Table 6 shows the ACE or ADE variance components estimates and model fitting results for the cross-sectional genetic analyses. Since the MZ correlation was smaller than twice the DZ correlation for the age groups 15–17, 18–20 and 30–32, the ACE model was fitted for these age groups. For the age groups 21–23, 24–26, and 27–29, the MZ correlation was more than twice the DZ correlation and thus the ADE model was fitted. Comparison of the full models showed an increase of unique environmental factors over time, explaining 38% of the variance in AAD symptoms at age 15–17 and 59% at age 30–32. Shared environmental influences decreased over time. While almost half of the variance (45%) was explained by shared environmental influences at age 15–17, and 19% of the variance at age 18–20, no shared environmental effects were present for the ages 21–29. At age 30–32, shared environmental influences accounted for 12% of the variance again. Genetic influences showed an increase in importance over age. At age 15–20, 18% of the variance in AAD symptoms was explained by genetic influences. At
