Abstract

There is now compelling evidence that growth patterns in early life are associated with risk of the metabolic syndrome in adulthood, although the relative importance of prenatal v. postnatal growth for such associations remains controversial. Body composition may play a key role in the 'programming' of such diseases, through itself being programmed by early growth, and perhaps also by being a mediator of the programming process. Early studies reporting positive associations between birth weight and adult BMI suggested a tendency for large babies to become obese adults. Such findings appeared contradictory to the many studies linking low birth weight with increased risk of the metabolic syndrome. Recent studies now indicate that birth weight is strongly predictive of later lean mass, and has a much weaker association with later fatness. Studies that link low birth weight with a more central adipose distribution in later life remain controversial, and require confirmation using more sophisticated methodologies. Findings for infant growth rate appear population-specific, with infant weight gain predicting subsequent lean mass in developing countries, but predicting subsequent fat mass and obesity in industrialised populations. Further studies are required on this issue, to ensure that appropriate public health policies are recommended for countries across the range of economic development. Although the links between early growth and later disease risk implicate early-life nutrition, either in utero or during infancy, few prospective studies have explored the influence of early diet on later body composition. Many studies have associated breast-feeding with a reduced prevalence of obesity categorised by BMI; however, the few studies directly evaluating childhood fatness provide little support for this hypothesis. Recent advances in the ability to measure body composition during the infant period offer a major opportunity to improve the understanding of the nutritional programming of body composition and its contribution, or lack thereof, to subsequent disease risk.