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 age 18–20, this increased to 28% and for the ages 21–29, 50% of the variance could be explained by genetic factors. At age 30–32 genetic influences were less important, explaining 28% of the variance.Table 6ACE and ADE variance component estimates and model fit results for the cross-sectional genetic analysesAgeADCE−2ll#par df χ2 Δdf p 15–17 ACE0.180.450.38831.1351,204 AE 0.68 0.32 834.0041,2052.871 0.090 CE 0.58 0.42 831.4641,2050.341 0.562 E1.00869.4531,20638.3220.00018–20 ACE0.280.190.533656.3753,636 AE 0.51 0.50 3658.0043,6371.631 0.202 CE 0.40 0.60 3658.7043,6372.331 0.127 E1.003719.7333,63863.3620.00021–23 ADE0.060.440.503644.0453,490 AE 0.46 0.54 3645.9843,4911.941 0.163 E1.003699.2433,49255.2020.00024–26 ADE0.240.260.523130.8553,035 AE 0.48 0.52 3131.3943,0350.541 0.462 E1.003178.6633,03647.8120.00027–29 ADE0.040.470.492620.0252,552 AE 0.47 0.53 2621.2742,5531.251 0.264 E1.002657.7832,55437.7620.00030–32 ACE0.280.120.592211.1552,225 AE 0.42 0.58 2211.4342,2260.281 0.597 CE 0.34 0.66 2212.1842,2261.031 0.310 E1.002233.5132,22722.3620.000For models printed in italics, the model fit does not differ significantly from the full (ACE or ADE) model (α = .05)
