Table 7.
Male | Female | |||||
---|---|---|---|---|---|---|
Coefficients | Estimate | 95%CI | p | Estimate | 95%CI | p |
Autoregressive | ||||||
ASB12→ASB13b | 0.789 | 0.658, 0.920 | <0.001 | 0.782 | 0.664, 0.900 | <0.001 |
ASB13→ASB15 | 0.746 | 0.673, 0.819 | <0.001 | 0.757 | 0.686, 0.828 | <0.001 |
ASB15→ASB17 | 0.645 | 0.559, 0.731 | <0.001 | 0.725 | 0.633, 0.817 | <0.001 |
ALC12→ALC13b | 0.670 | 0.564, 0.776 | <0.001 | 0.673 | 0.573, 0.773 | <0.001 |
ALC13→ALC15 | 0.497 | 0.436, 0.558 | <0.001 | 0.498 | 0.443, 0.553 | <0.001 |
ALC15→ALC17 | 0.507 | 0.436, 0.578 | <0.001 | 0.507 | 0.448, 0.566 | <0.001 |
Cross-lagged | ||||||
ALC12→ASB13 | −0.062 | −0.229, 0.105 | 0.468 | −0.057 | −0.202, 0.088 | 0.446 |
ALC13→ASB15 | 0.079 | −0.017, 0.175 | 0.102 | 0.019 | −0.071, 0.109 | 0.676 |
ALC15→ASB17 | 0.156 | 0.062, 0.250 | 0.001 | 0.057 | −0.051, 0.165 | 0.300 |
ASB12→ALC13 | 0.047 | −0.090, 0.184 | 0.503 | 0.078 | −0.051, 0.207 | 0.237 |
ASB13→ALC15 | 0.276 | 0.202, 0.350 | <0.001 | 0.269 | 0.202, 0.336 | <0.001 |
ASB15→ALC17 | 0.120 | 0.036, 0.204 | 0.005 | 0.131 | 0.055, 0.207 | 0.001 |
Correlationc | ||||||
ASB12-ALC12 | 0.676 | 0.625, 0.727 | <0.001 | |||
Residual correlationc | ||||||
ASB13-ALC13 | 0.238 | 0.115, 0.361 | <0.001 | |||
ASB15-ALC15 | 0.459 | 0.390, 0.528 | <0.001 | |||
ASB18-ALC17 | 0.649 | 0.580, 0.718 | <0.001 | |||
Fit indices | χ2 = 12,557.796, df = 5,413, p < 0.001 | |||||
CFI = 0.960, TLI = 0.961 | ||||||
RMSEA [90%CI] = 0.017 [0.017, 0.018] |
CFI, comparative fit index; RMSEA, root mean square error of approximation; TLI, Tucker-Lewis index.
In Model 2, autoregressive and cross-lagged paths were allowed to vary between the male and female subgroups, so separate autoregressive and cross-lagged paths by sex are presented.
ASB and ALC are factors for antisocial behavior and alcohol use, respectively.
Correlations were constrained equal across male and female subgroups in Model 2. Correlations were estimated at the initial age (age 12), and residual correlations were estimated at the rest of ages because ALC and ASB factors at ages 13 to 17 were endogeneous factors (i.e., dependent latent variables).