Our estimate of the heritability of consumption was far lower than estimates (Manolio et al., 2009; Zuk et al., 2012) obtained previously for consumption in young adults in previous studies (Rose et al., 2001; Palmer et al., 2013). Current methods used to calculate h2SNP typically result in estimates that are lower than those obtained using traditional biometric modeling. For example, a recent study of a Dutch sample assessed using the AUDIT reported a twin-based h2 estimate of 0.6, with a corresponding SNP-based estimate of h2SNP 0.33 (Mbarek et al., 2015). Such findings (“missing heritability”) have been discussed extensively (Manolio et al., 2009; Lee et al., 2011; Zuk et al., 2012; Brookfield, 2013; Koch, 2014), and may be due to rare variants, poor tagging of common variants, overestimation of heritability in twin studies, epistatic interactions, epigenetic factors, or other genomic phenomena. Accordingly, the low and non-significant h2SNP estimates for Problems and Maxdrinks may reflect the presence of other genetic factors, insufficient statistical power, or both (Supplementary Table 4). There are other potential explanations specific to the study and outcomes. First, recall
