ 108 ]. However, the anxiolytic effects of NMDA antagonists [ 175 ] also highlight the importance of glutamatergic activity in anxiety processes [ 176 ]. In line with behavioral findings, adolescents were less sensitive to changes in glutamate expression: adults showed heightened expression in the NAc, which has been suggested to underlie the higher levels of anxiety observed in adults compared to adolescents [ 106 ]. Importantly, across the various studies, different paradigms were used to assess anxiety, potentially contributing to the inconsistent results. Furthermore, most of the identified studies used a forced ethanol exposure paradigm. As alcohol-induced anxiety is likely also dependent on individual trait anxiety, voluntary consumption studies in high and low trait anxiety animals are important to further our understanding of the interaction between alcohol use and anxiety. Of note, the observed pattern suggestive of reduced anxiety in adolescents compared to adults diverges from conclusions of previous reviews such as Spear et al. [ 18 ] which concluded that adolescents are more likely to show augmented anxiety after alcohol exposure based on animal studies with adolescent animals only. Importantly, anxiety was included as a secondary outcome in this review because of the high comorbidity between anxiety disorders and alcohol addiction, warranting the inclusion of age-related differences in the relation between alcohol and anxiety. However, the search strategy was not specifically tailored to capturing all studies assessing age-related differences in the effect of alcohol on anxiety.

Translational considerations, limitations, and future directions

The reviewed studies revealed a high degree of variability in study designs and outcomes, hindering integration and evaluation of research findings. We were unable to differentiate our conclusions based on drinking patterns (i.e., comparing binge drinking, heavy prolonged use, AUD). The prevalence of binge-drinking in adolescence is very high and is associated with neurocognitive alterations [ 177 ]. Studies investigating the potential differential impact of binge-drinking compared to non-binge-like heavy alcohol use in adolescence and adulthood are critical for understanding the risks of chronic binge-like exposure in adolescence, even if it does not progress to AUD.

It is also important to acknowledge the limitations of the choice of adolescent and adult age ranges in our inclusion criteria. Rodent studies had to include an adolescent group exposed to alcohol between the ages of PND 25–42 and an adult group exposed after age PND 65. Ontogenetic changes may still be occurring between PND 42–55, and this period may more closely correspond to late adolescence and emerging adulthood in humans (e.g., 18–25 years). Studies that compared animals in this post-pubertal but pre-adulthood age range were not reviewed. Studies investigating age-related differences in the effects of ethanol on brain and cognitive outcomes in emerging adulthood are also translationally valuable given the high rates and risky patterns of drinking observed during this developmental period [ 178 ]. Indeed, an important future direction is to examine whether there are distinct vulnerability periods within adolescence itself for the effects of ethanol on brain and cognitive outcomes. Given that emerging adulthood is a period of continued neurocognitive maturation and heightened neural plasticity, studies comparing this age range to older adults (e.g., over 30) are also necessary for a more thorough understanding of periods of risk and resilience to the effects of alcohol.

Furthermore, we did not conduct a risk of bias assessment to examine the methodological quality of the animal studies. The applicability and validity of the risk of bias tools for general animal intervention studies, such as the SYRCLE risk of bias tool [ 179 ], remain in question at the moment. The lack of standardized reporting in the literature for many of the criteria (e.g., process of randomizing animals into intervention groups) would lead to many studies being labeled with an ‘unclear risk of bias’. Furthermore, there is still a lack of empirical evidence regarding the impact of the criteria in these tools on bias [ 179 , 180 ]. This is a significant limitation in evaluating the strength of the evidence for age-related differences based on the animal studies, which highlights the importance of more rigorous reporting standards in animal studies.

Moreover, most work is done in male rodents and is based on forced ethanol exposure regimes. In a recent opinion article, Field and Kersbergen [ 181 ] question the usefulness of these types of animal models to further our understanding of human substance use disorders (SUD). They argue that animal research has failed to deliver effective SUD treatment and that social, cultural, and other environmental factors crucial to human SUD are difficult, if not impossible, to model in animals. While it is clear that more sophisticated multi-symptom models incorporating social factors are needed to further our understanding of SUD and AUD specifically, a translational approach is still crucial in the context of investigating the more fundamental impact of alcohol use on brain and cognition. In humans, comparing the impact of alcohol use on brain and cognition between adolescents and adults is complicated by associations between age and cumulative exposure to alcohol; i.e., the older the individual, the longer and higher the overall exposure to alcohol. Although animal models may be limited in their ability to model every symptom of AUD, they can still provide critical insights into causal mechanisms underlying AUD by allowing direct control over alcohol exposure and in-depth investigation of brain mechanisms.

The intermittent voluntary access protocol resembles the patterns of alcohol use observed in humans, and also result in physiologically relevant levels of alcohol intake [ 182 , 183 , 184 ]. Only a minority of the studies included in this review employed a voluntary access protocol, with one study using beer instead of ethanol in water [ 158 ], which better accounts for the involvement of additional factors (e.g., sugar, taste) in the appeal of human alcohol consumption. Voluntary access protocols can also model behavioral aspects of addictive behavior such as loss of control over substance use and relapse [ 185 , 186 , 187 ], an important area in which little is known about the role of age. Ideally, one would also investigate choices between ethanol and alternative reinforcers, such as food or social interaction, that better mimic human decision-making processes [ 188 ]. However, studies on the effects of ethanol on social behavior are limited and show inconsistent results and studies assessing reward processes often lack a social reward component as an alternative reinforcer.

On a practical level, rodents mature quickly and choice-based exposure paradigms are more complex and time-consuming than most forced exposure paradigms. Consequently, by the time final behavioral measurements are recorded, both the adolescent and adult exposure groups have reached adulthood. To combat this, many of the included studies use forced ethanol exposure, such as ethanol vapor, to quickly expose rodents to very high doses of ethanol. Although the means and degrees of alcohol exposure may not directly translate to human patterns of alcohol use, such studies do allow for the assessment of the impact of high cumulative doses of ethanol within a relatively short period of time which allows for more time in the developmental window to test age-related differences in the outcomes. When considering the translational value of a study, it is therefore important to evaluate studies based on the goal, while not ignoring the practical constraints.

While human research is challenging due to the lack of experimental control and the inherent confounds in observational studies between age and alcohol exposure history, large-scale prospective longitudinal studies offer a gateway towards a better understanding. Comparisons of different trajectories of drinking from adolescence to adulthood (i.e., heavy drinking to light drinking, light drinking to heavy drinking, continuously heavy drinking, and continuously light drinking) could offer insight into the associated effects on cognitive and brain-related outcomes. Of course, different drinking trajectories are likely confounded with potentially relevant covariates which limits causal inference. Direct comparisons of low and heavy adolescent and adult drinkers, supported by a parallel animal model can help to bolster the causality of observed age-related differences in human studies. In addition, changes in legislation around the minimum age for alcohol consumption in some countries provide a unique opportunity to investigate how delaying alcohol use to later in adolescence or even young adulthood impacts cognitive functioning over time. Importantly, future studies investigating the moderating role of age in humans should carefully consider the impact of psychiatric comorbidities. While adolescence into young adulthood is the period in which mental health issues often emerge [ 189 , 190 ], there is some evidence that the prevalence of comorbidities is higher in adults with AUD [ 95 ]. This is an important to control for when considering age-related differences on cognition and the brain given the evidence of altered cognitive functioning in other common mental illnesses [ 191 , 192 ].

Concluding remarks

The aim of this systematic review was to extend our understanding of adolescent risk and resilience to the effects of alcohol on brain and cognitive outcomes compared to adults. In comparison to recent existing reviews on the impact of alcohol on the adolescent brain and cognition [ 17 , 18 , 19 , 22 , 23 ], a strength of the current review is the direct comparison of the effects of chronic alcohol exposure during adolescence versus adulthood. This approach allows us to uncover both similarities and differences in the processes underlying alcohol use and dependence between adolescents and adults. However, due to the large degree of heterogeneity in the studies included in sample, designs, and outcomes, we were unable to perform meta-analytic synthesis techniques.

In conclusion, while the identified studies used varying paradigms and outcomes, key patterns of results emerged indicating a complex role of age, with evidence pointing towards both adolescent vulnerability and resilience. The evidence suggests adolescents may be more vulnerable than adults in domains that may promote heavy and binge drinking, including reduced sensitivity to aversive effects of high alcohol dosages, reduced dopaminergic neurotransmission in the NAc and PFC, greater neurodegeneration and impaired neurogenesis, and other neuromodulatory processes. At the same time, adolescents may be more resilient than adults to alcohol-induced impairments in domains which may promote recovery from heavy drinking, such as cognitive flexibility. However, in most domains, the evidence was too limited or inconsistent to draw clear conclusions. Importantly, human studies directly comparing adolescents and adults are largely missing. Recent reviews of longitudinal human research in adolescents, however, revealed consistent evidence of alterations to gray matter, and to a lesser extent white matter, structure in drinkers [ 17 , 18 ], but also highlight the limited evidence available in the domains of neural and cognitive functioning in humans [ 17 ]. Future results from ongoing large-scale longitudinal neuroimaging studies like the ABCD study [ 193 ] will likely shed valuable light on the impact of alcohol use on the adolescent brain. However, our results also stress the need for direct comparisons with adult populations. Moreover, while the lack of experimental control and methodological constraints limit interpretations and causal attributions in human research, translational work aimed at connecting findings from animal models to humans is necessary to build upon the current knowledge base. Furthermore, the use of voluntary self-administration paradigms and incorporation of individual differences and environmental contexts are important steps forward in improving the validity of animal models of alcohol use and related problems. A more informed understanding of the effects of alcohol on adolescents compared to adults can further prevention efforts and better inform policy efforts aimed at minimizing harm during a crucial period for both social and cognitive development.

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This work was supported by grant 1RO1 DA042490-01A1 awarded to Janna Cousijn and Francesca Filbey from the National Institute on Drug Abuse/National Institutes of Health. The grant supported the salaries of authors Lauren Kuhns, Emese Kroon, and Janna Cousijn. Thank you to Claire Gorey (CG) for running the initial search and aiding in the screening process.

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Kuhns, L., Kroon, E., Lesscher, H. et al. Age-related differences in the effect of chronic alcohol on cognition and the brain: a systematic review. Transl Psychiatry 12 , 345 (2022). https://doi.org/10.1038/s41398-022-02100-y

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Drinking Age: Facts and Resources

There’s a lot of misinformation about the drinking age and it can be difficult to know what the facts are. For this reason, we’ve put together a list of talking points and references that you can use whether you are talking to your friends and family or your local legislator. We’ve also summarized some of the research that supports a lower drinking age or those who want a more in-depth analysis. And be sure to check out our Top Ten Reasons to Challenge the Drinking Age as well!

Drinking is less dangerous than other activities that you can do at 18.

