Education Resource from the Society for Endocrinology
Dr Ken Ong
Medical Research Council Epidemiology Unit, & Department of Paediatrics, University of Cambridge
Summer School 11-14 July 2006
The Møller Centre, Storeys Way, Cambridge, UK
Maternal obesity is a strong predictor of offspring obesity (Reilly et al. 2005). This relationship is multifactorial, being likely due to a combination of shared lifestyles and genetic influences; in addition, maternal obesity may lead to fetal macrosomia associated with gestational diabetes (Sermer et al. 1995). Overall, larger offspring birth weight is positively associated with subsequent greater BMI in childhood and later life, however the relationship is complex. Larger birth weight is associated with greater subsequent lean mass, rather than fat mass (Loos et al. 2002). In contrast, lower birth weight is associated with a subsequent higher fat mass to lean mass ratio, and also greater central fat and insulin resistance (Valdez et al. 1994). This paradoxical effect of lower birth weight is at least partly explained by the observation that these infants, who have been growth restrained in utero, tend to gain weight more rapidly, or “catch-up”, during the early postnatal period (Ong et al. 2002).
Other maternal factors associated with intra-uterine growth restraint include: first pregnancies, smoking during pregnancy, and lower mother’s own birth weight, which reflects maternal genetic factors. The greatest risk of childhood obesity and its adverse consequences may therefore be seen in babies born small relative to parental size, who have been more restrained in utero. Such infants grow more rapidly during infancy and have an increased tendency to central fat deposition, insulin resistance and cardiovascular disease risks in later life (Fagerberg et al. 2004; Ong et al. 2004).
There is still debate as to whether there are critical early periods for obesity: does excess weight gain during infant, childhood, or even very early neonatal life have a greater impact on long-term fat deposition and insulin resistance? Early prediction of childhood obesity risk will be aided by identification of maternal and fetal genes that regulate fetal nutrition and growth, and postnatal genes that regulate appetite, energy expenditure and the partitioning of energy intake into fat or lean tissue growth.
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The opinions expressed in this paper are those of the speaker and do not necessarily reflect the views of the Society
Revised:
23-Aug-2006