Objective To identify predictors of postnatal catch-up growth from birth to two years and its relation to size and obesity at five years. Design Regional prospective cohort study. Setting Avon longitudinal study of pregnancy and childhood, United Kingdom. Subjects 848 full term singletons from a 10% random sample of the Avon longitudinal study of pregnancy and childhood. Main outcome measures Maternal birth weight, prepregnancy weight, pregnancy weight gain, height, smoking, and parity, and paternal height. Weight and length of infants at birth, two years, and five years expressed as standard deviation (SD) scores from the UK reference scores for 1990. Percentage fat mass and total fat mass (estimated from skinfolds) and waist circumference at five years. Results Size at birth was representative of the national reference. Overall, 30.7% (260 of 848) of infants showed a gain in SD score for weight greater than 0.67 SD scores between zero and two years, indicating clinically significant catch-up growth. These children had lower weight, length, and ponderal index at birth than other children, and were more often from primiparous pregnancies. They also had taller fathers than other children, and their mothers had lower birth weights and were more likely to smoke during pregnancy. Children who showed catch-up growth between zero and two years were heavier, taller, and fatter (body mass index, percentage body fat, and waist circumference) at five years than other children. Conclusions In this contemporary well nourished cohort, catch-up growth was predicted by factors relating to intrauterine restraint of fetal growth. Children who showed catch-up growth between zero and two years were fatter and had more central fat distribution at five years than other children. Mechanisms that signal and regulate early catch-up growth in the postnatal period may influence associations between small size at birth and risks for disease in adulthood.Papers

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There is remarkably wide variation in rates of infancy growth, however, its regulation is not well understood. We examined the relationship between maternal smoking, parity, and breast- or bottle-feeding to size at birth and childhood growth between 0 and 5 y in a large representative birth cohort. A total of 1,335 normal infants had weight, length/height, and head circumference measured at birth and on up to 10 occasions to 5 y old. Multilevel modeling (MLwiN) was used to analyze longitudinal growth data. Infants of maternal smokers were symmetrically small at birth (p < 0.0005) compared with infants of nonsmokers, however, showed complete catch-up growth over the first 12 mo. In contrast, infants of primiparous pregnancies were thin at birth (p < 0.0005), showed dramatic catch-up growth, and were heavier and taller than infants of nonprimiparous pregnancies from 12 mo onwards. Breast-fed infants were similar in size at birth than bottle-fed infants, but grew more slowly during infancy. Among infants who showed catch-up growth, males caught up more rapidly than females (p = 0.002). In conclusion, early postnatal growth rates are strongly influenced by a drive to compensate for antenatal restraint or enhancement of fetal growth by maternal-uterine factors. The mechanisms that signal catch-up or catch-down growth are unknown but may involve programming of appetite. The importance of nutrition on early childhood growth is emphasized by the marked difference in growth rates between breast- and bottle-fed infants. The sequence of fetal growth restraint and postnatal catch-up growth may predispose to obesity risk in this contemporary population.

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Leptin may have a role in the initiation of puberty and the regulation of subsequent weight gain, but this hypothesis has not been tested by longitudinal study. We report data from 40 normal children (20 boys and 20 girls) followed from 8-16 yr of age with hormone measurements and auxology every 6 months. Before the onset of puberty, leptin levels were similar in boys and girls: G1, mean (95% confidence interval), 2.63 (2.17-3.20) ng/mL; B1, 2.47 (2.08-2.94) ng/mL (P = 0.64) and increased with age in both sexes (B, 0.107 +/- 0.042; P = 0.02). With the onset of puberty, leptin levels increased in girls (B2-B5, P < 0.0005), but decreased in boys (G2-G5, P < 0.0005). Similar positive independent relationships were seen between leptin and fat mass in girls (B, 0.106 +/- 0.022; P < 0.0005) and boys (B, 0.121 +/- 0.020; P < 0.0005), and negative relationships were found with fat-free mass [girls: B, -1.104 +/- 0.381 (P < 0.005); boys: B, -1.288 +/- 0.217 (P < 0.0005)]. Girls gained more fat mass than boys, whereas boys gained more fat-free mass, and this explained the sex difference in leptin levels. Leptin levels correlated significantly with a large number of other hormones, but none was independent of changes in body composition. In girls, but not in boys, low leptin levels during prepuberty (B1) predicted subsequent gains in the percent body fat during puberty (r = -0.75; P = 0.005). The sexual dimorphism in leptin levels during puberty reflects differential changes in body composition. Prepubertal leptin levels in girls also predict gains in the percent body fat.

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Recent discoveries of human genetic leptin deficiency have demonstrated its importance in regulating weight gain in early childhood. To investigate whether normal variation in leptin and insulin levels in cord blood could influence infancy growth, we assayed samples from 197 infants from a representative birth cohort, who were measured at birth, 4, 8, 12 and 24 months. Cord leptin levels correlated most closely with weight and ponderal index (kg/m3) at birth, but also with length and head circumference (all p<0.0005). Independent of birth size, females had higher leptin levels than males (p<0.0005). Cord levels of leptin, but not insulin, were negatively related to weight gain (p<0.005) from birth to 4 months, and accounted for 9.4% of the variance in weight gain, compared with breast/bottle feeding (3.5%) and early/late introduction of solids (1%). The effect of leptin levels on weight gain was independent of birthweight, and was still evident at 24 months. The wide variation in infancy growth ('catch-up' or 'catch-down') may be partly determined by leptin levels preset in utero. Our data support a role for leptin in the regulation of infancy weight gain, and suggest a mechanism whereby infants may 'catch-up' in growth postnatally following an adverse intrauterine environment.