• At 18, you can join the military, get married and raise a family, purchase a firearm, and serve on a jury—all of which require a significant amount of risk or responsibility. Strangely, though, alcohol is held to a different standard. Drinking alcohol is a serious activity, not to be engaged in without thought, but requiring a higher age to drink legally than activities that are either more dangerous or have a bigger impact on other people’s lives doesn’t make any sense.
• Tobacco is usually legal at 18 , though many states have moved to raise it to 21 , the same as the drinking age. However, smoking tobacco is still much more dangerous. Nicotine is arguably the most addictive drug people use. According to the CDC , smoking kills 1.3% of the smoking population each year. This makes tobacco over 20 times as deadly as alcohol , which only kills about 0.063% of the drinking population a year according to the CDC.
• Having sex requires far more physical and emotional maturity than drinking alcohol. Although the risks of sex do not primarily lie in the deaths it causes, sex does kill 36,000 people a year through STDs (and another 400 through pregnancy complications).
• Military service is more dangerous than drinking. Military service kills around  0.1% of the active duty population per year. This makes military service about 1.5 times as deadly as alcohol. And this is not even during a draft or a major war. During the Vietnam Era, the military death rate was 0.64% — 10 times as deadly as alcohol (By the way, 61% of Vietnam deaths were soldiers younger than 21).
• Your first sip of alcohol cannot possibly kill you , and is unlikely even to get you drunk. However, your first tour of duty in the military, your first week of basic training , or even your first time firing a gun, can kill you.
• It is possible to stop drinking whenever you want to . This comes in very useful when the situation begins to feel unsafe. However, it is not possible to stop serving in the military or stop being a parent whenever you want to, even if you feel you can’t handle the risk or the responsibility. Alcohol does not have this problem. We would never put someone in a situation where they had to keep drinking, and could not stop even when people’s lives were in danger.

We didn’t need to raise the drinking age in order to reduce the number of alcohol-related traffic deaths.

• The law did not prevent traffic deaths, it only delayed them. In an unrefuted study , Peter Asch and David Levy showed that raising the drinking age merely transferred drunk driving deaths from the 18-20 age group to the 21-24 age group. They argued that the problem with saying that the drinking age has saved lives is that it looks only at deaths for people aged 18-20. Raising the drinking age may have reduced deaths among people 18-20 but resulted in more deaths among people 21-24. This suggests that the real risk factor for drinking and driving is being an inexperienced drinker , regardless of age. If 18-year-olds have just started drinking, a disproportionate number will die from drunk driving. The same thing is true of 21-year-olds. The researchers wrote , “…it seems clear that the means by which we now make alcoholic beverages available to the young—proscribing consumption up to an arbitrarily specified age, and allowing it from that moment on—is a policy of little use in promoting highway safety.”
• Drunk driving was decreasing among all age groups before the National Minimum Drinking Age Act was fully implemented. The National Highway Traffic Safety Administration has shown that between 1982 and 1987 there was a reduction in the number of accidents related to intoxicated drivers. The number of alcohol-related accidents was already dropping before the age restriction laws were in place.
• Drunk driving decreased in places with that didn’t increase the drinking age.  According to the US Department of Transportation, Canada experienced almost the exact same reduction as the United States during the 1980s, without raising their drinking ages (18-19). This reduction in drunk driving also happened in states that have had a drinking age of 21 since the end of Prohibition. Raising the drinking age alone didn’t make a difference.
• The maximum Blood Alcohol Content level was lowered for everyone. Beginning in the 1970s and accelerating in the 1980s , states began lowering their legal maximum blood alcohol content for drivers, usually to 0.08%. Before this, the standard legal BAC was 0.1%, or even 0.15% . This new policy decreased the acceptable level of drunkenness for drivers, serving as a new deterrent for drunk driving among all age groups.
• Drunk driving became less socially acceptable . Organizations such as MADD caused a nationwide change in public opinion. Whereas previously, society had accepted drunk driving as a part of life, in the 1980s, people began to vilify drunk drivers . This could easily have deterred many people—including many young people—from drunk driving.
• It was a different generation. The people in their late teens and early 20s in the 1980s were the last members of the Baby Boom generation, and the earliest members of Generation X . The decrease in drunk driving was one of the many profound cultural changes that marked the transition from one generation to the next. These changes were already taking place before the drinking age was raised.

Other groups of people have a higher risk for alcohol problems, but their use is not restricted.

• Alcohol has many other risk groups that are not prohibited from drinking , including people with a history of alcoholism, pregnant women, and people previously convicted of alcohol-related crimes such as drunk driving, child abuse, and sexual assault. And yet aside from people under 21, all risk groups are allowed to drink. For example, let’s look at male drinkers.
• Me n are a far more serious risk group than people under 21 . They are 3 times as likely as women to die from alcohol , engage in drunk driving, reckless driving and commit seat belt violations . They are also twice as likely to be admitted to substance abuse treatment programs .
• Banning men from drinking could save lives. If the drinking age is supposed to save 900 lives a year, then by this same logic a law against men drinking would save far more lives. Like the drinking age, such a law would be hard to enforce. But if the government put the same amount of effort into enforcing restrictions on men’s drinking as it does into enforcing the drinking age, it would have a similar effect.
• The following chart shows the life-saving potential of a restriction on men’s drinking , if it had the same success rate people attribute to the restriction on underage drinking. Even if this policy had the same low success rate as the drinking age, it could save over 2 times as many lives on roads alone.

Numbers without a source are obtained by calculation.

• This is true even if we take different population sizes into account . Men make up about 50% of the population , whereas underage people make up about 25% of the population . This means that with a basic correction for population size, a law targeting men’s drinking would still save just as many lives per capita as our current law targeting underage drinking.

Countries with lower drinking ages have fewer alcohol-related problems.

• No other country has a higher drinking age. Other than the US, the only countries with a national minimum drinking age of 21 are Egypt, Indonesia, Kazakhstan, Oman, Sri Lanka, and Tonga. It is unusual for a country that prides itself on freedom and personal responsibility to be such an outlier.
• Australia, Canada, and New Zealand have nearly a mirror image history when it comes to alcohol . These countries also went through a Prohibition period and later set their drinking age at 21, which was the age of majority at the time. In the 1970s, like the United States, these countries lowered their drinking age as the age of majority was lowered to 18. These countries also have very similar stances on public health and safety, especially due to their high dependency on automobiles just like the United States, but never raised their drinking ages to 21. How can these countries, with their high standard of public safety and well-being, be able to consistently hold a drinking age of 18 or 19, and the United States cannot?
• Legal status of alcohol does not determine rates of liver cirrhosis deaths. Countries with more severe alcohol prohibition than the US have higher rates of death from liver cirrhosis —one of the main long-term consequences of alcohol use—than we do. These countries include Pakistan, Afghanistan, and India . Meanwhile, many countries across the world with easier access to alcohol than the US, such as Spain, Australia, Colombia, Japan, and Sweden, have lower rates of liver cirrhosis than we do.

Drunk driving is a serious problem – but not predominantly related to underage drinking.

• Many young people don’t drive. About 25% of people aged 18-21 do not have driver’s licenses, let alone cars (compared to 13% of the general population). An even larger number have licenses, but either choose not to drive or do not have opportunities to drive. This means that the drunk driving argument for the drinking age does not even apply to at least a quarter of the population aged 18-21.
• The law makes it easier to convict young people of DUI. For people over 21, getting convicted of DUI means they were driving drunk (BAC over 0.08%). But for people under 21, DUI only means that they had a measurable amount of alcohol in their blood (BAC over 0.00% or 0.02%). Many teenagers charged with DUI were arrested not because they were actually driving drunk, but because of their age.
• Alcohol-related does not mean alcohol-caused. We often hear this statistic : “Although drivers under the age of 21 represent 10 percent of licensed drivers they are responsible for 17 percent of fatal alcohol-related crashes.” But, “alcohol-related” does not mean “alcohol-caused.” In fact, in any number of these cases, it is possible that the driver was not drinking at all – accidents are classified as “alcohol-related” ”if at least one driver or nonoccupant (such as a pedestrian or pedalcyclist) involved in the crash is determined to have had a blood alcohol concentration (BAC) of .01 gram per deciliter (g/dL) or higher.” This way of classifying alcohol-related traffic accidents completely skews the results.

There are many negative consequences of current drinking age.

• In many states, ANY consumption of alcohol can result in fines from $100 to $1000, probation, and suspension of driver’s license, regardless of the case. Many states will also require an alcohol and drug educational program, substance abuse prevention, diversion, and/or restitution. In 23 states, jail time can result from any under 21 drinking, from a few days to a year.
• In New York , licensees charged with sale to minors face penalties of up to $10,000 per violation, with fines starting from $2,500 to $3,000 for the first time offense. Anyone under 21 found to be using fake IDs or false documents can have their licenses revoked for a minimum of 90 days or up to one year.
• Some places are actually increasing penalties for underage drinking , such as Pennsylvania and the city of Miami . If we think punishment is the answer to underage drinking and the earlier you start drinking, the more dangerous it is, why are we punishing 20 year olds more severely that 17 year olds? In the state of Rhode Island, those aged 18-21 face the most serious repercussions for underage drinking (compared to those under 18).
• If people are allowed to gather together at a bar, bartenders can stop serving drunken patrons , call cabs, and make sure there are “designated drivers.”
• In addition, the high legal age here in the US has many of the same effects as Prohibition, including increased over-indulgence, anti-social behavior, drinking in secret. “For an entire class of people, it’s the Roaring Twenties all over again .”
• The drinking age implements a system of segregation. When going out with friends the drinking age drives a wedge between friends over and under 21. Often they are unable to hang out at the same places. It also does not make sense for adults to be denied entrance to establishments that serve alcohol, be denied employment in a variety of industries and venues, or suffer under a system of segregation that treats them as second-class citizens. Adults under 21 are segregated, sometimes prohibited entirely from bars, nightclubs, certain restaurants, and liquor stores. The drinking age takes economic opportunities away from young people.
• The drinking age affects the jobs that younger people can get. In 2014, the alcoholic beverage industry accounted for $450 billion in total U.S. economic activity , $110 billion in wages, and nearly 4.6 million jobs for U.S. workers. There are over 600,000 bartenders in the country, earning a median income of $20,800 yearly, not including tips. And yet in many states, those under 21 can’t bartend . Small businesses that produce alcohol are a growing trend among millennials . However, those aged 18-20 either can’t partake in this popular venture or be an equal counterpart in the industry.
• Young people are punished just for trying to lessen the potential damage of drinking. People under 21 who try to serve as designated drivers can be charged merely for being at a party where alcohol is served. Taxi services that give free rides to prevent drunk driving during the holidays ban young people from using their services.

The drinking age prevents parents from teaching healthy drinking habits.

