Weight gain during lactation was significantly reduced in offspring nursed by a-casein deficient dams (p,0.001 for all comparisons of offspring nursed by a-casein deficient dams with the other two groups after day 3). This effect was seen when acasein deficient dams nursed their own pups and if the offspring of wild-type mice was nursed by deficient dams. This demonstrates that the effect is mediated by the genotype of the nursing female. This effect was also seen in two further litters after breeding of the a-casein deficient mice onto a CD1 background (Kolb et al., unpublished) . All females were able to nurse their pups, as indicated by the presence of milk in the stomach ('milk spot') in all groups of pups (Table 3) . However, by day 6, pups nursed by acasein deficient dams were visibly emaciated (Fig. 8a) in comparison with pups nursed by control dams (Fig. 8b) . By midlactation offspring nursed by a-casein deficient mice are significantly smaller than offspring nursed by control dams (Fig. 8c) . Pre-weaning mortality was low in all groups and unaffected by dam genotype. Weighing of individual pups throughout lactation demonstrates that offspring nursed by acasein deficient dams only reach a weight of around 3 g by the end of lactation, whereas pups nursed by control dams weigh around 12 g (Fig. 8d and Fig. 9a ). After weaning mice were maintained on a standard chow diet ad libitum. Offspring nursed by a-casein deficient dams display a significantly accelerated growth with respect to the control group between weaning and day 50 of life ( Fig. 9b and 10) . However, this brief growth spurt is insufficient to bring the weight of pups nursed by a-casein deficient dams up to the weight of control animals in the long term (Fig. 9c) . The difference in weight is displayed in both sexes (Fig. 9d) .