Twin modeling, based on biometrical genetics (Neale & Cardon, 1992), uses the natural contrast between monozygotic (MZ) twins (who share 100% of their genetic material) and dizygotic (DZ) twins (who share on average 50% of their segregating genes) to estimate genetic and environmental influences on behavior. In the current study, proportions of variance in risk for AUD and remission accounted for by additive genetic influences (A), environmental influences shared by twins, such as early family environment (C), and unique environmental influences, which distinguish twins from one another (E), were estimated using a two-stage model in which sources of variance on remission are partitioned into those shared with AUD and those specific to remission. All participants had data for the five-level AUD symptom variable, which represented the first stage of the model. Remission represented stage 2 of the model, with individuals having 0–1 AUD symptoms, or 0–2 in the case of more narrowly defined AUD, set to missing because, by definition, only those with AUD can remit from them. Under this two-stage model, twin pairs discordant for alcohol problems still contribute
