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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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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

Antioxidants & Redox Signaling, 23 (11), 985-997

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