Third, we excluded lifetime nondrinkers from these analyses. Statistical methods do exist that would permit us to include these subjects and formally model the genetic and environmental contributions to alcohol initiation and then consumption patterns and risk for subsequent AD (Kendler et al., 1999) contingent upon drinking. However, the lifetime abstainers constituted such a small proportion of our sample that the gain in completeness would be more than offset by a very large increase in the complexity of our models and the number of required statistical parameters.