• At age 18, young people are more likely to be living at home, where parents can set a good example for moderate use . By the age of 21, people are are more likely to be living on their own and are less likely to have role models to demonstrate moderate drinking habits. This can  lead to excessive binge drinking, which is most predominant among individuals below the legal age.
• Adults who supervise a party with alcohol to prevent drunk driving can be charged for allowing other people’s children to drink in their homes. Parents can face extremely harsh consequences such as jail time or losing custody of their children, their job, or professional license.

The National Minimum Drinking Age Act (NMDAA) may not even be legal.

• The Supreme Court of Louisiana ruled the drinking age of 21 violated the Louisiana Constitution. In the case of Manuel v. Louisiana (Louisiana Supreme Court, 1996) , the court decided that a drinking age of 21 “discriminates on the basis of age” and it wasn’t until the court faced pressure from advocacy groups and the federal government that the court reversed this decision.
• The federal government forced states to raise their drinking age by threatening to cut their federal funding. Congress threatened to withhold federal highway funding from states unless they raised their state drinking ages to 21.
• There are limits on how much the federal government can use removal of funds to coerce states into action . In National Federation Of Independent Business et al. v. Sebelius (U.S.Supreme Court, 2012) , the Supreme Court concluded that the federal government cannot threaten to withhold Medicaid funding from states that do not comply with the Affordable Care Act. According to the Court, the main difference between the Affordable Care Act (ruled coercive) and the NMDAA (ruled not coercive) was the amount of money Congress threatened to take away from states.
• The legal drinking age has nothing to do with highway safety . Justice O’Connor: “the establishment of a minimum drinking of 21 is not sufficiently related to interstate highway construction to justify so conditioning funds appropriated for that purpose.”
• The drinking age law doesn’t address the problem of drunk-driving and it unnecessarily curtails the rights of some people. Justice O’Connor: “…if the purpose of [the drinking age act] is to deter drunken driving, it is far too over- and under-inclusive. It is over-inclusive because it stops teenagers from drinking even when they are not about to drive on interstate highways. It is under-inclusive because teenagers pose only a small part of the drunken driving problem in this Nation.”
• The Twenty-first Amendment gave states, not the federal government, the right to regulate alcohol sales. O’Connor defined the NMDAA as “an attempt to regulate the sale of liquor, an attempt that lies outside Congress’ power to regulate commerce because it falls within the ambit of 2 of the Twenty-first Amendment.”
• Congress cannot “impose or change regulations in other areas of the State’s social and economic life because of an attenuated or tangential relationship to highway use or safety.”

List of of people and organizations that are critical of the current drinking age

Organizations.

Amethyst Initiative

Choose Responsibility

Youth for Colorado

Mary Kate Cary , former White House speechwriter and political commentator

Pete Coors , former chairman of Coors Brewing Company

David J. Hanson, Ph.D , Professor Emeritus of Sociology of the SUNY Potsdam

Gary Johnson , former Libertarian Presidential candidate and governor of New Mexico

John McCardell , former President of Middlebury, founder of Choose Responsibility

Jeffrey Miron , Professor, Harvard University

Papers and Reports

• Does the Minimum Drinking Age Affect Traffic Fatalities? Economists Peter Asch and David Levy studied the incidents of traffic fatalities after the minimum drinking age was raised and concluded that the legal drinking age had “no perceptible influence on fatalities.” A summary of this study is available here .
• Does the Minimum Legal Drinking Age Save Lives? Harvard professor Jeffrey A. Miron and attorney Elina Tetelbaum argue against a drinking age of 21 and show that it “fails to have the fatality-reducing effects” that other papers have reported.
• The Minimum Purchase Age for Alcohol and Young-Driver Fatal Crashes: A Long-Term View Sociologist Mike Males takes a critical look at the National Minimum Drinking Age Act by pointing out to the flaws in research that suggested that raising the drinking age would decrease drunk driving incidents.
• The true effect of MLDA reform: An analysis of the mortality displacement in youth traffic accidents caused  by the drinking age reform of the 1980s This paper looks at the differing points of view over the effectiveness of the 21 drinking age.
• Young Driver Fatalities: The Roles of Drinking Age and Drinking Experience Economists Peter Asch and David Levy take another look at the extent to which age is a factor in drunk driving incidents. They argue that the safety effects of raising the drinking age are overstated and therefore focusing on a higher drinking age is misdirected and that it would be better to focus on alcohol consumption more generally.

“It is the single most regrettable decision of my entire professional career.” – Dr. Morris Chafetz , appointee to the Presidential Commission on Drunk Driving who helped to raise the drinking age.

“Prohibition… goes beyond the bounds of reason in that it attempts to control a man’s appetite by legislation and makes a crime out of things that are not crimes… A prohibition law strikes a blow at the very principles upon which our government was founded.” – Abraham Lincoln

Related Pages

Drinking Age

Reasons to Challenge the Drinking Age

Solutions and Alternatives to the Drinking Age

State Guide to Drinking Age Law

The National Minimum Drinking Age Act

Start a Chapter

Death at TRAILS Carolina Wilderness & Media Response

Gavin Newsom Won on Youth Rights

A Youth Rights Lesson from Superbad

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Events, news & press, underage drinking and the drinking age.

The Amethyst Initiative’s harmful remedy

T he problem of underage drinking on college campuses has been brewing for many years to the continued vexation of higher education administrators. In 2008 , John McCardell, president emeritus of Middlebury College, began to circulate for signature a public statement among colleagues titled “The Amethyst Initiative,” 1 which calls for elected officials to reexamine underage drinking laws. The project grew out of outreach efforts of a nonprofit organization he founded in 2007 called Choose Responsibility. The nonprofit advocates lowering the drinking age to 18 and licensing alcohol use for young people in much the same manner as driving — following coursework and an exam. Choose Responsibility also favors the repeal of the laws that set 21 as the mandatory minimum age for drinking (known as the “ 21 laws”) and encourages states at the least to adopt exceptions to the 21  laws that would allow minors to drink at home and in private clubs. It also favors social changes that shift the focus on alcohol use among youth to the home, family, and individual.

The Amethyst Initiative’s statement has been signed by 135 college presidents and chancellors at schools from Duke to Bennington. The majority is private; most are in the Northeast. The statement takes no formal position, unlike Choose Responsibility. It does, however, drop heavy hints as to where the debate ought to come out. The statement says “ 21 is not working” and asks “How many times must we relearn the lessons of Prohibition?” It draws comparisons to other age-of-majority rights conferred on 18 -year-olds, such as voting and serving in the military, and calls upon elected officials to consider “whether current public policies are in line with current realities.”

It seems that the presidents of 135 colleges, including elite schools, large universities, and small state schools find themselves so exasperated with the amount of alcohol guzzled by undergraduates — or more to the point, the trouble the undergraduates get into while inebriated — that they now beseech lawmakers to “rethink 21 ,” an elegant and rather roundabout way of saying: Let undergrads drink with the sanction of the law.

The primary argument made in the Initiative’s statement in favor of repealing the 21 laws is that the 21 laws make alcohol taboo, thus driving underage drinking underground and causing more binge drinking to take place than otherwise would, due to the allure of forbidden fruit and the need for secrecy. Hence, by lowering the drinking age, youth consumption would come out in the open and binge drinking would be largely reduced or even eliminated. The second salutary effect of lowering the drinking age, the Initiative argues, would be educational: Colleges would be allowed to have open, frank discussions about responsible drinking. In other words, institutions of higher education could teach young people how to drink responsibly. The Initiative makes vague references to the “unintended consequences” of 21 “posing increasing risks to young people,” and says that the original impetus for the 21  laws — reduction of highway fatalities by young drivers — has outlived its usefulness.

Since its launch, the Initiative has created a public dialog about the drinking age, resulting in media coverage and a hearing before the New Jersey state legislature in November 2008 . Despite its gravity as a public health problem, even among children younger than 18 , the topic of underage alcohol abuse has been underaddressed in the popular media and in public funding compared to illicit drug abuse. The Initiative is a welcome development insofar as it challenges us to examine whether 21 “is working.” The answer: It is not, as currently enforced. So should 21 be scrapped or salvaged? First, a look at how we got here, and why the 21  laws are broken.  

The 21 laws

A mericans generally have not allowed young people to drink. Older teens were allowed to drink legally during part of the 1970 s and early 1980 s — a blip on the American-history radar screen. Here is how it happened.

During the 19 th century, cultural and social norms prevented young people from drinking. The expense and limited availability of liquor also helped keep it out of youthful hands. After Prohibition, it was left up to the states to regulate alcohol, and most states made the legal drinking age 21 , the same as the age for voting and other adult rights. The issue remained largely untouched until the late 1960 s when protests over the Vietnam War raised the question of the national voting age. For the first time, the question of the draft age and the voting age were linked in the popular imagination, at least among the left. “If a boy is old enough to fight and die for his country, why isn’t he old enough to vote?” was the popular refrain.

The legal drinking age got swept up in the political upheaval of the era, as states generally reexamined their age-of-majority laws. Between 1970 and 1976 , 29 states lowered their age for drinking alcohol. The results were catastrophic. Highway deaths among teenagers and young adults skyrocketed. Almost immediately, states began raising the minimum drinking age again — years before Congress in 1982 and 1984 dangled the carrot of federal highway monies as an incentive. Between 1976 and 1984 , 24 of the 29 states raised the age back up again. By 1984 , only three states allowed 18 -year-olds to drink. Five states and the District of Columbia regulated various degrees of alcohol consumption among those 18 and over. The remaining states had a patchwork of minimum ages ranging from 19 to 21 . 2

While states experimented with age-of-majority laws, a cultural shift was taking place in how society regarded drunk driving. In 1980 , a 13 -year-old California girl named Cari Lightner was walking to a carnival when she was struck by a hit-and-run drunk driver and killed instantly. Her mother became enraged when she learned that drunk driving was not treated seriously in the American judicial system. What followed was one of the great stories of American grassroots activism. Together with a friend, Candace Lightner founded Mothers Against Drunk Driving ( madd ), which quickly garnered local and later national support in a campaign that focused on putting a human face on the damage done by drunk drivers. By 1982 , with madd 100 -chapters strong, President Reagan created a presidential commission to study drunk driving and Congress authorized highway funds to states that passed stiffer drunk driving laws. In 1984 , Congress passed the Uniform Drinking Age Act, which required states to have a minimum drinking age of 21 < for all types of alcohol consumption if they wanted to receive federal highway monies. The legal drinking age has stayed at 21  since then.

In most of the television debates about the Amethyst Initiative, the success or failure of 21 has been primarily linked to the issue of highway deaths, with the debaters arguing fatality statistics to prove whether the 21 laws should be shelved because of the advent of safer cars. But that suggests, wrongly, that the debate largely begins and ends with the question of teenage bodies splattered across the interstates. While drunk driving among underage drinkers remains a problem, unfortunately it is only one of several ways that underage drinking threatens young people. Time has not stood still since 1984 . American campuses and drinking patterns have changed, and not for the better.

