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 vs. 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 Lifetime 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 fit to the data. The heritability was 37% (95%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 almost entirely due to common genetic risk factors.