It has recently been shown that genetic defects in proteins involved in creatine synthesis or transport are associated with neurological problems in children; these include mental retardation, epilepsy and speech delay, implying an important role for creatine in brain development, although it is not known whether the role is different from the classic function of creatine and creatine phosphate in energy metabolism. The objective of this study was to determine the extent to which milk creatine could account for creatine accretion in the neonatal pig. Sow milk at peak lactation (day 18) contains about 800 μM creatine and no detectable guanidinoacetate (GAA), creatine’s immediate biosynthetic precursor. Arterial plasma creatine and GAA concentrations in lactating sows were 288 ± 112 μM and 2.4 ± 0.7 μM, respectively. No detectable arterial‐venous difference for creatine across the mammary glands of lactating sows was found. In the first 10 days of life, the neonatal pig acquires, from milk, about 320 μmoles of creatine/day/100 g weight gain. It is likely that milk is a minor source of creatine compared to de novo synthesis by the neonatal pig. This finding is consistent with that of human infants with genetic defects in creatine synthesis. Data will also be presented on the accretion of creatine in piglets over the first 10 days of life. (Supported by CIHR and NSERC).