Binge drinking

T he logic of the Initiative is that if we take away the allure of illegality, American youth will stop binging. That conclusion is wrong. Alcohol should be forbidden to 18 - to 20 -year-olds precisely because they have a propensity  to binge drink whether the stuff is illegal or not — especially males.

Henry Wechsler and Toben F. Nelson, in the landmark Harvard School of Public Health College Alcohol Study, or cas , which tracked college student drinking patterns from 1992 to 2001 , explained that binge drinking is five or more drinks on one occasion. Binge drinking brings the blood alcohol concentration to 0.08 gram percent or above (typically five drinks for a man or four for a woman within two hours). To understand just how drunk that makes a person, consider that it violates criminal laws to drive with a blood alcohol level of 0.08  gram percent or above.

To call alcohol taboo implies that drinking is done in secret and rarely. Yet college drinking is so common as to have lost all tinge of intrigue. Drinking greases the social wheels, and college life for many is saturated with popular drinking games that no doubt seem brilliant to the late-adolescent: Beerchesi, Beergammon, BeerSoftball, coin games like Psycho, Quarters, and BeerBattleship, and card and dice games linked to beer.

When undergraduates binge drink, they get into trouble — a lot of it. They endanger and sometimes kill their fellow students by setting fires. 3 They sexually assault their female companions (approximately 100,000 incidents annually). They get into fights with other young undergrads (some 700,000 assaults annually). On average 1,100 a year die from alcohol-related traffic crashes and another 300 die in nontraffic alcohol-related deaths. According to the cas , among the 8 million college students in the United States surveyed in one study year, more than 2 million drove under the influence of alcohol and more than 3 million rode in cars with drivers who had been drinking. Eight percent of students — 474,000 — have unprotected consensual sex each year because they have been drinking. 4  In short, college students do stupid, illegal, dangerous, and sometimes deadly things when they drink.

Moreover, the drinking doesn’t begin in college. More kids drink alcohol than smoke pot, which is the most commonly used illicit drug. A third of our youth taste their first drink before the age of 13 and have drinking patterns as early as 8 th to 10 th grade. In a pattern that continues in college, boys fall into binge drinking patterns in greater numbers than girls by 12 th grade. 5 The Pacific Institute for Research and Evaluation has estimated the social cost of underage drinking (for all youth) at some $ 53  billion. That includes only highway deaths and injuries and does not factor in brain damage associated with early adolescent drinking, or the array of other injuries and social problems such as opportunity costs that crop up when children drink.

The majority of those who binge drink in college started down that road long before they matriculated — they simply continue their drinking habits once they arrive on campus. Brett Sokolow, president of the consulting firm National Center for Higher Education Risk Management ( ncherm ), which counsels colleges on reducing “risk” through educational programs and institutional policies, said in an interview that based on his anecdotal experience, 60 to 70 percent of the students attending his on-campus alcohol seminars have had drinking experiences prior to attending college and about 40  percent have “deeply engrained drinking habits” by the time they get to college.

Consider the scope of college drinking. Among the general population in America, 15 percent of 18 - to 25 -year-olds binge drink, according to the Centers for Disease Control. Among college students, 80 percent reported drinking and of those, 40 percent binge drink once a month — that is more than twice the rate of their peers in the general population. 6 About one fourth drank in this way frequently — three or more times in a two week period. 7

If college life, with its basic structure and lack of privacy, forces drinking underground as the Amethyst Initiative posits, then one should see far less binge drinking among youth who are not in college. A study drawn on data from the National Household Survey on Drug Abuse, which looked at heavy episodic drinking among all 18 - to 24 -year-olds, comparing those in college to those outside the ivy-covered walls, does not bear out the Initiative’s theory. While 41 percent of those in college binge drank at least once a month, according to that study, so did 36  percent of other youth. And as we shall see, in the military and in countries where they may drink legally, the young guzzle apace.

U.S. military

T he initiative, as  well as students arguing in favor of the right to go to keggers, invoke the plight of the parched soldier — old enough to die for his country but not allowed to have a beer. The cascading images on Choose Responsibility’s Web site even include the wordless image of a young soldier.

Reality check: The U.S. Department of Defense takes substance abuse among military personnel very seriously and has been addressing drug and alcohol issues for many years. While it has made great progress against illicit drugs, it has found alcohol more intractable. dod devotes substantial resources to counseling and prevention programs. Heavy alcohol use is regarded as a drain on morale and productivity and a potential threat to unit readiness. dod in 2005  undertook a comprehensive study of health-related behaviors among active-duty military personnel that compared alcohol use among men and women in the four branches of the service and the civilian population.

It found high rates of binge drinking among young service members, especially men aged 18 to 25 . Binge drinking was especially high in the Army and the Marines, where binge drinking rates of young men were similar to those of male college students. The consequences of heavy alcohol use in the military can be severe, including being passed over for promotion and punishment under the Uniform Code of Military Justice.

Not all military drinking by young men and women is illegal, depending on where soldiers and sailors are stationed. Under federal law, military personnel must comply with the law of the jurisdiction in which their installation is located. Contrary to the lure-of-the-illicit theory, the dod study showed that soldiers drink more when it is legal . Among the entire military (all ages), 15 percent are heavy users of alcohol in the continental United States, while outside the United States, 25  percent are heavy users. The study found that one of the factors that made binge drinking less likely was being located in the United States.

This throws into doubt two fundamental assumptions of the Initiative: that young people drink because of the allure of forbidden fruit; and that enforcement does not work. Young men in the military, who clearly have a very strong propensity to drink, do less of it when stationed in the United States. While one can surmise that some of the decrease could be due to lower levels of stress, it is a comparison that bears further inquiry. There is something about young males being grouped together in bonding experiences, whether in college or in the military, that seems to lend itself to heavy drinking.  

The military experience of lower drinking levels in the U.S. could also mean that factors such as enforcement, fear of consequences, and difficulty in obtaining alcohol influences the amount of binge drinking. The Air Force has the lowest rate of binge drinking among the service branches and the Navy has made an effort to change the culture of sailors on liberty engaging in binge drinking. Clearly, drinking is influenced by organizational culture. The cas study came to similar conclusions: It found that drinking cultures differ among schools and states, sometimes depending on the level of binge drinking among adults  and the type of enforcement in the state. The environment in which young people are placed and the adult support systems and level of enforcement count.

Other settings bear comparison. American students studying abroad in France or Italy notice that college students there don’t drink like fish, and assume that is the case among young people everywhere in Europe. While many Americans cling to the belief that Europeans are better than us, studies of drinking habits across all of Europe show that their binge drinking problems are worse than ours in many countries, start at younger ages, and continue into adulthood.

The legal drinking ages in Europe generally range from 16 to 18 with varying rules as to when youth may purchase and consume alcohol. Serious binge drinking begins at age 15 in countries across the European Union. The highest rates are seen in the Nordic countries, Slovenia, Latvia, the uk , and Ireland. 8 Young teenagers, 15 - to 16 -year-olds, are drinking six drinks at a clip when they go out (even more in the uk and Ireland), and 18 percent of that age group is binge drinking three times a month. Things aren’t much better south of the equator. When New Zealand lowered its drinking age to 18 it experienced a “sharp increase in binge drinking among teenagers and young adults.” 9

The alcohol-sex cocktail

M an does not  live by drink alone. There is something else college students, far from the confines of home, like to do: have sex. And when we consider that the vast majority of binge drinkers are male and then factor in their role as the initiator in sexual adventures, the role of sex drive in campus alcohol abuse becomes clearer.

One of the results of the fall of in loco parentis in the early 1970 s was the rise of the ivory-towered Sodom and Gomorrah. Mind you, today we are not talking about dating as the Baby Boomer generation understands it. We are talking about “hooking up.” That means young people go out in groups and then pair off, have casual sex, and quite possibly never get together again. Alcohol, sadly, is directly linked to the hookup culture. It fuels casual and often dangerous sexual encounters on campuses. (The danger lies in unprotected sex and date rape.)

It’s important to think about the hookup culture as we weigh whether lowering the drinking age, coupled with education and licensing, would work. Picture this: A 19 -year-old male has heard the lectures and has an alcohol license in his hip pocket. Yet he knows that plying himself and his female companions with beer will vastly increase his chances that the evening will end with a hookup. Oh, and he’s at a bar selling 25 -cent beer pitchers. Care to wager how that night will turn out?

Brett Sokolow of ncherm said in an interview that the alcohol-related campus workshops he conducts grew out of sexual assault presentations he has done. In speaking with students and exploring how assault situations arose, he found that alcohol played an integral role. His anecdotal observations of the connection between alcohol and problematic sexual encounters on campus are reflected in research in the field. In 2001 , 474,000 college students had unprotected sexual intercourse as a result of their drinking. In the same year, more than 696,000 reported being assaulted or hit by another drinking student and of those episodes, 97,000 were alcohol-related sexual assault or date rape victims. 10

Sexual misconduct hearings are now “no longer rare occurrences on many college campuses,” Sokolow wrote in a white paper. The paper (available on the ncherm  website) provides painstaking guidelines for college administrators to follow in conducting disciplinary hearings to determine if the victim of an alleged assault was truly “incapacitated” or just plain “drunk,” “under the influence,” “intoxicated,” or “inebriated.” Parsing such terms is a job skill for today’s college administrator, since only “incapacitation” renders a victim unable to give consent to a sexual encounter.

Just another privilege?

T he initiative takes pains to refer to college students as “adults,” and argues that the 21 laws should be brought “into sync” with age-of-majority rights such as voting, military service, or contract. These are not apt comparisons because the basis of those rights is the doctrine of emancipation. Given the grave consequences of underage alcohol consumption, the legal test for emancipation is helpful in thinking about whether the typical American 18 -year-old is mature enough for the rights and responsibilities of legal drinking.

When a minor enters the military (with parental permission), he or she automatically  becomes emancipated in the eyes of the law. The law assumes that the military will only accept someone who demonstrates the necessary level of maturity for duty. In the event the military is wrong, it has an excellent system for weeding out mistakes: basic training. The military can discharge those not up to the challenge. For a minor to become emancipated under other circumstances, it’s a tougher process. He must show a court that he is self-supporting, can handle his own personal affairs, and understands what emancipation means.

Although a typical 18 -year-old is technically emancipated, it is the rare college student who could pass such a test. Rather than living a life of real emancipation like his married or enlisted counterparts, the college student exists in a strange netherworld suspended between adolescence and real adulthood. While college students demonstrate a good deal of independence in the sense that they live away from home, make friends, study, and do their own laundry, they are nonetheless dependent on their parents financially and demonstrate varying degrees of autonomy and good sense. They are often busy having the time of their lives. Indeed, a common suggestion for reigning in campus drinking is to hold classes on Friday mornings, thus preventing the weekend revelry from beginning on Thursday nights.

