Impact of age at first drink on vulnerability to alcohol-related problems: Testing the marker hypothesis in a prospective study of young adults
Introduction
Early experimentation with alcohol is highly prevalent among youth in Western countries (Hibell et al., 2005; Johnston et al., 2005), making adolescence a critical age period for the onset and increase of alcohol use. During the past two decades, a burgeoning literature has emerged establishing an association between age of drinking onset and risk for later hazardous alcohol consumption and dependence. Both cross-sectional (Grant and Dawson, 1997, Hingson et al., 2006, McGue et al., 2001b) and longitudinal studies (Grant et al., 2001a, Pitkanen et al., 2008, Warner et al., 2007; Grant et al., 2001b) have indicated that the age at drinking onset is one of the strongest predictors for the development of later alcohol-related problems.
Although well described, the mechanisms underlying this relationship remain unclear. On the one hand, a direct causal relationship between early age at first alcohol use and the vulnerability to subsequent problem drinking has been suggested. Adolescence is a stage of life that is associated with various significant transitions and psychological changes. The early initiation of alcohol use is assumed to affect important developmental processes that determine healthy functioning in later life and thereby causes an escalation towards heavier and more frequent drinking (DeWit et al., 2000). From a neurobiological perspective, it has been argued that prominent alterations in brain function and structure during adolescence are associated with a higher sensitivity towards external influences. The most affected brain regions during this transitional period are the prefrontal cortex, the mesolimbic dopamine system and its connections to the forebrain (Spear, 2002). Given the important role of these brain areas in mediating the reinforcing effects and motivational salience of alcohol and other drugs, it is suggested that the adolescent brain is particularly vulnerable to the progression of neural changes underlying addiction (Chambers et al., 2003).
Numerous preclinical studies document that the acute and chronic effects of drug exposure differ significantly depending on the developmental stage (Smith, 2003). Adolescent rats were found to be less sensitive to the sedative effects of ethanol compared with older animals (Little et al., 1996, Pian et al., 2008). As a consequence of heavy alcohol intake, adolescent but not adult rats showed frontal cortex degeneration and more persistent impairments on spatial learning memory (Crews et al., 2000, White et al., 2000). Analogous to these findings in rodents, altered brain structure and cognitive performance were found in heavy-drinking human adolescents. 15–16-year-olds with repeated heavy use displayed significantly poorer learning and memory function than nonabusing youths (Brown et al., 2000). Studies using MRI volumetry demonstrated reduced volumes of the hippocampus (De Bellis et al., 2000) and prefrontal cortex in alcohol-abusing adolescents compared with matched controls (De Bellis et al., 2005). These probable alcohol-related alterations may promote persistent drinking and impede the adaptation to developmental challenges, thus explaining the high risk of lifetime alcohol dependence among those who started drinking in early adolescence.
Another explanation for the association between early drinking initiation and a greater risk of alcohol-related problems posits that drinking onset at an early age is rather a correlate of shared predisposing factors. This contrary theoretical position emphasizes a common genetic determination of both phenomena and is sustained by twin studies showing substantial genetic influence on the association between early alcohol use and alcohol dependence (Prescott and Kendler, 1999, McGue et al., 2001a). Possible mechanisms for an indirect genetic transmission include parental alcoholism and offspring psychopathology, particularly externalizing disorders. Moreover, important psychosocial predictors of alcohol misuse were identified as indicators of a negative developmental trajectory that leads to later alcohol-related problems and have also been linked to early onset alcohol use (Hawkins et al., 1997, Pitkanen et al., 2008, Windle et al., 2008).
Male gender and a positive family history of alcoholism, both of which are known risk factors for problem drinking and dependence (Chassin et al., 1999, Grant et al., 2008), were repeatedly shown to be predictive for early alcohol initiation (Hill et al., 2000, Sartor et al., 2007). There is some evidence that environmental conditions and stressors, i.e. adverse familial attitudes, family conflict and availability of alcohol, promote early drinking onset rather than family history of alcoholism per se (Kuperman et al., 2005, Komro et al., 2007). Not only do substance abuse and disinhibitory/antisocial traits and disorders frequently co-occur (Compton et al., 2005, Ohlmeier et al., 2008), but childhood and adolescent externalizing symptoms have been described as important predictors of adult alcohol use and alcohol use disorders (Alati et al., 2005, Molina and Pelham, 2003, Pitkanen et al., 2008). Drinking alcohol at an early age was repeatedly found to be preceded by aggressive/antisocial and hyperactivity/impulsivity symptoms in boys and girls (Elkins et al., 2007, McGue et al., 2001a, Sartor et al., 2007), suggesting that the association of early onset drinking with later alcohol problems might reflect a common vulnerability to externalizing behavior.
