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      Maternal Nutrition and Fetal Development

      1 , 2 , 3 , 1 , 2
      The Journal of Nutrition
      Oxford University Press (OUP)

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          Abstract

          Nutrition is the major intrauterine environmental factor that alters expression of the fetal genome and may have lifelong consequences. This phenomenon, termed "fetal programming," has led to the recent theory of "fetal origins of adult disease." Namely, alterations in fetal nutrition and endocrine status may result in developmental adaptations that permanently change the structure, physiology, and metabolism of the offspring, thereby predisposing individuals to metabolic, endocrine, and cardiovascular diseases in adult life. Animal studies show that both maternal undernutrition and overnutrition reduce placental-fetal blood flows and stunt fetal growth. Impaired placental syntheses of nitric oxide (a major vasodilator and angiogenesis factor) and polyamines (key regulators of DNA and protein synthesis) may provide a unified explanation for intrauterine growth retardation in response to the 2 extremes of nutritional problems with the same pregnancy outcome. There is growing evidence that maternal nutritional status can alter the epigenetic state (stable alterations of gene expression through DNA methylation and histone modifications) of the fetal genome. This may provide a molecular mechanism for the impact of maternal nutrition on both fetal programming and genomic imprinting. Promoting optimal nutrition will not only ensure optimal fetal development, but will also reduce the risk of chronic diseases in adults.

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          Most cited references36

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          Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals.

          Cells of a multicellular organism are genetically homogeneous but structurally and functionally heterogeneous owing to the differential expression of genes. Many of these differences in gene expression arise during development and are subsequently retained through mitosis. Stable alterations of this kind are said to be 'epigenetic', because they are heritable in the short term but do not involve mutations of the DNA itself. Research over the past few years has focused on two molecular mechanisms that mediate epigenetic phenomena: DNA methylation and histone modifications. Here, we review advances in the understanding of the mechanism and role of DNA methylation in biological processes. Epigenetic effects by means of DNA methylation have an important role in development but can also arise stochastically as animals age. Identification of proteins that mediate these effects has provided insight into this complex process and diseases that occur when it is perturbed. External influences on epigenetic processes are seen in the effects of diet on long-term diseases such as cancer. Thus, epigenetic mechanisms seem to allow an organism to respond to the environment through changes in gene expression. The extent to which environmental effects can provoke epigenetic responses represents an exciting area of future research.
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            Obesity and the environment: where do we go from here?

            J O Hill (2003)
            The obesity epidemic shows no signs of abating. There is an urgent need to push back against the environmental forces that are producing gradual weight gain in the population. Using data from national surveys, we estimate that affecting energy balance by 100 kilocalories per day (by a combination of reductions in energy intake and increases in physical activity) could prevent weight gain in most of the population. This can be achieved by small changes in behavior, such as 15 minutes per day of walking or eating a few less bites at each meal. Having a specific behavioral target for the prevention of weight gain may be key to arresting the obesity epidemic.
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              The risk of maternal nutritional depletion and poor outcomes increases in early or closely spaced pregnancies.

              An adequate supply of nutrients is probably the single most important environmental factor affecting pregnancy outcome. Women with early or closely spaced pregnancies are at increased risk of entering a reproductive cycle with reduced reserves. Maternal nutrient depletion may contribute to the increased incidence of preterm births and fetal growth retardation among these women as well as the increased risk of maternal mortality and morbidity. In the past, it was assumed that the fetus functioned as a parasite and withdrew its nutritional needs from maternal tissues. Studies in both animals and humans demonstrate, however, that if the maternal nutrient supply is inadequate, the delicate balance between maternal and fetal needs is disturbed and a state of biological competition exists. Furthermore, maternal nutritional status at conception influences how nutrients are partitioned between the mother and fetal dyad. In severe deficiencies maternal nutrition is given preference; in a marginal state the fetal compartment is favored. Although the studies of nutrient partitioning have focused on energy and protein, the partitioning of micronutrients may also be influenced by the maternal nutritional status. Marginal intakes of iron and folic acid during the reproductive period induce a poor maternal status for these nutrients during the interpregnancy interval. Poor iron and folic acid status has also been linked to preterm births and fetal growth retardation. Supplementation with food and micronutrients during the interpregnancy period may improve pregnancy outcomes and maternal health among women with early or closely spaced pregnancies.
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                Author and article information

                Journal
                The Journal of Nutrition
                Oxford University Press (OUP)
                0022-3166
                1541-6100
                September 2004
                September 01 2004
                September 2004
                September 01 2004
                : 134
                : 9
                : 2169-2172
                Affiliations
                [1 ]Cardiovascular Research Institute, The Texas A&M University System Health Science Center; College Station, TX 77843
                [2 ]Departments of Animal Science, Texas A&M University
                [3 ]Veterinary Physiology and Pharmacology, Texas A&M University
                Article
                10.1093/jn/134.9.2169
                15333699
                04fc4bd5-639d-4933-a207-a2b933e5be07
                © 2004
                History

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