Alcohol consumption is unique among the rights conferred by age-of-majority laws because it alters brain chemistry, and the risk of conferring it on the wrong person can be immediate and violent. Bear in mind that under various provisions of state and federal law, even minors emancipated at an early age through marriage or military service see no change in their right to drink.

In addition, colleges are not the bastions of the hale and hearty they were for most of the 20 th century. Today, students attend college while managing chronic illnesses such as arthritis, diabetes, multiple sclerosis, asthma, depression and other psychiatric maladies, endocrine disorders, and attention deficit disorder. College populations even include cancer survivors in various stages of remission. “Two generations ago [ill students] would not have been mainstreamed,” said Patricia Fennell, head of Albany Health Management Associates and an expert on managing chronic health conditions. Now they are coping with chronic illnesses far from the watchful eyes of their parents — which means taking medicines and dealing with the temptations of college life — including alcohol.

Emancipation is not always desirable. Indeed, there is a tradition in the law to that effect. Many states have an express, statutory exception to age-of-majority emancipation rules. Exceptions usually relate to special rights conferred on the disabled, who are entitled to certain protections beyond the age of 18 . Many state and federal child poverty programs cover children through age  21 . Given the rates of binge drinking on campus and the number of deaths, injuries, and social costs associated with underage alcohol use, the emancipation-exception doctrines provide a useful perspective from which to think about the 21 laws. By delaying legal drinking, the 21 laws provide a valuable, partial exception to emancipation for 18 -, 19 - and 20 -year-olds on the grounds that when it comes to alcohol, they can benefit from society’s protection.

The question is not whether we should protect youth from alcohol, but why has society done such a lousy job of it by largely failing to enforce the 21  laws? The Initiative, in its rhetorical question about “repeating the lessons of Prohibition,” intimates that laws proscribing alcohol are simply doomed to failure. Are they?

Prohibition

I n the early 20 th century, the nation was a hodgepodge of “dry” and “wet” states. During the 1910 s, dry states became frustrated that liquor was entering their borders via railroad shipments to individuals under a legal loophole. The powerful Anti-Saloon League lobbied successfully for the Webb-Kenyon Act, which President Taft later vetoed. A court challenge followed in 1917 . The decision, Clark Distilling Co. v. Western Maryland Railway Co. , upheld the constitutionality of the Act, despite concerns that had been raised about it under the commerce clause of the Constitution. With power becoming centralized in Washington as World War I approached, the dry congressmen who dominated at the time saw their moment to take on the alcohol industry. Congress passed the 18 th Amendment, which was quickly ratified in January, 1919 . 11

The 18 th Amendment banned the manufacture, sale, and importation of “intoxicating liquors” for use as beverages. It gave “concurring jurisdiction” for enforcement to the federal and state governments. Congress soon passed the Volstead Act, which defined “intoxicating liquor” to include even light beer. The Volstead Act was far more draconian than many dry advocates anticipated and cost the movement supporters.

Prohibition’s impact was immediate: It lowered the rates of alcohol-related deaths, illnesses, and pathologies such as cirrhosis, alcoholism, and drunkenness arrests, and dramatically lowered the consumption of beer and liquor. So intense was the regulatory effort during Prohibition that 85 percent of distilleries went out of business, with the remainder producing mostly industrial alcohol. The social tradition of the male saloon vanished from American life. All of this was done at a substantial sacrifice to the national purse. 12

Nonetheless, the “concurring jurisdiction” clause wreaked havoc. The U.S. Supreme Court held in the National Prohibition Cases  that “concurring jurisdiction” meant that the federal government got to call the shots and enforce its teetotaling agenda under the Volstead Act even where local or state law was more lenient. That was a formula for hostility between state and federal governments and an invitation to subverting the law through illegal trafficking and speakeasies. Moreover, Southern states didn’t want Washington sticking its nose in their business — wet or dry. Consequently, Southern states put the kibosh on federal enforcement by making sure it was underfunded by Congress. Not surprisingly, the feds ended up doing most of the enforcement — underfunded — competing with overlapping, often uncooperative state entities, involved in their own local, wet-dry politics.

A combination of factors sank Prohibition, both social and political. In the end, however, it was the Great Depression that broke the back of Prohibition. By the late 1920 s, business titans such as Pierre DuPont, who had been dry advocates, felt pummeled by the taxman of the Roaring Twenties and suddenly were singing the praises of the British liquor tax system. Just one year after the election of the “wet” Roosevelt ticket in 1932 , ratifying conventions were held for the 21 st Amendment with the hope that the resurgence of the alcohol industry would replenish tax revenues and provide “relief to suffering families.” 13

There is much to learn from Prohibition. The 21 laws are not as sweeping as the Volstead Act. They are not a ban on an industry, nor are they a ban on the sale of all alcohol to all drinkers; they do not create a bootleg market or leave a void for organized crime. The political factions that undermined Prohibition enforcement are not a factor in underage drinking. The 21  laws ban alcohol for a small segment of society, extending the childhood ban on alcohol for only three years. Choose Responsibility argues that the violence and illegal excesses of Prohibition — the homemade booze that made people sick, the organized crime, the shootouts — bear a direct parallel to the secretive ways of today’s underage binge drinking.

This isn’t so. American youth don’t distill liquor in their dorm rooms, they aren’t involved in organized crime, they don’t shoot federal marshals or transport truckloads of bootleg spirits. We are faced with the opposite problem: Underage drinkers are surrounded by easily available alcohol and need expend no special efforts to obtain it. A phony id , an invitation to a party, or a 21 -year-old friend does the trick. There is no underground market in alcohol — they are buying their alcohol from neighborhood pubs and liquor stores or obtaining it from older buddies.

There already exist many laws relating to the sale of liquor to those under 21  that, if better enforced, could prevent underage drinking. Enactment of additional laws in some states would aid enforcement. For example, purchasing alcohol for underage drinkers or selling large quantities of beer or renting unregistered kegs are not illegal in some states — but should be. These types of state and local laws do not conflict with each other, nor do they overlap with federal enforcement efforts, which was a central point of policy contention that gave rise to criminality and weak enforcement during Prohibition. The federal Department of Education regulations that can penalize schools for failure to comply with federal alcohol-related campus policies do not overlap with local law enforcement powers to arrest, prosecute, or fine those who sell liquor to minors.

A fundamental change in outlook is required, because selling liquor to young people in the United States is big business. Underage drinkers account for 19.4 percent of alcohol revenues (about $ 22.5 billion). 14 The absurdly low price of beer near college campuses — it is not unusual for a pitcher of beer to cost 25 cents — creates temptations that are very hard for young people in college to resist. A discussion in the National Academy of Sciences report on underage drinking revealed that when alcohol is “readily accessible” to young people, it “represents a powerful message within the social environment that encourages youth consumption and undermines other messages regarding the risks alcohol poses to their well being.” 15 The low price of beer has been shown to be an important factor in underage drinking and the overall accessibility of alcohol to young people. During the decade from 1981 to 1992 , underage drinking declined because of intense public education, a shift in youth culture away from the 1970 s model of getting wasted, and — significantly — a lack of spending money available to young people. 16

Why not just educate?

C hoose responsibility would replace the 21 laws with alcohol education at home and on campus. But colleges already educate college students about drinking. Even though schools are required to have anti-underage drinking policies under federal law, there is nothing to prevent them from teaching moderation or techniques to prevent alcohol poisoning. Indeed, college students get alcohol education from numerous sources: official school policy and abstinence programs and alcohol moderation programs provided by colleges; moderation programs provided by outside consulting groups; an online program called AlcoholEdu that has reached almost a quarter of a million students on over 400 college campuses; and normative marketing programs. Sokolow estimates that 10 to 20  percent of colleges now have outside consultants come to campus to provide alcohol moderation programs.

A large role is also played by social-norms marketing programs in which “latent healthy norms” about college drinking are made known to students through posters, flyers, and other forms of high-profile communication on campus. In other words, messages on billboards and flyers all over campus model the way grown-ups drink. A program may present the idea that a typical young drinker consumes five or fewer drinks when he parties with friends. Such marketing programs carry a positive message and do not discuss the dangers of drinking. About half of all four-year residential colleges have conducted social-norms marketing programs for alcohol. 17

They are not necessarily a good idea. A study of alcohol-related social-norms marketing was done based on the data gathered in the Harvard cas that compared the 118  schools in the survey. The social-norms study included the schools that had experienced social-norms marketing programs and those that didn’t. The study showed that social-norms marketing did not reduce college drinking. In fact, in the schools that had the programs, drinking increased. In the schools without the programs, no change in drinking rates occurred.

The study did not show why drinking increased at schools with the programs, but it is a cautionary tale. The college drinking scene is a battleground with two fronts: coping with those who already are binge drinkers and fighting for the hearts and souls of the others. We know that about half of freshman classes enter with no history of alcohol use and can be lured into drinking. Hearing a message sanctioned by the college that some drinking is all right could tip the balance.

We do know that many environmental factors influence the likelihood of a nondrinking student continuing on that course, including diversity of the student body, the number of female students, the risk and cost of obtaining alcohol and the presence of “zero-tolerance” dorms. Much depends on the state and its culture of enforcement. Measures such as increasing prices, imposing excise taxes, and local laws that regulate the density of liquor-selling establishments close to campus can have a strong impact on underage drinking. 18

The Institute of Alcohol Studies in London looked at individual as well as meta-analyses of European, Australian, and American youth alcohol education efforts. It found that although there were “individual examples of the beneficial impacts of school-based education,” there was not enough evidence to conclude that education has an impact on binge drinking among young people. The Institute said it was not implying that education should not be done, but it “should not be seen as the answer to reduce the harm done by binge drinking.” Education, the Institute concluded, plays only a supportive role. 19

The Amethyst Initiative says, in essence, that the phenomenon of underage drinking is a tidal wave that society cannot stop. Our only hope is to ride the wave along with our children, give them an oar, and hope they don’t drown. That relies on the very big — and untested — assumption that their young minds have the capacity to listen when it comes to alcohol, no matter how badly they want to party, hook up, fit in.

Given the stakes, America should not throw in the towel on the 21 laws until we have actually enforced them as they were meant to be enforced — though it will require a clear dedication of political will. It can be done; a similar revolution occurred during the 1980 s with respect to driving under the influence laws. Disparities in enforcement do not mean that the laws are impossible to enforce. It signals that we have not gotten serious as a nation about using the laws we have — and improving them where needed.  

Carla T. Main writes often on law and society. She is the author of Bulldozed (Encounter Books, 2007), about an eminent domain battle in a small city in Texas.

