Adolescent Alcohol Use: Risks and Consequences
Adolescent Alcohol Use: Risks and Consequences
The adolescent brain undergoes profound neuro-developmental change, in turn influenced by genetic, environmental and sex hormonal factors (Arain et al., 2013). Glutamatergic neurotransmission is predominant and the maturation of neural circuits facilitates social-emotional development (Nelson et al., 2005). At the same time puberty manifests itself in outward bodily change.
The risk factors for adolescent AUDs can be divided into environmental, genetic and phenotypic. Genetic-environmental interaction determines individual alcohol use and AUDs.
As adolescents become more autonomous so the influence of the peer group becomes more important and family influences wane (Bremner et al., 2011). Adolescence sees a clustering of risk-taking behaviours such as smoking, drinking, drug-taking and sexual activity. Peer effects on risk-taking are strong in this age group, and adolescents affiliated with substance-using peers are at greater risk of engaging in similar behaviours themselves (Gardner and Steinberg, 2005). Peer acceptance is a potent social reward for adolescents (Rubin et al., 2006; Guyer et al., 2012) and is associated with high self-esteem and social competence. Having friends who drink increases the likelihood that young people will drink too. Young people are also influenced by how much their friends are drinking. Having older friends and spending more time with drinking friends are likely to promote excessive drinking (Bremner et al., 2011).
Parental expectation and involvement in social activities has been shown to moderate alcohol use (Nash et al., 2005; Wichers et al., 2013) and religious affiliation also shows a protective effect. Factors that influence drinking, drinking frequently and drinking to excess include lower levels of parental supervision, exposure to a close family member who drinks or becomes intoxicated, easy access to alcohol and positive expectations of alcohol (Bremner et al., 2011).
Genetic predisposition accounts for about half of the risk in the development of alcohol dependence. Adolescents with a positive family history of alcohol problems are at greater risk of developing an alcohol problem, and at a younger age, than their peers with negative family histories. Genetic factors may have more influence on drinking behaviour in late than in earlier adolescence (Rose et al., 2001).
Certain childhood characteristics are thought to increase the risk of adolescent AUDs and early identification of these characteristics can be helpful in preventing or attenuating the risk (Thatcher and Clark, 2008). For instance childhood psychological dysregulation is a behavioural phenotype that reflects an individual's vulnerability to developing an AUD in adolescence (Tarter et al., 2003; Thatcher and Clark, 2008). Other characteristics that have been identified and can be measured, but cannot be seen, are known as endophenotypes. Endophenotypes are not an element of the disorder but are associated with it, contribute to individual vulnerability and are seen in the families of affected individuals (Laucht et al., 2007). A range of endophenotypes has been identified as markers for AUDs in young people, including behavioural sensitivity to alcohol and event-related potentials (e.g. P300). Schuckit and colleagues have shown that a low level of response (LR) to alcohol is associated with heavier drinking and alcohol problems (Schuckit et al., 2005, 2008). Adolescent children of alcoholics have been shown to have an abnormal P300 response and abnormalities in brain structure and function (Hill and Steinhauer, 1993; Iacono et al., 2002; Yoon et al., 2006).
Sensation seeking and behavioural disinhibition are associated with an increased risk of developing substance use disorders in adolescence and may mediate genetic risk (Laucht et al., 2007; Iacono et al., 2008).
Externalizing problems in childhood, in particular conduct disorder, have been shown to predict adolescent alcohol and substance use disorders (White et al., 2001; King et al., 2004; Fergusson et al., 2007; Young et al., 2008). A longitudinal study from the West of Scotland (N = 2586 pupils) explored the causal effects of alcohol (mis)use and antisocial behaviour in pupils followed up between the ages of 11 and 15 years (Young et al., 2008) and the findings suggested that antisocial behaviour was the main predictor of alcohol misuse and alcohol-related trouble in this under-age cohort. An American study of 429 rural youths found that delinquency at the age of 11 was a positive predictor of alcohol use at 16 for both boys and girls (Mason et al. (2007). However other studies have reported a reciprocal relationship (D'Amico et al., 2008) and Iacono et al. (2008) propose that a common genetic liability to behavioural disinhibition underlies the co-occurrence of early onset substance use disorders and these other disorders. A recent study of male twins found that genetic risk of externalizing disorder and peer deviance predicted the greatest risks of unfavourable alcohol trajectories (Wichers et al., 2013).
Adolescents with attention deficit hyperactivity disorder appear to have an increased risk of drug use disorders but the evidence for an association with AUDs is mixed (Molina and Pelham, 2003; Molina et al., 2007, 2012). Parental knowledge may confer a protective effect in relation to alcohol use in adolescents with ADHD (Walther et al., 2012).
Of internalizing disorders, only depression at the age of 11 years was shown to have a significant relationship with substance use at the age of 14 years (King et al., 2004).
Adolescents with poor affect regulation and depression or who are experiencing high levels of environmental stress may drink or use drugs to self-medicate as a maladaptive coping mechanism. The association between low mood and alcohol use appears to be stronger in adolescents with fewer conduct problems (Hussong et al., 2008)
Adolescents are able to tolerate higher levels of alcohol than adults and they are also more likely to experience the positive effects of alcohol. This may contribute to the development of binge drinking.
