(Bukowski et al., 2009; Vahratian et al., 2004), preeclampsia (Bodnar et al., 2006; Catov et al., 2007), and infants with low birth weight and who are small for their gestational age (Timmermans et al., 2009). For example, the First and Second Trimester Evaluation of Risk (FASTER) trial found that preconceptional folate supplementation for at least 1 year was associated with a lower risk of spontaneous extreme preterm birth (20–28 weeks) and that the risk was inversely proportional to the duration of preconceptional folate supplementation.
Although the biological mechanisms linking periconceptional nutrition with specific reproductive outcomes are not clearly understood, Lu indicated that some evidence makes connections that are biologically plausible. For example, nutrition plays a role in host susceptibility to infection and inflammation, and these in turn may be related to placental complications. In approximately one-third of the cases of preterm birth, the placental vessels show failure of vascular remodeling, and in 15 to 25 percent they show residual vascular pathology characterized by thrombosis and atherosis (see Figure 2-1).
Lu briefly reviewed evidence of the role of the placenta in fetal programming and future disease risk (see Godfrey, 2002) and noted potential effects of periconceptional nutrition on epigenetic modification (Sinclair et al., 2007; Steegers-Theunissen et al., 2009). In particular, he emphasized periconceptional nutrition as it relates to allostasis and allostatic load. Allostasis refers to the maintenance of stability through change, and allostatic load refers to the cumulative physiological toll from chronic stress. Chronic, repeated stress causes the body to lose its ability for self-regulation (McEwen, 1998). Lu postulated that chronically “bombarding” the body with high-sugar and high-fat diets and with high stress will gradually re-