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However, as discussed in the next sections of this paper, we cannot exclude that maternal polymorphisms of folate pathway genes, their preferential transmission to a DS embryo, as well as epigenetic modifications and expression levels of folate-related genes mapping to chromosome 21, could contribute to the DS phenotype, including the development of congenital defects or that of other diseases later in life

Several studies reports impaired GSH and 25(OH)VD 3 in obese and type 2 diabetic subjects 8,9,12,19,21

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