Risk Factors for Drinking in Adolescents
The adolescent brain undergoes profound neuro-developmental change, in turn influenced by genetic, environmental and sex hormonal factors (Arain et al., 2013). Glutamatergic neurotransmission is predominant and the maturation of neural circuits facilitates social-emotional development (Nelson et al., 2005). At the same time puberty manifests itself in outward bodily change.
The risk factors for adolescent AUDs can be divided into environmental, genetic and phenotypic. Genetic-environmental interaction determines individual alcohol use and AUDs.
Environmental Factors
As adolescents become more autonomous so the influence of the peer group becomes more important and family influences wane (Bremner et al., 2011). Adolescence sees a clustering of risk-taking behaviours such as smoking, drinking, drug-taking and sexual activity. Peer effects on risk-taking are strong in this age group, and adolescents affiliated with substance-using peers are at greater risk of engaging in similar behaviours themselves (Gardner and Steinberg, 2005). Peer acceptance is a potent social reward for adolescents (Rubin et al., 2006; Guyer et al., 2012) and is associated with high self-esteem and social competence. Having friends who drink increases the likelihood that young people will drink too. Young people are also influenced by how much their friends are drinking. Having older friends and spending more time with drinking friends are likely to promote excessive drinking (Bremner et al., 2011).
Parental expectation and involvement in social activities has been shown to moderate alcohol use (Nash et al., 2005; Wichers et al., 2013) and religious affiliation also shows a protective effect. Factors that influence drinking, drinking frequently and drinking to excess include lower levels of parental supervision, exposure to a close family member who drinks or becomes intoxicated, easy access to alcohol and positive expectations of alcohol (Bremner et al., 2011).
Genetic Factors
Genetic predisposition accounts for about half of the risk in the development of alcohol dependence. Adolescents with a positive family history of alcohol problems are at greater risk of developing an alcohol problem, and at a younger age, than their peers with negative family histories. Genetic factors may have more influence on drinking behaviour in late than in earlier adolescence (Rose et al., 2001).
Certain childhood characteristics are thought to increase the risk of adolescent AUDs and early identification of these characteristics can be helpful in preventing or attenuating the risk (Thatcher and Clark, 2008). For instance childhood psychological dysregulation is a behavioural phenotype that reflects an individual's vulnerability to developing an AUD in adolescence (Tarter et al., 2003; Thatcher and Clark, 2008). Other characteristics that have been identified and can be measured, but cannot be seen, are known as endophenotypes. Endophenotypes are not an element of the disorder but are associated with it, contribute to individual vulnerability and are seen in the families of affected individuals (Laucht et al., 2007). A range of endophenotypes has been identified as markers for AUDs in young people, including behavioural sensitivity to alcohol and event-related potentials (e.g. P300). Schuckit and colleagues have shown that a low level of response (LR) to alcohol is associated with heavier drinking and alcohol problems (Schuckit et al., 2005, 2008). Adolescent children of alcoholics have been shown to have an abnormal P300 response and abnormalities in brain structure and function (Hill and Steinhauer, 1993; Iacono et al., 2002; Yoon et al., 2006).
Sensation seeking and behavioural disinhibition are associated with an increased risk of developing substance use disorders in adolescence and may mediate genetic risk (Laucht et al., 2007; Iacono et al., 2008).
Externalizing problems in childhood, in particular conduct disorder, have been shown to predict adolescent alcohol and substance use disorders (White et al., 2001; King et al., 2004; Fergusson et al., 2007; Young et al., 2008). A longitudinal study from the West of Scotland (N = 2586 pupils) explored the causal effects of alcohol (mis)use and antisocial behaviour in pupils followed up between the ages of 11 and 15 years (Young et al., 2008) and the findings suggested that antisocial behaviour was the main predictor of alcohol misuse and alcohol-related trouble in this under-age cohort. An American study of 429 rural youths found that delinquency at the age of 11 was a positive predictor of alcohol use at 16 for both boys and girls (Mason et al. (2007). However other studies have reported a reciprocal relationship (D'Amico et al., 2008) and Iacono et al. (2008) propose that a common genetic liability to behavioural disinhibition underlies the co-occurrence of early onset substance use disorders and these other disorders. A recent study of male twins found that genetic risk of externalizing disorder and peer deviance predicted the greatest risks of unfavourable alcohol trajectories (Wichers et al., 2013).
Adolescents with attention deficit hyperactivity disorder appear to have an increased risk of drug use disorders but the evidence for an association with AUDs is mixed (Molina and Pelham, 2003; Molina et al., 2007, 2012). Parental knowledge may confer a protective effect in relation to alcohol use in adolescents with ADHD (Walther et al., 2012).
Of internalizing disorders, only depression at the age of 11 years was shown to have a significant relationship with substance use at the age of 14 years (King et al., 2004).
Adolescents with poor affect regulation and depression or who are experiencing high levels of environmental stress may drink or use drugs to self-medicate as a maladaptive coping mechanism. The association between low mood and alcohol use appears to be stronger in adolescents with fewer conduct problems (Hussong et al., 2008)
Adolescents are able to tolerate higher levels of alcohol than adults and they are also more likely to experience the positive effects of alcohol. This may contribute to the development of binge drinking.
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