The name is absent

Autism prodrome 38 of 89

intrauterine environment in which it is developing. When the fetal environment is
deprived of nutrients, an adaptive change occurs, with optimization of the growth of key
body organs at the expense of other organs (Hales & Barker, 1992). This adaptation
involves changes in the epigenetic (‘epi’: on the gene) program and has long-term
consequences (Gicquel, El-Osta, & Le Bouc, 2008). Epigenetics relates to stable and
heritable patterns of gene expression that do not involve changes in DNA sequence.
Epigenetic mechanisms manage gene expression and are required to achieve the stable
repression or expression of genes at defined developmental stages. Prenatal and
perinatal environmental challenges during the course of pregnancy are likely causes
of deleterious epigenetic modifications to the fetal brain with long-term
developmental consequences, including risk and vulnerability to ASD. Moreover,
there is increasing evidence that prenatal psychological stressors program fetal and
neonate Hypothalamus-Pituitary-Adrenal (HPA) axis reactivity with long-term effects
on future development, and investigators have been identifying the epigenetic
machinery mediating the impact of prenatal stressors on the child development (McGill
et al., 2006; Weaver et al., 2004). Fetal programming involving epigenetic changes
might be a mediating mechanism between prenatal risk factors and subsequent
developmental outcome.

Recent investigations focused attention on the crucial prenatal and perinatal
periods and identified potential risk factors for ASD (Gillberg & Cederlund, 2005;
Glasson et al., 2004; Kinney, Munir, Crowley, & Miller, 2008; Kolevzon, Gross, &
Reichenberg, 2007; Larsson et al., 2005; Maimburg & Vaeth, 2006; Williams, Helmer,
Duncan, Peat, & Mellis, 2008). Croen, Grether and Selvin (2002) investigated a total
population of more than 3.5 million live births from 1989-1994 in California.
Participants included 4356 children known to the state as diagnosed with full

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