Most psychiatric disorders are likely a consequence of complex gene x gene and gene x environment interactions (Heath et al., 2002; Rutter et al., 2006). Our study presents age at 1st drink as a potential risk factor in the etiology of AD symptoms. From a gene-finding perspective, investigators may be able to enhance their ability to isolate genes for AD by considering them in the context of early age at 1st drink. From a public health standpoint, later age at 1st drink may serve to protect against a familial predisposition to subsequent AD symptomatology. Even though this environmental measure may share genetic vulnerability with AD, it is a modifiable environmental factor that needs further consideration.
