In order to study the mechanisms underlying low LR it would be important to know whether a single set of mechanisms contribute to all measures of low LR or if different mechanisms underlie the individual measures. Given the range of domains considered in this review, it seems unlikely that the human low LR is a monolithic phenotype. Most studies exploring the genetic basis for low LR as a risk factor in humans have employed individual response variables, differentiating among subjective, body sway, and hormonal variables. Others, however, have created composite “low LR” indices. Several studies have attempted to sort out the genetic and environmental contributions to paths that link family history, LR and eventual diagnosis using statistical approaches including multiple regression, path analysis, or structural equation modeling. These have typically used the composite variables, making it difficult to tell exactly which aspects of LR might be predictive or have different mechanisms (Schuckit, Smith 1996;Schuckit, Smith 2000;Trim et al., 2009). Despite these difficulties, linkage and association studies have found some evidence for genomic localization of risk -promoting alleles for the global