1  The use of the word “amethyst” alludes to an ancient myth associating the stone with the ability to ward off drunkenness.

2  Richard J. Bonnie and Mary Ellen O’Connell, eds., Reducing Underage Drinking: A Collective Responsibility, Committee on Developing A Strategy to Reduce and Prevent Underage Drinking (National Academies Press, 2004 ), 25–26 .

3   Robert Davis and Anthony DeBarros, “Alcohol and Fire a Deadly Mix,” USA Today , Dec. 18, 2008 .

4  Ralph W. Hingson et al., “Magnitude and Morbidity Among U.S. College Students Ages 18–24 ,” Journal of Studies on Alcohol (March 2002 ); Ralph W. Hingson, et al., “Magnitude and Morbidity Among U.S. College Students Ages 18–24 : Changes from 1998 to 2001 , Ages 18–24 ,” Annual Review of Public Health ( 2005 ); and “The Surgeon General’s Call to Action to Prevent and Reduce Underage Drinking” (Office of the Surgeon General, 2007 ), available at http://www.surgeongeneral.gov/topics/underagedrinking/calltoaction.pdf (accessed May 4, 2009 ).

5  J.A. Grunbaum, et al., “Youth risk behavior surveillance — United States, 2003,” Morbidity and Mortality Weekly Report Summary  53:2 (May 21, 2004), and L.D. Johnston, et al., “Teen Drug Use Continues Down in 2006, Particularly Among Older Teens; but Use of Prescription-Type Drugs Remains High,” University of Michigan News and Information Services (2006).

6  “The Surgeon General’s Call to Action to Prevent and Reduce Underage Drinking.”

7  “Magnitude and Morbidity Among U.S. College Students Ages 18–24 .”

8  Bjorn Hibell., et al., “The espad Report 2003 : Alcohol and Other Drug Use Among Students in 35 European Countries” ( 2004 ).

9  Institute of Alcohol Studies, “Binge Drinking — Nature, prevalence and causes, ias Fact Sheet” ( 2006 ).

10  “Magnitude and Morbidity Among U.S. College Students Ages 18–24 : Changes from 1998 to 2001 , Ages 18–24 <.”

11  Thomas R. Pegram, Battling Demon Rum (Ivan R. Dee, 1998 ), 144 .

12  Jack S. Blocker Jr., “Did Prohibition Really Work? Alcohol as a Public Health Innovation,” American Journal of Public Health 26:2 (February 2006 ).

13  Blocker, “Did Prohibition Really Work? Alcohol as a Public Health Innovation.”

14  Bonnie and O’Connell, Reducing Underage Drinking , 23 .

15  James Mosher, et al., “Reducing Underage Drinking: The Role of Law,” Journal of Law, Medicine & Ethics 32:4 (Winter 2004 ).

16  Bonnie and O’Connell, Reducing Underage Drinking , 100 .

17  Henry Wechsler and Toben F. Nelson, “What We Have Learned From the Harvard School of Public Health College Alcohol Study: Focusing Attention on College Student Alcohol Consumption and the Environmental Conditions That Promote It,” Journal of Studies on Alcohol and Drugs (July 2008 ).

18  Robert Zimmerman and William DeJong, “Safe Lanes on Campus: A Guide for Preventing Impaired Driving and Underage Drinking” (Higher Education Center for Alcohol and Other Drug Prevention, 2003 ).

19  Peter Anderson, “Binge Drinking and Europe,” (Institute of Alcohol Studies, 2008 ).

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Why Are Older Americans Drinking So Much?

The pandemic played a role in increased consumption, but alcohol use among people 65 and older was climbing even before 2020.

By Paula Span

The phone awakened Doug Nordman at 3 a.m. A surgeon was calling from a hospital in Grand Junction, Colo., where Mr. Nordman’s father had arrived at the emergency room, incoherent and in pain, and then lost consciousness.

At first, the staff had thought he was suffering a heart attack, but a CT scan found that part of his small intestine had been perforated. A surgical team repaired the hole, saving his life, but the surgeon had some questions.

“Was your father an alcoholic?” he asked. The doctors had found Dean Nordman malnourished, his peritoneal cavity “awash with alcohol.”

The younger Mr. Nordman, a military personal finance author living in Oahu, Hawaii, explained that his 77-year-old dad had long been a classic social drinker: a Scotch and water with his wife before dinner, which got topped off during dinner, then another after dinner, and perhaps a nightcap.

Having three to four drinks daily exceeds current dietary guidelines , which define moderate consumption as two drinks a day for men and one for women, or less. But “that was the normal drinking culture of the time,” said Doug Nordman, now 63.

At the time of his 2011 hospitalization, though, Dean Nordman, a retired electrical engineer, was widowed, living alone and developing symptoms of dementia. He got lost while driving, struggled with household chores and complained of a “slipping memory.”

He had waved off his two sons’ offers of help, saying he was fine. During that hospitalization, however, Doug Nordman found hardly any food in his father’s apartment. Worse, reviewing his father’s credit card statements, “I saw recurring charges from the Liquor Barn and realized he was drinking a pint of Scotch a day,” he said.

Public health officials are increasingly alarmed by older Americans’ drinking. The annual number of alcohol-related deaths from 2020 through 2021 exceeded 178,000, according to recently released data from the Centers for Disease Control and Prevention : more deaths than from all drug overdoses combined.

An analysis by the National Institute on Alcohol Abuse and Alcoholism shows that people over 65 accounted for 38 percent of that total. From 1999 to 2020, the 237 percent increase in alcohol-related deaths among those over age 55 was higher than for any age group except 25- to 34-year-olds.

Americans largely fail to recognize the hazards of alcohol, said George Koob, the director of the institute. “Alcohol is a social lubricant when used within the guidelines, but I don’t think they realize that as the dose increases it becomes a toxin,” he said. “And the older population is even less likely to recognize that.”

The growing number of older people accounts for much of the increase in deaths, Dr. Koob said. An aging population foreshadows a continuing surge that has health care providers and elder advocates worried, even if older people’s drinking behavior doesn’t change.

But it has been changing . The proportions of people over 65 who report using alcohol in the past year (about 56 percent) and the past month (about 43 percent) are lower than for all other groups of adults. But older drinkers are markedly more likely to do it frequently, on 20 or more days a month, than younger ones.

Moreover, a 2018 meta-analysis found that binge drinking (defined as four or more drinks on a single occasion for women, five or more for men) had climbed nearly 40 percent among older Americans over the past 10 to 15 years.

What’s going on here?

The pandemic has clearly played a role. The C.D.C. reported that deaths attributable directly to alcohol use, emergency room visits associated with alcohol, and alcohol sales per capita all rose from 2019 to 2020, as Covid arrived and restrictions took hold.

“A lot of stressors impacted us: the isolation, the worries about getting sick,” Dr. Koob said. “They point to people drinking more to cope with that stress.”

Researchers also cite a cohort effect. Compared to those before and after them, “the boomers are a substance-using generation,” said Keith Humphreys, a psychologist and addiction researcher at Stanford. And they’re not abandoning their youthful behavior, he said.

Studies show a narrowing gender divide, too. “Women have been the drivers of change in this age group,” Dr. Humphreys said.

From 1997 to 2014, drinking rose an average of 0.7 percent a year for men over 60, while their binge drinking remained stable. Among older women, drinking climbed by 1.6 percent annually, with binge drinking up 3.7 percent.

“Contrary to stereotypes, upper-middle-class, educated people have higher rates of drinking,” Dr. Humphreys explained. In recent decades, as women grew more educated, they entered workplaces where drinking was normative; they also had more disposable income. “The women retiring now are more likely to drink than their mothers and grandmothers,” he said.

Yet alcohol use packs a greater wallop for older people, especially for women, who become intoxicated more quickly than men because they’re smaller and have fewer of the gut enzymes that metabolize alcohol.

Seniors may argue that they are merely drinking the way they always have, but “equivalent amounts of alcohol have much more disastrous consequences for older adults,” whose bodies cannot process it as quickly, said Dr. David Oslin, a psychiatrist at the University of Pennsylvania and the Veterans Affairs Medical Center in Philadelphia.

“It causes slower thinking, slower reaction time and less cognitive capacity when you’re older,” he said, ticking off the risks.

Long associated with liver diseases, alcohol also “exacerbates cardiovascular disease, renal disease and, if you’ve been drinking for many years, there’s an increase in certain kinds of cancers,” he said. Drinking contributes to falls, a major cause of injury as people age, and disrupts sleep.

Older adults also take a lot of prescription drugs, and alcohol interacts with a long list of them. These interactions can be particularly common with pain medications and sleep aids like benzodiazepines, sometimes causing over-sedation. In other cases, alcohol can reduce a drug’s effectiveness.

Dr. Oslin cautions that, while many prescription bottles carry labels that warn against using those drugs with alcohol, patients may shrug that off, explaining that they take their pills in the morning and don’t drink until evening.

“Those medications are in your system all day long, so when you drink, there’s still that interaction,” he tells them.

One proposal for combating alcohol misuse among older people is to raise the federal tax on alcohol, for the first time in decades. “Alcohol consumption is price-sensitive, and it’s pretty cheap right now relative to income,” Dr. Humphreys said.

Resisting industry lobbying and making alcohol more expensive, the way higher taxes have made cigarettes more expensive, could reduce use.

So could eliminating barriers to treatment. Treatments for excessive alcohol use, including psychotherapy and medications, are no less effective for older patients , Dr. Oslin said. In fact, “age is actually the best predictor of a positive response,” he said, adding that “treatment doesn’t necessarily mean you have to become abstinent. We work with people to moderate their drinking.”

But the 2008 federal law requiring health insurers to provide parity — meaning the same coverage for mental health, including substance use disorders, as for other medical conditions — doesn’t apply to Medicare. Several policy and advocacy groups are working to eliminate such disparities.

Dean Nordman never sought treatment for his drinking, but after his emergency surgery, his sons moved him into a nursing home, where antidepressants and a lack of access to alcohol improved his mood and his sociability. He died in the facility’s memory care unit in 2017.

Doug, whom his father had introduced to beer at 13, had been a heavy drinker himself, he said, “to the point of blackout” as a college student, and a social drinker thereafter.

But as he watched his father decline, “I realized this was ridiculous,” he recalled. Alcohol can exacerbate the progression of cognitive decline, and he had a family history.

He has remained sober since that pre-dawn phone call 13 years ago.

Research Suggests That Drinking Coffee Or Tea Could Lessen The Risk Of Frailty As You Get Older

Posted: April 13, 2024 | Last updated: April 13, 2024

Research Suggests That Regularly Drinking Coffee Or Tea During Middle Age Could Lessen The Risk Of Physical Frailty As You Get Older

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ORIGINAL RESEARCH article

This article is part of the research topic.

