The modern era of genetic studies regarding alcohol and other drug-related problems was built upon many years of observations that these problems cluster in families. Thus, children of parents with AUD have a three to four times higher risk of having AUD themselves than children of parents without AUD.1,2 However, the presence of a familial influence does not by itself demonstrate whether this familial link relates to shared genes, a shared environment, or their combination. Those distinctions were subsequently addressed in part through twin studies demonstrating that twins of people with AUD were at significantly higher risk to have AUD themselves if they were identical twins, who shared 100% of their genes, than if they were fraternal twins, who shared only 50% of their genes. An identical twin of someone with AUD has about a 60% risk of AUD compared to about a 40% risk for fraternal twins. Therefore, even in identical twins, the risk that the second twin also developed AUD was not 100%, indicating the involvement of additional factors.3–5
