Early age at first drink may modify tween/teen risk for alcohol dependence

  • People who begin drinking at an early age are more likely to subsequently develop alcohol dependence (AD).
  • A new study has found that age at first drink (AFD) may enhance the role of genetic factors that are already associated with vulnerability to AD symptoms.
  • Heritable influences on AD symptoms were considerably greater in those who reported an AFD younger than 15 years of age.

Individuals who begin drinking at an early age are more likely to subsequently develop alcohol dependence (AD). While age at first drink (AFD) and AD are influenced by similar genetic and environmental factors, AFD may also have an impact on the risk for AD. A new study has found that AFD may facilitate the expression of genes that are already associated with vulnerability to AD symptoms.

Results will be published in the December issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

“Drinking at an early age may create an environment where individuals can more easily transition from normative to problematic drinking,” said Arpana Agrawal, assistant professor of psychiatry at Washington University School of Medicine and corresponding author for the study. “Early AFD is often part of other precocious/non-normative behaviors such as conduct problems, experimentation with drugs, and deviant peers. From a biological perspective, early AFD may induce changes in the highly sensitive adolescent brain, which may also modify an individual’s subsequent genetic vulnerability to AD.”

“This would mean that, for someone who is vulnerable, an experience or exposure leads to the expression of their pre-existing risk to develop AD,” added Carol A. Prescott, professor of psychology at the University of Southern California. “AFD could be said to have moderating effects if early alcohol exposure alters the trajectory an adolescent is on, for example, if early involvement then led to changes in academic achievement or peer group composition in ways that increased risk for later development of AD.”

Agrawal and her colleagues examined previously collected data on 6,257 adult, identical and fraternal, male and female Australian twins. They statistically examined the extent to which: AFD increased AD symptoms, and whether the magnitude of additive genetic, shared, and non-shared environmental influences on AD symptoms varied as a function of a lower AFD.

“In this sample of young adults of Caucasian ancestry from Australia, earlier AFD was associated with increased likelihood of a lifetime history of onset of AD symptoms, and with reporting more AD symptoms. It was also associated with increased genetic vulnerability to AD symptoms,” said Agrawal. “Compared with those who consumed their first alcohol drink after age 13 to15 years, early-onset drinkers appeared to be more genetically susceptible to later AD problems.”

“These results may be interpreted in two ways,” said Prescott. “Early drinking changes the course an individual is on, and is thus a direct cause of increased AD risk; and early drinking is correlated with AD risk, and is thus an indirect indicator of AD risk. The results from this study suggest that both explanations are partially correct.”

Agrawal believes it is possible that use of alcohol at a particularly early age may lead to modifications in the developing brain which, in turn, may modify expression of AD-related genes. “However,” she added, “it is equally likely that a set of common genes contribute to the likelihood of early AFD and AD.”

Neither Agrawal nor Prescott were surprised that heritable influences on AD symptoms were considerably greater in those who reported an AFD of younger than 15 years of age. “At least 12 studies from several different countries have found that individuals whose (genetic or environmental) predispositions lead them to try alcohol at an earlier age have greater risk to develop alcohol-related problems,” said Prescott.

“Additionally,” said Agrawal, “we found that in individuals who began drinking at a later age, genetic influences played a much smaller part and that non-shared environment gained prominence. This suggests that AD problems in those with later AFD, while less common, are attributable to unique experiences of those individuals, for example, a traumatic life event.”

Agrawal noted that these findings have implications for future research. “From a gene-finding standpoint, which is now gaining even more momentum, we urge scientists to consider the role of AFD,” she said. “Our work and that of others suggests heterogeneity in the role of genes acting on AD risk as a consequence of early or late AFD.”

These findings also have public-health and education implications, particularly for “tweens” and teens, about problems associated with early drinking. “We show that even though there are common, underlying risk and protective factors for AFD and AD,” said Agrawal, “encouraging youth to initiate drinking alcohol at a later age may reduce the likelihood of expression of genetic vulnerability to later alcohol problems. This does not imply that later-onset drinkers will never develop AD, but their risk seems largely attributable to individual environmental experiences.”

Given that this study is based on a sample of twins from Australia, as noted by Prescott, which has a different drinking culture and practices than in the U.S., Agrawal and her colleagues will next try to replicate these findings in other older and younger Australian and U.S. samples to see if these findings are unique to this group of young adult Australians or more general in nature.

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, “Evidence for an Interaction between Age at 1st Drink and Genetic Influences on DSM-IV Alcohol Dependence Symptoms,” were: Carolyn E. Sartor, Michael T. Lynskey, Julia D. Grant, Michele L. Pergadia, Richard Grucza, Kathleen K. Bucholz, Elliot C. Nelson, Pamela A.F. Madden, and Andrew C. Heath of Washington University School of Medicine; and Nicholas G. Martin of Queensland Institute of Medical Research, Australia. The study was funded by the National Institute on Alcohol Abuse and Alcoholism, and ABMRF/Foundation for Alcohol Research. This release is supported by the Addiction Technology Transfer Center Network at http://www.ATTCnetwork.org.

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