Catch up is a property of human growth whereby children return to their genetic trajectory after a period of growth arrest or delay, for example, because of illness.
12 It may occur at any stage of growth, but is most commonly observed in the first 1-2 years of life, and pronounced catch-up growth postnatally is often seen after severe intrauterine growth restraint.
13In this contemporary and representative birth cohort, a large proportion of children (30.7%) showed catch-up growth between zero and two years, sufficient to result in a move upwards by the width of at least one percentile band on standard growth charts. These children were lighter and thinner at birth than other children, and their mothers had had lower birth weights and also higher prevalence of primiparous pregnancy and smoking than the other mothers, indicating that fetal growth in these children had been restrained. The main determinants of fetal growth restraint in contemporary societies are not known. In this cohort, maternal diets during pregnancy have been shown to be adequate
14 and unrelated to size at birth.
15 Pregnancy induced hypertension and other maternal disease are also unlikely to be major factors as this cohort was recruited from healthy singletons at full term.
Children who showed catch-up growth had taller fathers than the other children. This may indicate a postnatal effect of paternal genes on childhood growth but could also be explained by increased maternal restraint in response to greater fetal growth potential, as suggested by crossbreeding experiments in animals.
16 Catch-up growth was also related to low maternal birth weight. From observations of birth weights among extended human kindreds, Ounsted concluded that maternal restraint may be inherited as a trait through the maternal line.
17 In this ALSPAC cohort, we recently showed an association between a common genetic variant in mitochondrial DNA and thinness at birth in infants who subsequently showed catch-up growth.
18 Thus, interaction between maternally and paternally derived fetal genotypes could be an important determinant of fetal growth restraint and postnatal catch-up growth.
19How infants who were restrained in utero catch up postnatally is largely unknown, although greater food intake has been observed compared with other infants.
20 Concentrations of cord blood leptin are positively related to ponderal index at birth but inversely related to weight gain in infancy, and thus low concentrations of this hormone at birth may provide a signal for catch-up growth through reduced inhibition of satiety.
21Children who showed catch up in weight or length between zero and two years were heavier and taller than other children at five years and they were also taller in relation to their mothers' and fathers' heights. Furthermore, these children had greater body mass index, percentage body fat, total fat mass, and central fat distribution, which are variables of childhood size linked to metabolic markers for risk of disease in adulthood
22,23 and are predictive for adulthood obesity.
24 Thus, in contemporary, affluent societies the biological predisposition to catch-up growth conferred by intrauterine restraint may result in an acceleration of growth postnatally that overshoots the genetic trajectory. A similar growth pattern has been observed in rodents exposed to experimental growth restraint in utero but allowed a plentiful food supply postnatally.
25It is not known whether children who show postnatal catch-up growth will achieve final heights in excess of their genetic target, or rather whether their larger size at five years represents a faster rate of maturation. It is clear, however, that early postnatal catch-up growth, in a contemporary setting, leads to increased risk of central and peripheral obesity in childhood and potential risk for disease in adulthood. In contrast, catch-down growth in babies of large birth weight was related to thin size at five years and this finding is consistent with the continuum in decreasing risk of disease in adulthood with increasing size at birth, which extends across the whole range of birth weights.
5,6 Further exploration of genetic and postnatal environmental factors that influence postnatal catch-up growth could uncover mechanisms whereby associations between size at birth and risks for disease in adulthood may be modified.
What is already known on this topic
The increased risks for diseases in adulthood, such as type 2 diabetes and hypertension, associated with small size at birth are exacerbated, and in some population studies only seen, in those subjects who become obese
What this study adds
The greatest variation in rates of weight gain occurs in the first 1-2 years of postnatal life
Infants who showed catch-up growth during this period were smaller and thinner at birth and had more maternal indicators of intrauterine growth restraint but were larger and fatter than other children at five years
Factors that signal and regulate postnatal catch-up growth may therefore contribute to the pathogenesis underlying the fetal origins hypothesis