In order to take into consideration the noted inherent and environmental characteristics when examining the effects of early drinking onset, longitudinal studies are needed. Such studies provide the possibility to prospectively investigate the relationship between different risk factors and their impact across different developmental stages. Previous attempts to explore whether there is a causal or merely correlative relationship between the age at drinking onset and the risk for alcohol dependence yielded conflicting results. When estimating the effects of risk factors in early adolescence on alcohol misuse in young adulthood, Hawkins et al. (1997) found that age of drinking initiation fully mediated the effects of relevant parental behavior as well as school and peer influences. Although this result suggests that environmental and family factors may only be significant for the development of alcohol use disorders due to their involvement in determining age at drinking onset, this study did not account for factors that represent genetic transmission, e.g. parental alcoholism and child psychopathology. In a more recent prospective study, King and Chassin (2007) showed that early-adolescent drinking onset was no longer a predictor of alcohol dependence in young adults after controlling for parental characteristics, the family environment and externalizing symptoms. This finding, in turn, supports the notion that early onset of alcohol use does not influence the risk for later dependence in itself but may merely be a marker of a genetically determined vulnerability to alcoholism.
The current study represents a further step in gaining an understanding of this complex issue. To examine the association of age at first alcohol use with drinking habits and hazardous drinking in young adulthood, we prospectively investigated a German birth cohort, considering various preceding risk factors from childhood to adolescence. In addition, we were able to incorporate genotype information in order to explore its effect on the age at drinking onset. Research on the molecular genetics influencing the liability for alcoholism is complicated due to the multiple genes contributing to this complex disorder. Previously, in our own study, we found evidence that two haplotype-tagging single nucleotide polymorphisms (SNP) covering the CRHR1 gene (rs242938, rs1876831) affected adolescent alcohol use (Blomeyer et al., 2008, Treutlein et al., 2006). Recently, we also observed an involvement of the CRHR1 gene in predicting earlier drinking onset. In addition, we demonstrated an association between the level of response to alcohol during adolescence and a functional polymorphism in the promoter region of the serotonin transporter (5-HTTLPR, Hinckers et al., 2006). This well-studied polymorphism is purported to play a role in determining various personality traits and psychiatric disorders, including alcohol dependence, but to date, there is only one study indicating its importance for the early initiation of alcohol use, which was conducted among Korean male alcoholics (Kweon et al., 2005).
The aim of the present study was to replicate the results from US surveys, by investigating whether age at drinking initiation is associated with young adult alcohol consumption and problem drinking in a German cohort. In addition, we examined whether age at first drink remains a predictor of drinking behavior in adulthood when controlling for shared risk factors that precede first alcohol use, including family and individual characteristics and relevant genotypes.
Section snippets
Sample
The participants of the Mannheim Study of Children at Risk, a prospective longitudinal study on the outcome of early risk factors from birth into adulthood, were utilized for the present investigation. The initial sample consisted of 384 children of predominantly (>99.0%) European descent born between 1986 and 1988. Infants were recruited from two obstetric and six children’s hospitals of the Rhine-Neckar Region of Germany and were included consecutively into the sample according to a
Results
Table 1 presents descriptive data for drinking variables and potential risk factors for early onset drinking. On average, participants reported drinking alcohol once a week and more than half of the sample (53.6%) reported at least one heavy drinking occasion during the last 45 days. This rate corresponds well with the results from a recent epidemiological survey of substance abuse in Germany (Pabst and Kraus, 2008), which showed the highest prevalence of binge drinking in young adults (61.1% in
Discussion
The current study confirms previous research demonstrating that early age at drinking onset is significantly associated with increased alcohol consumption in adulthood. To our knowledge, this is the first investigation to prospectively assess this issue in a cultural setting which differs from the US in terms of having a lower legal drinking age, among others, by examining the question of whether this relationship is accounted for by shared factors contributing to the risk for alcohol
Contributors
A. Buchmann wrote the first draft of the manuscript. B. Schmid managed the literature searches and analyses. D. Blomeyer was responsible for the acquisition of data. K. Becker, J. Treutlein, M. Rietschel and G. Schumann contributed to the molecular genetic analyses. C. Jennen-Steinmetz provided statistical expertise. U.S. Zimmermann contributed to the analysis and interpretation of the data. M. Schmidt, G. Esser and T. Banaschewski contributed to the conception and funding of the study. M.
Role of funding source
Funding for this study was provided by grants from the German Research Foundation (DFG) and the Federal Ministry for Education and Research. None of these institutions had any further role in study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the paper for publication.
Conflict of interest
All authors declare that they have no conflicts of interest.
Acknowledgments
This study was supported by grants from the German Research Foundation (DFG) and the Federal Ministry for Education and Research as part of the ‘Baden- Wuerttemberg Consortium for Addiction Research´ and the ‘National Genome Research Network’.
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