Abstract

Infant nutrition in the 1970s was concerned with the high solute content of milk formula and its attendant risks of thirst, excess energy intake and infantile obesity. Campaigns encouraged a return to breast-feeding, and milk formulae were modified. The success of these campaigns has resulted in breast-fed children becoming less heavy even than children reared on newly formulated artificial milks. This raises the question of defining the optimal weight and height gain. Once these are defined, then new recommendations on intake can be developed. The intakes of breast-fed children cannot be used to define recommended intakes of formula since the energetic responses to the two seem to be different, and with so many differences in nutrient content, a comparison based only on energy intake is misleading.

Intakes of children differ by racial group, geographical area, time, season and social class, and there are substantial inter-individual variations in need. There is a tendency for excessive weight gain in obese families with below-normal intakes in obesity-prone infants and children. High intakes for a group of babies are associated with an increased prevalence of infantile adiposity.

The 1985 FAO/WHO/UNU allowances for energy in affluent societies could result in a 7% prevalence rate for obesity in children. There has been a secular decline in energy consumption in bottle-fed babies and in weaned children, but it is uncertain whether this is true of breast-fed babies. The secular decline in intake may reflect warmer homes and clothing and less physical activity than formerly. It is therefore difficult to specify appropriate energy intakes without taking into account physical activity, social and environmental factors, and individual susceptibility to weight gain.

If obesity is established in infancy or childhood, then there is now substantial evidence that this increases the probability of obesity in adolescence and in adult life. Experimental findings on baboons support a long-term programming of adiposity not mediated by an adipocyte hypercellular mechanism. This evidence supports a lowering of recommended intake in childhood. However, some data now suggest that rapid growth in infancy is advantageous on a long-term basis, thus casting doubt on the wisdom of accepting slower growth rates in breast-fed children. Early feeding practices, e.g., in relation to iron, fatty acid and cholesterol metabolism, also program long-term metabolism.

It is concluded that, given the uncertainty about the impact of different infant growth rates on adult risk of morbidity and mortality, a reduction in the recommended intakes for infants should only be undertaken when more reassuring data become available.