of the association; that fetal nutrition as a programming stimulus affects fetal growth rather than birthweight. 60 This distinction between fetal growth and birthweight is difficult to make in human pregnancy, although repeated ultrasound measures of fetal size during pregnancy are beginning to assist here. However, the distinction can be readily demonstrated in animals. Fetal sheep growing rapidly in late gestation slow their growth promptly in response to 10 days of maternal undernutrition and resume growth on maternal (and hence fetal) refeeding. When examined after 10 days of refeeding, these fetuses have the same birthweight and length as control fetuses of well-fed ewes, but have increased heart and kidney size and increased blood pressure. 45 , 61 In this case fetal weight does not reflect the direct causal relationship between fetal nutrition, fetal growth and altered physiology. A similar situation can be imagined in human pregnancy where fetuses of similar birthweight may arrive at that point via very different growth trajectories (Figure 2). It seems likely that these trajectories would be associated with different patterns of physiological function and likely programming and thus disease risk, although this remains to be demonstrated. A fetus can reach a given birthweight via a variety of possible different growth trajectories. These fetuses may be of different body composition, and may have differing disease risk in adulthood. A Late growth restriction and fetal wasting. B Early growth restriction. C Normal growth. D Late growth restriction followed by catch-up growth. If fetal growth is poorly reflected