Genes and environment contribute to personal and peer drinking during adolescence and beyond

Alcohol use typically begins during adolescence, within social contexts, and is often correlated with the drinking of one’s peers. A new study of how a person’s drinking is related to the alcohol use of their peers from early adolescence through to early adulthood has found that both genetic and environmental factors contribute to the correlation between one’s own drinking and peer drinking.

Results will be published in the February 2015 online-only issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

“Peers can influence adolescent drinking in different ways,” said Alexis C. Edwards, assistant professor in the department of psychiatry at Virginia Commonwealth University as well as corresponding author for the study. “Peer pressure can work in both directions: some kids feel pressured, others are the ones exerting the pressure for whatever reason. Peer pressure doesn’t have to be explicit; kids can perceive pressure that’s never verbalized. Another way that peers can influence drinking is simply by providing access to alcohol. Furthermore, adolescent drinking behavior often occurs in the context of peer groups rather than in solitary situations. Therefore, it’s important not to overlook the role that choice plays in all these scenarios: to varying extents, kids select which peers they hang out with, which in turn has consequences for alcohol use.”

“Peer behavior is perhaps the most enduring social correlate of both contemporaneous and subsequent alcohol use, so studies specifically designed to explore the etiology underlying these associations, and particularly those that examine mechanistic processes, are tremendously important to the field,” added Shawn J. Latendresse, assistant professor in the department of psychology & neuroscience at Baylor University.

“We have access to a rich twin dataset that uniquely allows us to tease apart the complicated relationships of peer selection and peer influence, all in the context of genetic and environmental influences underlying behavior,” said Edwards. “We examined men simply because we only had the necessary data for men. It would be very interesting to see if the same patterns hold among women, because there are some differences in drinking behaviors across the sexes.”

Alcohol use typically begins during adolescence, in social settings, and is influenced by peer drinking.

  New findings indicate that both genetic and environmental factors contribute to the correlation between one’s own drinking and peer drinking.

  The influence of genetic factors increases as an individual moves from adolescence into adulthood.

Edwards and her colleagues used data collected in Wave Three of the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders. From that larger study of adult Caucasian twins, study authors analyzed data from a sample of 1,790 men, provided through structured clinical interviews that included retrospective reports of their own drinking as well as their peers’ alcohol-related behaviors from adolescence into young adulthood, ages 12 to 25 years. The influence of three plausible models of genetic and environmental influences on the relationship between phenotypes was examined over time.

Genes and environment contribute to personal and peer drinking during adolescence and beyond “There seem to be two take-home messages,” said Edwards. “First, genetic and environmental factors contribute to the correlation between one’s own drinking and their peers’ drinking. Second, apart from these shared genetic and environmental liabilities, there are causal processes at play: your own drinking phenotype causes you to select peers based on their drinking, and your peers’ drinking influences your own drinking.”

“Most notable, from the perspective of developmental science, is the fact that this study provides initial evidence of bidirectional influences among the drinking behaviors of individuals and their peers,” added Latendresse. “Yet, despite increasing additive genetic influences across adolescence, the majority of the variance in alcohol consumption continues to be attributable to environmental factors. This is particularly encouraging, as there remains great potential within the research community to identify modifiable aspects of the environment that can then serve as the focus of applied prevention/intervention efforts.”

Both Edwards and Latendresse commented on the finding of a clear increase in the influence of genetic factors as the adolescents moved into adulthood, and a corresponding decrease in the influence of shared environmental factors.

Alcohol use and heavy drinking are common during adolescence and young adulthood, although the minimum legal drinking age across the United States is 21 years. Some individuals may start hazardous alcohol consumption earlier in childhood. The prevalence of problematic alcohol use continues to escalate into the late adolescent and young-adult age range of 18 to 20 years. Drinking by college-aged students remains a major issue. Results of recent research that have demonstrated that brain development continues well into early adulthood and that alcohol consumption can interfere with such development indicate that alcohol use by youth is an even greater pediatric health concern.

Use of alcohol at an early age is associated with future alcohol-related problems. Data from the National Longitudinal Alcohol Epidemiologic Study substantiated that the prevalence of both lifetime alcohol dependence and alcohol abuse show a striking decrease with increasing age at onset of use. For those aged 12 years or younger at first use, the prevalence of lifetime alcohol dependence was 40.6%, whereas those who initiated at 18 years was 16.6% and at 21 years was 10.6%. Similarly, the prevalence of lifetime alcohol abuse was 8.3% for those who initiated use at 12 years or younger, 7.8% for those who initiated at 18 years, and 4.8% for those who initiated at 21 years. The contribution of age at alcohol use initiation to the odds of lifetime dependence and abuse varied little across gender and racial subgroups in the study. Early alcohol initiation has been associated with greater sexual risk-taking (unprotected sexual intercourse, multiple partners, being drunk or high during sexual intercourse, and pregnancy); academic problems; other substance use; and delinquent behavior in mid- to later adolescence. By young adulthood, early alcohol use is associated with employment problems, other substance abuse, and criminal and violent behavior. Independent of genetic risk, exposure to alcohol or other drug use disorders of parents predicts substance use disorders in children.


Adolescent drinking behaviors cover the alcohol use spectrum, from primary abstinence to alcohol dependence. The Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision (DSM-IV-TR)10 defines alcohol abuse as a maladaptive pattern of use that leads to clinically significant impairment or distress, as manifested by 1 or more of the following within a 12-month period:

  •   recurrent alcohol use that results in a failure to fulfill major role obligations at work, school, or home;
  •   recurrent alcohol use in situations in which it is physically hazardous;
  •   recurrent alcohol-related legal problems;
  •   continued alcohol use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the alcohol; and
  •   the symptoms have never met the criteria for alcohol dependence.

