C H A P T E R 1 posure to infection after birth, determine its susceptibility to chronic disease in later life”. Adequate and balanced protein, energy and micronutrient intake during pregnancy might be a protective factor for adult obesity. Thus, improving women’s nutritional status prior to and during pregnancy can substantially reduce the risk of low birth weight. Children born with low birth weight appeared to have less lean body mass, lower BMI and greater fat mass in adults19. In SGA children, poor nutritional conditions during gestation can modify metabolic systems to adapt to expectations of chronic under nutrition. These children are potentially poorly equipped to cope with energy-‐dense diets and are possibly pro-‐ grammed to store as much energy as possible, leading to later obesity, metabolic syndrome, disturbed regulation of normal puberty and early onset of cardiovascu-‐ lar disease35. A follow up of 5654 men born from 1911 to 1930 in England demon-‐ strated that men with the lowest weights at birth had highest death rates from is-‐ chemic heart disease36. Fetal growth restraint is associated with maternal-‐uterine factors such as primipar-‐ ity, smoking, restrictions in the maternal diet, maternal insulin resistance, and ges-‐ tational diabetes. Alternatively, if an insulin resistant state was manifested in utero, then diminished fetal growth with SGA might be anticipated, because insulin is a powerful prenatal growth hormone14. Insulin plays a central role in fetal growth. During the first two years of life, espe-‐ cially during the first 12 months of life, SGA newborns are usually able to catch-‐up growth velocity above the 50th percentile37. Not only does this trend improve the final height, but it has also been associated with changes in insulin sensitivity38,39. If a SGA child shows a growth pattern that transcends the normal trend, the risk to develop obesity is evident. Also children with growth hormone deficiency (GHD) are at risk to develop obesity. GDH children appear to have a higher fat mass. In children who do not suffer from growth hormone deficiency, the growth in length compensates the increase in weight. In GDH children this compensation mechanism does not work. In GHD chil-‐ dren it is shown that besides its positive effect on growth, rhGH influences metabo-‐ lism too40,41. The basal metabolic rate increases visible as a change in body compo-‐ sition by an increase in fat-‐free mass (FFM)42,43. Adults with GHD are characterized by disturbances in body composition, lipid me-‐ tabolism, cardiovascular risk profile and bone mineral density. It is well-‐known that adult GHD usually is accompanied by an increase in fat accumulation. Growth hor-‐ mone replacement in adult patients with GHD results in reduction of fat mass and abdominal fat mass in particular44. 16
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