BPA, Phthalates & Stress: Mechanisms and Interactions For Childhood Obesity

Investigadores: Martha Maria Tellez Rojo Solis, Gabriela Elizabeth Rueda Hernández, Alejandra de Jesús Cantoral Preciado, Maritsa Solano Gonzalez, Ana Benito Vinós.

Childhood obesity is a growing crisis. The prevalence of obesity among U.S. children aged 6-11 years increased from 7% in 1980 to 20% in 2008.1,2 Among U.S. Hispanics, 1 in 4 children are obese.1 Increasingly, obese children show signs of cardiometabolic dysfunction, including insulin resistance, and dyslipidemia.3 While increased caloric intake plays a role, the underlying cause is likely not as simple as just caloric imbalance. The rise of obesity is nested in profound transformations in our environment and society. Increased manufacturing has led to widespread fetal exposure to endocrine disrupting chemicals (EDCs), and modern lifestyles have created an increasing burden of chronic psychosocial stress, both of which are potential causes of obesity.4,5 In animals, fetal exposure to EDCs such as Bisphenol A (BPA) and phthalates,6-10 or stress11-13 reprograms the metabolic set point towards obesity, but human research is still sparse. Pregnancy is a potential key life stage for programming, but it is also a key life-stage at which future interventions may be targeted. Determining the role of fetal life experiences on programmed obesity is therefore critical.

Pregnancy-stressOur project’s primary goal is to characterize the effect of prenatal exposure to BPA and phthalates on child obesity. We will also investigate whether prenatal-BPA & phthalate effects are modified in the context of high social stress, in order to better understand susceptibility to EDC exposure. Finally, we will identify epigenetic marks that program altered metabolic trajectories. In animals, EDCs14-17 and stress11-13 cause fetal re-programming via altered signaling in the hypothalamic-pituitary-adrenal (HPA) axis.

To our knowledge, interactions of psychosocial stress with BPA/phthalates have not been studied in humans, nor have human studies assessed cortisol metabolism or epigenetics in EDC obesity research. We are uniquely poised to conduct this research because we can leverage the PROGRESS study (Programming Research in Obesity, GRowth, Environment and Social Stressors) in Mexico, an existing prospective birth cohort focused on early childhood neurocognitive phenotypes with extensive measures of prenatal stress and cortisol metabolism.

Acerca de cieeinsp

Centro de Investigación en Evaluación y Encuestas del Instituto Nacional de Salud Pública de México.
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