Female Male Normal

Female Male Undernourished

Figure 2 Locomotor behavior and food intake in Wistar rats as a consequence of a normal or adverse fetal environment (n = 6-8/ group). (A) Food intake (kcal per gram body weight per day over a 5-day period) in females at day 145; P< 0.005 for effect of fetal programing, P < 0.05 for postnatal hypercaloric diet. (B) Locomotor activity at 14months in males and females; P<0.005 for effect of fetal programing and gender. Data analyzed by factorial ANOVA, and data are shown as means ┬▒SE. (Reproduced from Vickers MH, Breier BH, McCarthy D, and Gluckman PD (2003) Sedentary behavior during postnatal life is determined by the prenatal environment and exacerbated by postnatal hypercaloric nutrition. American Journal of Physiology. Regulatory Integrative and Comparative Physiology 285(1): R271-273 with permission from the American Physiological Society.)

weight. Leptin may relate to subsequent growth by affecting appetite and energy intake.

Depending on the outcome under study, there are differences in whether linear growth or growth in weight, particularly weight relative to height, matters. Most often, more rapid weight gain is the risk factor, owing to the fact that excess adiposity is an important risk factor for many chronic diseases of adulthood. Another key issue concerns the timing of effects. There is controversy about whether early infancy compensatory growth following intrauterine growth restriction confers risk, or whether it is only later growth that matters.

Where many potential adverse outcomes might be affected by postnatal growth, the following sections focus on adiposity, blood pressure and coronary heart disease, insulin resistance and diabetes, and cancer.

Adiposity and Obesity

Early undernutrition followed by later overnutrition as well as early overfeeding independent of prior growth restriction are thought to increase risk of later obesity. Rapid postnatal weight gain occurs in a significant proportion of infants who are born small for gestational age. Prospective studies in US, South African, and British cohorts show that rapid growth in early infancy increases later risk of overweight. Longitudinal data from the US National Perinatal Collaborative study show that, independent of birth weight, one-third of obesity at age 20 is attributable to rapid weight gain in the first 4 months of life. In a Bristol, UK cohort, nearly one-third of children had an increased weight standard deviation (SD) score of more than 0.67units from birth to age 2 years, and these children remained fatter, having more central fat distribution at age 5 years compared to children with lower early growth rates. Similarly, data from the South Africa Birth to Ten cohort showed that children with rapid weight gain in infancy were significantly lighter at birth and significantly taller, heavier, and fatter throughout childhood.

Early postnatal growth rates may program insulin-like growth factors, IGF-I and IGF-II. Figure 3 illustrates this point with data on 5-year-old children from Bristol, UK in whom IGF levels were strongly related to current body size, but also that, independent of current size, children who had experienced catch up growth (change in Z-score >0.67 SD) from birth to age 2 had higher IGF levels. Childhood IGF levels are important as determinants of later linear growth and timing of puberty, and are associated with later risk of hormone-dependent cancers.

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