Plant-Based Products for Healthy Neurological Aging

Amelioration of age-related cognitive decline and anxiety in mice by Centella asiatica extract varies by sex, dose and mode of administration Provisionally Accepted

• 1 Oregon Health and Science University, United States
• 2 Oregon State University, United States
• 3 Oregon's Wild Harvest, United States
• 4 VA Portland Health Care System, Veterans Health Administration, United States Department of Veterans Affairs, United States

The final, formatted version of the article will be published soon.

A water extract (CAW) of the Ayurvedic plant Centella asiatica administered in drinking water has been shown to improve cognitive deficits in mouse models of aging and neurodegenerative diseases.Here the effects of CAW administered in drinking water or the diet on cognition, measures of anxiety and depression-like behavior in healthy aged mice are compared.Three-and eighteen-month-old male and female C57BL6 mice were administered rodent AIN-93M diet containing CAW (0, 0.2, 0.5 or 1% w/w) to provide 0, 200 mg/kg/d, 500 mg/kg/d or 1000 mg/kg/d for a total of 5 weeks. An additional group of eighteen-month-old mice were treated with CAW (10 mg/mL) in their drinking water for a total of five weeks to deliver the same exposure of CAW as the highest dietary dose (1000 mg/kg/d). CAW doses delivered were calculated based on food and water consumption measured in previous experiments. In the fourth and fifth weeks, mice underwent behavioral testing of cognition, anxiety and depression (n=12 of each sex per treatment group in each test).Aged mice of both sexes showed cognitive deficits relative to young mice while only female aged mice showed increased anxiety compared to the young female mice and no differences in depression were observed between the different ages. CAW (1000 mg/kg/d) in the drinking water improved deficits in aged mice in learning, executive function and recognition memory in both sexes and attenuated the increased measures of anxiety observed in the aged female mice. However, CAW in the diet only improved executive function in aged mice at the highest dose (1000 mg/kg/d) in both sexes and did so less robustly than when given in the water. There were no effects of CAW on depression-like behavior in aged animals regardless of whether it was administered in the diet or the water.These results suggest that CAW can ameliorate age-related changes in measures of anxiety and cognition and that the mode of administration is important for the effects of CAW on resilience to these age-related changes.

Keywords: Aging, Cognition, Anxiety, Depression, Centella asiatica

Received: 19 Dec 2023; Accepted: 10 Apr 2024.

Copyright: © 2024 Gray, Hack, Brandes, Zweig, Yang, Marney, Choi, Magana, Cerruti, McFerrin, Koike, Nguyen, Raber, Quinn, Maier and Soumyanath. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Mx. Nora E. Gray, Oregon Health and Science University, Portland, United States

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• v.100(6); Jun 2010

Will Increasing Alcohol Availability By Lowering the Minimum Legal Drinking Age Decrease Drinking and Related Consequences Among Youths?

H. Wechsler was the principal investigator of the College Alcohol Study. T. F. Nelson was a co-investigator of the College Alcohol Study. Both authors contributed to the conceptualization, writing, editing, and approval of the article.

Alcohol use health consequences are considerable; prevention efforts are needed, particularly for adolescents and college students. The national minimum legal drinking age of 21 years is a primary alcohol-control policy in the United States. An advocacy group supported by some college presidents seeks public debate on the minimum legal drinking age and proposes reducing it to 18 years.

We reviewed recent trends in drinking and related consequences, evidence on effectiveness of the minimum legal drinking age of 21 years, research on drinking among college students related to the minimum legal drinking age, and the case to lower the minimum legal drinking age.

Evidence supporting the minimum legal drinking age of 21 years is strong and growing. A wide range of empirically supported interventions is available to reduce underage drinking. Public health professionals can play a role in advocating these interventions.

SINCE 1984 THE NATIONAL minimum legal drinking age in the United States has been 21 years. During the intervening 25 years there have been periodic efforts to lower the minimum legal drinking age, including recent legislation introduced in 7 states, although none of these bills have been enacted. In 2008 a group of university and college presidents expressed their discontent with the minimum legal drinking age of 21 years by signing on to the Amethyst Initiative, a much publicized advocacy effort to encourage public debate about lowering the drinking age. This group of college presidents, and their partner organization, Choose Responsibility, propose reducing the minimum legal drinking age to 18 years. This policy change is a central feature of a campaign its organizers contend will help young adults aged 18 to 20 years make healthy decisions about alcohol and lead to reductions in drinking and its negative effects. Because the consequences of alcohol use are considerable, and changes in the minimum legal drinking age may have important ramifications for health and safety, this issue requires serious consideration and participation from the public health community.

ALCOHOL AND PUBLIC HEALTH

Alcohol consumption is the third leading actual cause of death in the United States, a major contributing factor to unintentional injuries, the leading cause of death for youths and young adults, and accounts for an estimated 75 000 or more total deaths in the United States annually. 1 – 3 Alcohol use is associated with a wide range of adverse health and social consequences, including physical and sexual assault, unintended pregnancy, sexually transmitted infection, violence, vandalism, crime, overdose, other substance use, and high-risk behavior, resulting in a heavy burden of social and health costs. 2 , 4 , 5 Drinking alcohol most commonly begins during adolescence and early initiation of alcohol use is associated with alcohol problems in adulthood. 6 , 7 Underage drinkers drink on fewer occasions, but when they drink they are more likely to binge drink. 8 , 9 In recognition of the harms caused by underage drinking the US Surgeon General issued a Call to Action in 2007 to prevent and reduce drinking among youths. 5

MINIMUM LEGAL DRINKING AGE IN THE UNITED STATES

Minimum legal drinking age laws have been a primary alcohol-control strategy in the United States for 75 years. When the 21st Amendment to the US Constitution repealed Prohibition in 1933, most states set a minimum legal drinking age of 21 years, although the specific provisions of the law in each state varied. 10 These laws began to change in the 1970s when many states lowered the minimum legal drinking age along with reducing the minimum age to vote during the Vietnam War. 11

The lower minimum legal drinking age was followed by increases in the sale and consumption of alcohol and in alcohol-involved traffic fatalities, particularly among young adults aged 18–20 years. 12 – 14 On the basis of these unintended health consequences of the lower drinking age, some states reinstated the minimum legal drinking age of 21 years. 15 By the early 1980s, this situation created a patchwork of differential legal restrictions across states and contributed to the problem of underage youths in states with a minimum legal drinking age of 21 years driving to states with a lower minimum legal drinking age to purchase and consume alcohol. In direct response to these concerns, Congress and President Ronald Reagan worked to create a consistent national drinking age. The National Minimum Drinking Age Act became law in 1984, requiring that states prohibit the purchase and public possession of alcohol for persons aged younger than 21 years in order to receive all of their federal highway funds. 16 By 1988 all states had a minimum legal drinking age of 21 years.

TRENDS IN ALCOHOL USE AND RELATED PROBLEMS

Overall in the United States, alcohol consumption, heavy drinking, and daily alcohol use have declined among young adults aged 18–20 years since the early 1980s, whereas shifts in drinking behavior among young adults aged 21 to 24 years have been more gradual and less consistent. 17 , 18 Increases in binge drinking have been observed among young adults aged 21–24 years in the past decade, but drinking among those aged 18–20 years has remained stable during this time period for both college students and their peers who were not in college. 19 Consistent with declining trends in consumption, the percentage of traffic fatalities involving alcohol declined dramatically from the early 1980s (when reliable national data first existed) through 1997, when rates leveled off. 13 Figure 1 shows these national trends in alcohol-involved motor vehicle fatalities for youths aged 16 to 20 years and those aged 21–24 years with data from the National Highway Traffic Safety Administration Fatality Analysis Reporting System, a census of deaths from traffic fatalities in the United States.

Percentage of alcohol-related motor vehicle fatalities among young adults aged 16 to 24 years, by age group: United States, 1982–2007.

Source . National Highway Traffic Safety Administration Fatality Analysis Reporting System.

COLLEGE STUDENTS AND THE MINIMUM LEGAL DRINKING AGE

Although heavy drinking among older adolescents and young adults has declined over the past decades, no such declines have occurred among college students. 17 , 18 , 20 , 21 College students are more likely to engage in heavy drinking than their peers who do not attend college, 19 , 22 – 24 with 2 in 5 students nationally engaging in binge drinking on at least 1 occasion in the past 2 weeks. 18 , 21 Approximately three quarters of college students aged 18–20 years drank alcohol in the past year, although they are less likely than their peers of legal drinking age to drink and to engage in binge drinking. 8 , 19 The heaviest-drinking college students are more likely to have been heavy drinkers in high school. 25 – 29

College students are heavy drinkers as a group, but drinking behavior varies widely by college. 30 , 31 College environments that afford easy access to low-cost alcohol, have few policies restricting accessibility to alcohol, and have lax enforcement of existing policies create the conditions for heavy drinking among college students. 8 , 30 , 32 – 43 The Safe and Drug-Free Schools and Communities Act requires college administrators to enforce the minimum legal drinking age of 21 years, a restriction that targets approximately half of the traditional college student population. However, surveys of college administrators indicate that enforcement of alcohol policies at most colleges is limited, and colleges tend to focus their prevention efforts on educational programs for students. 44 , 45 One national survey found that fewer than 1 in 10 underage students who drink alcohol reported experiencing any consequences for violating alcohol policies imposed by their college. 8

Although the level of enforcement of the minimum legal drinking age of 21 years is low nationally, enforcement and comprehensiveness of policy restrictions do make a difference. At colleges where campus security strongly enforces the alcohol policy, students perceive the stronger enforcement efforts and are less likely to binge drink. 34 Underage students who attend college in states with a comprehensive set of control policies restricting underage drinking are less likely to binge drink than underage students in states with no similar policies. 8

THE AMETHYST INITIATIVE ARGUMENT

The overall lack of progress in reducing drinking and related problems among college students nationally is of concern to many college officials. 44 As of November 2009, presidents and chancellors of 135 colleges and universities have signed on to the Amethyst Initiative ( http://www.amethystinitiative.org ) calling for a public debate about lowering the minimum legal drinking age to 18 years. 46 Specifically, they suggest that the current minimum legal drinking age of 21 years is not working to prevent youths from using alcohol and experiencing the negative consequences of drinking. The Amethyst Initiative suggests that the observed declines in drinking, traffic fatalities, and related harms since the minimum legal drinking age of 21 years became law are a result of other factors, such as improvements in motor vehicle safety, and not the change in the minimum legal drinking age. Furthermore, they contend that drinking among young adults aged 18–20 years is being driven underground by the minimum legal drinking age away from bars—where it is more carefully monitored—to private parties, which are less safe. Some college presidents have expressed concern that these unsafe drinking environments have contributed to an increase in alcohol poisoning deaths among youths and young adults. They also argue that young adults aged 18–20 years drink more responsibly in Western European countries where the minimum legal drinking age is lower.

