BEC and not on intake, the intakes have increased as a genetically correlated response to selection (Fig. 3). The S7 HDID-2 mean ethanol intake was 6.45 ± 0.33 g/kg, while that for the S7 HDID-1 mean was 5.89 ± 0.26 g/kg. That mice achieving higher BECs drank more makes logical sense. That there was a smaller increase in intake than there was in BEC over generations is consistent with there being partial, but not total, overlap between the pools of genes affecting the two traits. Within genetically homogeneous C57BL/6J mice, the correlation (which is traditionally taken as environmental in origin) between intake and BEC was r = 0.71 (Rhodes et al. 2005). Within HDID-1 mice of the S11 generation, where the correlation represents a mix of genetic and environmental influences depleted to the extent that selection has fixed some relevant genes, we found r = 0.45 (Crabbe et al. 2009). In the foundation population (S0) of HS/Npt animals, the correlation was r = 0.44 (unpublished data). We believe that across populations and estimates, intake typically explains about 25% of BEC variation, whether considered phenotypically or ‘genetically’ [i.e., from inbred strain means (Crabbe et al. 2009)].
