To address the relationships between genetic influences on AD symptomatology, AD symptom clustering (whether 3 or more symptoms occurred within a 12-month period; undefined in those with 0–2 AD symptoms), alcohol abuse (undefined in those with 3 or more AD symptoms), and heaviness of consumption (undefined in those with 3 or more AD symptoms), we used an approach described by Heath et al. (30). In a twin analysis containing an unconditional phenotype (e.g. AD symptomatology) and a conditional phenotype (e.g. heaviness of consumption, defined only in unaffected individuals) and using the assumption of underlying normally distributed risk (‘liability’) distributions, they showed that although a full bivariate genetic model is underidentified if the unconditional phenotype is binary, this problem no longer applies if the unconditional phenotype includes at least two non-zero categories for which the conditional phenotype is defined (e.g. consumption is defined in those reporting 0, 1 or 2 AD symptoms).
