ABSTRACT
Epidemiological studies have suggested a link between the fetal environment (including nutrition) and postnatal health, particularly cardiovascular function or dysfunction, in humans (Barker and Osmond 1986; Chmurzynska 2010; Hill and Duville 2000; Phillips 2007). For example, high rates of death from ischemic heart disease and the metabolic syndrome are positively correlated with low birth weight, which may result, in part, from a reduced availability of nutrients to the fetus in utero (Barker 2007; Hales and Barker 1992). The concept of fetal programming has been experimentally tested in a number of species, including nonhuman primates (Nijland et al. 2010), rats (Anderson et al. 2006), mice (Dunn and Bale 2009), cattle (Cafe et al. 2009), and sheep (Symonds et al. 2009). Of particular interest, effects of changes in nutrition or endocrine status during fetal or neonatal life can be carried forward to subsequent developmental stages (Figure 6.1). This phenomenon may be explained by epigenetics, which is deˆned as stable and inheritable alterations of genes through covalent modiˆcations of DNA and core histones without changes in DNA sequences (Evertts et al. 2010).
