Epidemiologic studies have shown an association between an adverse intrauterine environment (eg, exposure to malnutrition) and an increased risk of developing cardiometabolic disease in adulthood. These studies laid the foundation for the developmental origins of health and disease hypothesis, which states that limited nutrient supply to the fetus results in physiologic and metabolic adaptations that favor survival but result in unfavorable consequences in the offspring if there is excess nutrition after birth. This discrepancy in the pre- and postnatal milieus, perceived as stress by the offspring, may confer an increased risk of developing cardiometabolic disease later in life. Thus, early life exposures result in programming or changes in cellular memory that have effects on health throughout the life course. One of the mechanisms by which programming occurs is via epigenetic modifications of genes, processes that result in functionally relevant changes in genes (ie, gene expression) without an alteration in the genotype. In this review, we will describe how fetal exposures, including under- and overnutrition, affect neonatal and childhood growth and the future risk for cardiometabolic disease.
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