Early age of alcohol initiation is not the cause of alcohol use disorders in adulthood, but is a major indicator of genetic risk. A population-based twin study
Version of Record online: 19 AUG 2014
© 2014 Society for the Study of Addiction
Volume 109, Issue 11, pages 1824–1832, November 2014
How to Cite
Ystrom, E., Kendler, K. S. and Reichborn-Kjennerud, T. (2014), Early age of alcohol initiation is not the cause of alcohol use disorders in adulthood, but is a major indicator of genetic risk. A population-based twin study. Addiction, 109: 1824–1832. doi: 10.1111/add.12620
- Issue online: 8 OCT 2014
- Version of Record online: 19 AUG 2014
- Accepted manuscript online: 20 MAY 2014 07:08AM EST
- Manuscript Accepted: 9 MAY 2014
- Manuscript Revised: 12 AUG 2013
- Manuscript Received: 29 MAY 2013
- National Institutes of Health. Grant Number: MH-068643
- Norwegian Research Council. Grant Number: 190509
- Norwegian Foundation for Health and Rehabilitation
- Norwegian Council for Mental Health
- European Commission. Grant Number: QLG2-CT-2002-01254
- Alcohol abuse;
- alcohol dependence;
- alcohol use;
- alcohol use disorders;
- confounding factors;
- cohort studies;
- twin study
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.
A population-based twin study using biometric twin modelling.
A population-based sample of 1336 Norwegian twins.
Life-time DSM-IV AUDs were assessed by structured clinical interview and AAI by questionnaire.
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.
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.