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Chunk #21 — Methods — Data analysis — Longitudinal genetic analyses

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Stable genetic effects on symptoms of alcohol abuse and dependence from adolescence into early adulthood.
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First, in submodel 3a a unique environmental simplex structure was specified (Guttman 1955; Boomsma and Molenaar 1987) that allowed for both stable and dynamic influences. This model contained six latent unique environmental variance components, each with one observed measurement as its (only) indicator. The unique environmental variance underlying the observed measurement at a particular age group was determined by the transmission terms (ß) that describe the amplification or attenuation of the unique environmental variance that was already present in the previous age group (E i−1 ), plus the innovation terms (ζ) that allow for new unique environmental variance ‘coming on line’: E i = ße i2 × E i−1 + ζe i2 (Neale and Cardon 1992). Since 15–17 was the first age group, no unique environmental variance could be transmitted from an earlier age group. Therefore, the unique environmental variance for this age group reduced to ζe 12. For the CAGE at age 18–20, the unique environmental variance equaled ße 12 × ζe 12 + ζe 22 and for age 21–23 ße 22 × (ße 12 × ζe 12 +