Table 1, when X, the path representing moderation of genetic influences on AD symptoms by age at 1st drink, was set to zero, there was a substantial deterioration of model fit. This statistically significant change in model fit was also noted when Z (path denoting moderation of non-shared environmental influences) was set to zero. However, both the shared environmental path (C) and its moderation (Y) could be constrained to zero. Thus, there was support for age of 1st drink modifying the magnitude of additive genetic and non-shared environmental influences on AD symptoms. These first sets of analyses were conducted jointly in men and women, allowing parameters to vary across sexes (hence, the 2 degree of freedom change in Table 1). Next, we tested for sex differences and some evidence was found. While the main effects of age at 1st drink on AD symptoms (via B) and the path denoting genetic factors and their moderation (A, via X) could be equated across sexes, the path denoting non-shared environment and its moderation (E, via Z) could not. Thus, our best-fitting model allowed for the main effects of age at 1st drink on AD symptoms and moderation of additive genetic and non-shared environmental