Alcohol dependence is defined as a maladaptive pattern of use that leads to clinically significant impairment or distress, as manifested by 3 or more of the following within the same 12-month period:

  •   tolerance;
  •   withdrawal;
  •   alcohol is often taken in larger amounts or over a longer period than was intended;
  •   there is a persistent desire or unsuccessful efforts to cut down or control use;
  •   a great deal of time is spent in activities necessary to obtain alcohol, use alcohol, or recover from its effects;
  •   important social, occupational, or recreational activities are given up or reduced because of use; or
  •   alcohol use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by alcohol.

“The increase in the relevance of genetic factors is pretty typical,” said Edwards. “As we age and gain more autonomy, our behavior is driven more by our own genetic liabilities and we are less influenced by the familial environment.”

“In general, as twins mature and become more independent of one another - for example, attend different schools, live in separate homes - they tend to share fewer of the influences within their physical and social environments, while their genetic similarities remain constant,” added Latendresse. “Of course, unique aspects of the twins’ environments are just as influential as their shared biology, and often more so, when it comes to their own alcohol consumption and the perceived consumption of their peers.”

“I hope that our study helps clarify the relationship observed between self and peer drinking behaviors across adolescence into adulthood,” said Edwards. “But there’s no way around the fact that this relationship is complicated. Our contribution is to provide evidence that shared genetic/environmental liabilities and causal processes are at play simultaneously: the association isn’t an either/or situation.”

Risk Factors for Adolescent Alcohol Use, Abuse, and Dependence

Genetic Risk Factors. Animal studies and studies of twins and adoptees demonstrate that genetic factors influence an individual’s vulnerability to alcoholism. Children of alcoholics are significantly more likely than children of nonalcoholics to initiate drinking during adolescence and to develop alcoholism, but the relative influences of environment and genetics have not been determined and vary among people.

Biological Markers. Brain waves elicited in response to specific stimuli (e.g., a light or sound) provide measures of brain activity that predict risk for alcoholism. P300, a wave that occurs about 300 milliseconds after a stimulus, is most frequently used in this research. A low P300 amplitude has been demonstrated in individuals with increased risk for alcoholism, especially sons of alcoholic fathers. P300 measures among 36 preadolescent boys were able to predict alcohol and other drug (AOD) use 4 years later, at an average age of 16.

Childhood Behavior. Children classified as “undercontrolled” (i.e., impulsive, restless, and distractible) at age 3 were twice as likely as those who were “inhibited” or “well-adjusted” to be diagnosed with alcohol dependence at age. Aggressiveness in children as young as ages 5-10 has been found to predict AOD use in adolescence. Childhood antisocial behavior is associated with alcohol-related problems in adolescence and alcohol abuse or dependence in adulthood.

Psychiatric Disorders. Among 12- to 16-year-olds, regular alcohol use has been significantly associated with conduct disorder; in one study, adolescents who reported higher levels of drinking were more likely to have conduct disorder.

Six-year-old to seventeen-year-old boys with attention deficit hyperactivity disorder (ADHD) who were also found to have weak social relationships had significantly higher rates of alcohol abuse and dependence 4 years later, compared with ADHD boys without social deficiencies and boys without ADHD.

Whether anxiety and depression lead to or are consequences of alcohol abuse is unresolved. In a study of college freshmen, a DSM-III diagnosis of alcohol abuse or dependence was twice as likely among those with anxiety disorder as those without this disorder. In another study, college students diagnosed with alcohol abuse were almost four times as likely as students without alcohol abuse to have a major depressive disorder. In most of these cases, depression preceded alcohol abuse. In a study of adolescents in residential treatment for AOD dependence, 25 percent met the DSM-III-R criteria for depression, three times the rate reported for controls. In 43 percent of these cases, the onset of AOD dependence preceded the depression; in 35 percent, the depression occurred first; and in 22 percent, the disorders occurred simultaneously.

Latendresse agreed. “It is also important to note that the increasing role of genes across development that is evidenced in this, and many other studies, might not be as straight forward as it appears. For example, because one’s genes generally aren’t subject to change, any change in the influence or expression of one’s genes is likely ‘triggered’ by other biological and/or environmental processes. However, within the types of statistical models employed in this study, all of these conditional effects would necessarily be partitioned in with the additive genetic variance. In this way, environmental influence has the potential to be misallocated.”


Alcoholism: Clinical & Experimental Research (ACER) is the official journal of the Research Society on Alcoholism and the International Society for Biomedical Research on Alcoholism. Co-authors of the ACER paper, “Multiple Mechanisms Influencing the Relationship between Alcohol Consumption and Peer Alcohol Use,” were: Hermine H. Maes of the Virginia Institute for Psychiatric and Behavioral Genetics, and the Department of Human and Molecular Genetics at Virginia Commonwealth University; Carol A. Prescott of the Department of Psychology at the University of Southern California, Los Angeles; and Kenneth S. Kendler of the Virginia Institute for Psychiatric and Behavioral Genetics, and the Department of Psychiatry at Virginia Commonwealth University. The study was funded by the National Institutes of Health, and the Carman Trust and W. Keck, John Templeton, and Robert Wood Johnson Foundations.


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