Prenatal maternal stress (PNMS) in animals and humans predicts obesity and metabolic dysfunction in the offspring. Epigenetic modification of gene function is considered one possible mechanism by which PNMS results in poor outcomes in offspring. Our goal was to determine the role of maternal objective exposure and subjective distress on child BMI and central adiposity at 13½ years of age, and to test the hypothesis that DNA methylation mediates the effect of PNMS on growth. Mothers were pregnant during the January 1998 Quebec ice storm. We assessed their objective exposure and subjective distress in June 1998. At age 13½ their children were weighed and measured (n = 66); a subsample provided blood samples for epigenetic studies (n = 31). Objective and subjective PNMS correlated with central adiposity (waist-to-height ratio); only objective PNMS predicted body mass index (BMI). Bootstrapping analyses showed that the methylation level of genes from established Type-1 and -2 diabetes mellitus pathways showed significant mediation of the effect of objective PNMS on both central adiposity and BMI. However, the negative mediating effects indicate that, although greater objective PNMS predicts greater BMI and adiposity, this effect is dampened by the effects of objective PNMS on DNA methylation, suggesting a protective role of the selected genes from Type-1 and -2 diabetes mellitus pathways. We provide data supporting that DNA methylation is a potential mechanism involved in the long-term adaptation and programming of the genome in response to early adverse environmental factors.

An adverse environment in utero, including exposure to prenatal maternal stress (PNMS), can result in poor birth outcomes such as low birth weight, which increases risk of later cardiometabolic diseases such as hypertension and obesity. It is unclear to what extent PNMS influences obesity risk independent of its impact on birth characteristics, especially among humans. Our objective was to determine whether PNMS resulting from a natural disaster influenced risk of childhood obesity. Eight children with high objective PNMS exposure (14.5%) were obese compared to one child (1.8%) with low exposure (P = 0.02). Objective PNMS increased obesity risk (model 1, P = 0.02, odds ratio = 1.37) after controlling for other potential risk factors. Results suggest that PNMS might be an independent risk factor in the development of childhood obesity. Participants included 111 women who were pregnant during the January 1998 Québec Ice Storm or who conceived within the following 3 months and their children. We tested associations between objective and subjective PNMS from the storm and childhood obesity status at age 5½, controlling for children’s birth characteristics and breastfeeding status; household socioeconomic status; maternal obstetric complications, life events and smoking during pregnancy, psychological functioning, and height (model 1, n = 111) or BMI (for a subset of 69 participants, model 2).