Several researchers have examined these and other assertions regarding the minimum legal drinking age of 21 years in detail with available scientific evidence. 46 – 48 Public health professionals should become familiar with these arguments and the evidence to advocate effective public policy.

RESEARCH ON THE MINIMUM LEGAL DRINKING AGE

The minimum legal drinking age has been perhaps the single most studied alcohol-control policy. 12 , 46 , 48 , 49 Differences in laws among states and within states over time have allowed researchers to study the effect of this policy and come to some reliable conclusions. A review of 241 studies published between 1960 and 2000 that examined the effects of lowering or raising minimum drinking age laws identified 135 high-quality studies in terms of sampling, research design, and having an appropriate comparison group. 12 Of the 79 quality studies that examined the relationship between the minimum legal drinking age and traffic crashes, 58% found fewer crashes associated with a higher minimum legal drinking age, whereas no study found fewer crashes associated with a lower minimum legal drinking age. 12 Consistent with these findings, a higher minimum legal drinking age was associated with lower rates of alcohol consumption and other alcohol-related problems. 12

Similar conclusions have been reached by subsequent studies that have accounted for other prevention policies and demographic shifts over time. 13 , 50 – 52 Although 1 recent study cited by proponents of lowering the minimum legal drinking age concluded that the minimum legal drinking age does not save lives, the authors used methods that differed from those of other studies. 53 The study compared states that adopted the minimum legal drinking age of 21 years early with those who adopted it later and concluded that later-adopting states (i.e., states that were compelled by the national policy) had no significant reduction in traffic fatalities. The analysis shows that early and late adopting states both had declines that were similar in magnitude, but these trends were not directly compared. They also examined overall fatalities, including those that did not involve alcohol, which would not be sensitive to changes in the minimum legal drinking age.

Another study of adults in the United States found that those who were legally able to purchase alcohol before age 21 years were more likely than those who could not to meet criteria for alcohol use disorder or another drug use disorder later in life. 54 Despite uneven and sometimes lax enforcement, the best available evidence suggests that the minimum legal drinking age of 21 years has saved more than 800 lives annually among young adults aged 18–20 years in the United States. 55 , 56

The minimum legal drinking age is not a single law or the sole policy designed to reduce heavy drinking and related harms among youths. It works in concert with other laws and alcohol-control policies. In addition to the effect of the primary restrictions on possessing and purchasing alcohol, other state laws that are designed to restrict underage drinking include zero tolerance laws for drinking and driving, administrative driver's license revocation, restrictions on possession of a false age identification, and mandatory training for servers on policies and procedures to prevent alcohol sales to minors and persons who are obviously intoxicated. In 1982, only 36 laws of this type were passed in all states. By 1997 the cumulative total grew to 204 and reached 245 in 2005. 13

Recent research has examined the relative contribution of these policies and found that, in addition to the effect of the national minimum legal drinking age of 21 years, each of these policy restrictions is independently associated with lower levels of drinking and alcohol-involved fatalities among youths aged younger than 21 years. 8 , 12 , 13 , 50 – 52 Drinking among youths and college students varies by state and is strongly associated with the level of drinking among adults and state alcohol control policies. 33 , 57 States that had more alcohol control policies and laws to complement the minimum legal drinking age of 21 years had lower levels of drinking and related problems among underage youths. 8 , 33 , 50 , 51

Private, off-campus residences and bars are the most frequently cited venues for heavy drinking among underage college students. 8 , 58 However, licensed establishments are not the safe and controlled venues for drinking claimed by the Amethyst Initiative. Despite state-level restrictions on the purchase and consumption of alcohol for persons aged younger than 21 years, many college communities have local ordinances that allow persons aged 18–20 years entry into bars. Underage patrons are frequently able to obtain alcohol and drink heavily in off-campus bars, and heavy drinking is associated with disruptive and aggressive behavior and physical altercations in these venues. 58 , 59 Studies in licensed establishments across multiple communities have shown that a high level of purchase attempts by underage and obviously intoxicated patrons are successful. 60 – 63 Yet when establishment staff are trained and policies are enforced, illegal alcohol sales to these patrons are reduced. 60 , 62

Countries with lower minimum legal drinking ages do not fare better. Contrary to the assertion of the Amethyst Initiative, heavy alcohol use among adolescents is a common problem across Europe. Frequent binge drinking among adolescents aged 15 to 16 years in many countries occurs at more than double the rate as in the United States. 5 , 64 , 65 The European region has the highest overall consumption of alcohol among adults and the highest proportion of alcohol-attributable deaths in the world. 65 Further, the experience with lowering the minimum legal drinking age in other countries is consistent with what occurred in the United States in the 1970s. In 1999 New Zealand lowered its national drinking age from 20 years to 18 years, resulting in significant increases in the occurrence of alcohol-involved emergency room admissions and traffic crashes among youths aged 15 to 19 years. 66 , 67

One impetus for the reduction in the US minimum legal drinking age to 18 years in the 1970s was the institution of the Selective Service System to draft eligible males aged 18 to 25 years into compulsory military service during the Vietnam War. The rationale was that men old enough to serve in the military were old enough to drink alcohol. Recent research has pointed to the significant problem of binge drinking among active duty military personnel, particularly among personnel who are underage, and prompted concern over the negative impact drinking has on job performance and preparedness. 68

Alcohol-related deaths among adolescents and young adults have increased in recent years. The Centers for Disease Control and Prevention provides the Alcohol-Related Disease Impact software to assess alcohol-attributable mortality trends with data from the National Vital Statistics System ( https://apps.nccd.cdc.gov/ardi/HomePage.aspx ). Table 1 shows that alcohol deaths rose among young adults aged 18 to 24 years for 2001 to 2006, with slightly higher increases among those aged 21–24 years. Most of the increase in deaths resulted from poisonings attributable to alcohol mixed with other substances, including opioids and other narcotics. However, alcohol poisoning deaths for young adults aged 18–20 years in this category did not increase and remain at about 9 or 10 deaths per year. Although a limitation of the ARDI system is that it assumes that the proportion of poisoning deaths over time that are attributable to alcohol is constant, these findings are consistent with an observed increase in the use of prescription drugs such as Vicodin and OxyContin among young adults. 18

Trends in Alcohol-Attributable Mortality Among Young Adults Aged 18–24 Years: United States, 2001–2006

Source . Centers for Disease Control and Prevention Alcohol-Related Disease Impact software ( http://www.cdc.gov/Alcohol/ardi.htm ).

The public discussion about the minimum legal drinking age has focused on such arguments as whether the minimum legal drinking age was indeed responsible for observed declines in drinking and related problems. Less attention has been given to the central tenet of the Amethyst Initiative that a lower drinking age would lead to declines in drinking among college students and related problems. There is no scientific evidence to suggest that a lower minimum legal drinking age would create conditions for responsible drinking or would lead young adults aged 18–20 years to make healthy decisions about drinking.

EXPERTS ASSESS THE MINIMUM LEGAL DRINKING AGE

The minimum legal drinking age of 21 years has a strong legal basis and considerable political and empirical support. 46 On the basis of the collective weight of evidence about the minimum legal drinking age, panels of experts and government agencies have consistently concluded that the national minimum legal drinking age of 21 years is effective public policy for reducing drinking and related problems and recommend closing loopholes in the law and strengthening enforcement. A report issued by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) in 2002 recognized the distinct problem of drinking among college students and outlined a set of empirically based interventions to prevent and reduce drinking by college students. 69 A prominent recommendation of this report was to increase enforcement of minimum drinking age laws. 69 Other groups that have concluded that the minimum legal drinking age of 21 years is an effective policy include the National Highway Traffic Safety Administration, the Substance Abuse and Mental Health Services Administration, the National Research Council and Institute of Medicine of the National Academies, the Centers for Disease Control and Prevention, the Office of the US Surgeon General, and the Governors Highway Safety Association. The American Public Health Association has been vocal on this issue as well, 70 and in 2008 members supported Policy Statement LB-08-02: “Maintaining and Enforcing the Age-21 Legal Drinking Age.”

REDUCING UNDERAGE DRINKING AND RELATED CONSEQUENCES

The Amethyst Initiative highlights the important and challenging problem of heavy drinking among college students. Despite considerable attention to this issue since the early 1990s, very little progress has been made in reducing drinking and binge drinking among students. 18 , 20 , 21 Colleges and communities can do a number of things to reduce and prevent underage drinking. The NIAAA College Drinking Task Force recommendations included implementation of public information campaigns about, and enforcement of, laws to prevent alcohol-impaired driving, restrictions on alcohol retail outlets, increasing prices and excise taxes on alcoholic beverages, and implementing responsible beverage service policies at on- and off-campus venues. 69 Few colleges have implemented these recommended policies and practices since the release of that report (T. F. Nelson, ScD, unpublished data, 2009). The Amethyst Initiative has not advocated, or taken a position on, any of these empirically based initiatives. 46 It is difficult to imagine how the college presidents who may question the minimum legal drinking age of 21 years can enforce it on their campuses. Public health professionals can partner with colleges and help acquaint administrators with effective alcohol-control strategies, including policies such as the minimum legal drinking age, and counter the misleading messages issued by the Amethyst Initiative.

A major challenge to understanding and evaluating the best available interventions is the lack of consistent, ongoing surveillance research from a national perspective. The Monitoring the Future Study and the National Survey on Drug Use and Health collect data on young people of college age, but, because of their designs, these surveys lack the depth to evaluate changes at the college level that can reduce student drinking. The Harvard School of Public Health College Alcohol Study has contributed to the understanding of these issues because it specifically studied students within colleges and assessed the college environments, including policy and programmatic initiatives. 30 However, the most recent nationally representative study of the College Alcohol Study was conducted in 2001. A dedicated, ongoing survey is needed to understand whether progress is being made to reduce heavy drinking among college students.

The weight of the scientific evidence, evaluated by many experts and government agencies, demonstrates that the minimum legal drinking age of 21 years is effective public policy for reducing underage drinking and preventing the negative consequences that can result from underage drinking. The evidence suggests that making alcohol more available by reducing the minimum legal drinking age to 18 years will lead to an increase in drinking and related harms. The evidence shows instead that strengthening enforcement and establishing policies to support the existing minimum legal drinking age are effective approaches to lower alcohol-related morbidity and mortality among youths. Public health professionals can play an important leadership role to prevent and reduce the impact alcohol has on health by advocating effective, empirically supported alcohol-control policy initiatives at the local, state, and national level.

Acknowledgments

The Harvard School of Public Health College Alcohol Study was generously supported by multiple grants from the Robert Wood Johnson Foundation.

We thank M. Stahre of the Centers for Disease Control and Prevention Alcohol Team for analysis of the Alcohol-Related Disease Impact system.