Background and aims: An early age of alcohol initiation (AAI) is associated with and has been hypothesized to be a cause of alcohol use disorders (AUD) in adulthood. Results from twin studies, however, indicate that AAI is an indicator of risk for AUD. We aimed to test a causal hypothesis versus a risk indicator hypothesis for the relationship between early AAI and AUD.
Design: A population-based twin study using biometric twin modelling.
Setting: Norway.
Participants: A population-based sample of 1336 Norwegian twins.
Measurements: Life-time DSM-IV AUDs were assessed by structured clinical interview and AAI by questionnaire.
Findings: The risk indicator model in which the association between AAI and AUD was explained by common vulnerability was the best fitted to the data. The heritability was 37% [95% confidence interval (CI) = 21%, 53%] for AAI and 62% (95% CI = 51%, 73%) for AUD. Genetic risk for AAI accounted for 44% (95% CI = 17%, 71%) of the total genetic risk for AUD and the correlation between genetic factors for AAI and AUD was -0.66 (95%CI -0.87, -0.46). Individual-specific environmental risk for AAI explained only 1% (95% CI = 0%, 3%) of the risk for AUD. Shared environmental factors did not influence AUD, but accounted for 25% (95% CI = 7%, 35%) of the variance in AAI.
Conclusions: The association between early age of alcohol initiation and alcohol use disorders in later life does not reflect a causal relationship, but is due almost entirely to common genetic risk factors.
Keywords: Alcohol abuse; alcohol dependence; alcohol use; alcohol use disorders; causality; cohort studies; confounding factors; genetics; sex; twin study.
© 2014 Society for the Study of Addiction.