Contributions of enriched cereal-grain products, ready-to-eat cereals, and supplements to folic acid and vitamin B-12 usual intake and folate and vitamin B-12 status in US children: National Health and Nutrition Examination Survey (NHANES), 2003-2006
ABSTRACT US children consume folic acid from multiple sources. These sources may contribute differently to usual intakes above the age-specific tolerable upper intake level (UL) for folic acid and to folate and vitamin B-12 status.
We estimated usual daily folic acid intakes above the UL and adjusted serum and red blood cell folate, serum vitamin B-12, homocysteine, and methylmalonic acid (MMA) concentrations in US children by age group and by the following 3 major folic acid intake sources: enriched cereal-grain products (ECGP), ready-to-eat cereals (RTE), and supplements containing folic acid (SUP).
We analyzed data in 4 groups of children aged 1-3, 4-8, 9-13, and 14-18 y from the National Health and Nutrition Examination Survey (NHANES), 2003-2006 (n = 7161).
A total of 19-48% of children consumed folic acid from ECGP only. Intakes above the UL varied from 0-0.1% of children who consumed ECGP only to 15-78% of children who consumed ECGP+RTE+SUP. In children aged 1-8 y, 99-100% of those who consumed ≥ 200 μg folic acid/d from supplements exceeded their UL. Although < 0.5% of children had folate deficiency or low vitamin B-12 status, the consumption of RTE or SUP with folic acid was associated with higher mean folate and vitamin B-12 concentrations and, in some older children, with lower homocysteine and MMA concentrations.
Our data suggest that the majority of US children consume more than one source of folic acid. Postfortification, the consumption of RTE or SUP increases usual daily intakes and blood concentrations of folate and vitamin B-12.
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ABSTRACT: 'Discretionary fortification' refers to the addition of vitamins and minerals to foods at the discretion of manufacturers for marketing purposes, but not as part of a planned public health intervention. While the nutrients added may correspond to needs in the population, an examination of novel beverages sold in Toronto supermarkets revealed added nutrients for which there is little or no evidence of inadequacy in the population. This is consistent with the variable effects of manufacturer-driven fortification on nutrient adequacy observed in the US. Nutrient intakes in excess of Tolerable Upper Intake Levels are now observed in the context of supplement use and high levels of consumption of fortified foods. Expanding discretionary fortification can only increase nutrient exposures, but any health risks associated with chronically high nutrient loads from fortification and supplementation remain to be discovered. Regulatory bodies are focused on the establishment of safe levels of nutrient addition, but their estimation procedures are fraught with untested assumptions and data limitations. The task of determining the benefits of discretionary fortification is being left to consumers, but the nutrition information available to them is insufficient to allow for differentiation of potentially beneficial fortification from gratuitous nutrient additions.Nutrients 10/2014; 6(10):4421-4433. DOI:10.3390/nu6104421 · 3.15 Impact Factor
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ABSTRACT: Increased consumption of folic acid is prevalent, leading to concerns about negative consequences. The effects of folic acid on the liver, the primary organ for folate metabolism, are largely unknown. Methylenetetrahydrofolate reductase (MTHFR) provides methyl donors for S-adenosylmethionine (SAM) synthesis and methylation reactions. Our goal was to investigate the impact of high folic acid intake on liver disease and methyl metabolism. Folic acid-supplemented diet (FASD, 10-fold higher than recommended) and control diet were fed to male Mthfr(+/+) and Mthfr(+/-) mice for 6 mo to assess gene-nutrient interactions. Liver pathology, folate and choline metabolites, and gene expression in folate and lipid pathways were examined. Liver and spleen weights were higher and hematologic profiles were altered in FASD-fed mice. Liver histology revealed unusually large, degenerating cells in FASD Mthfr(+/-) mice, consistent with nonalcoholic fatty liver disease. High folic acid inhibited MTHFR activity in vitro, and MTHFR protein was reduced in FASD-fed mice. 5-Methyltetrahydrofolate, SAM, and SAM/S-adenosylhomocysteine ratios were lower in FASD and Mthfr(+/-) livers. Choline metabolites, including phosphatidylcholine, were reduced due to genotype and/or diet in an attempt to restore methylation capacity through choline/betaine-dependent SAM synthesis. Expression changes in genes of one-carbon and lipid metabolism were particularly significant in FASD Mthfr(+/-) mice. The latter changes, which included higher nuclear sterol regulatory element-binding protein 1, higher Srepb2 messenger RNA (mRNA), lower farnesoid X receptor (Nr1h4) mRNA, and lower Cyp7a1 mRNA, would lead to greater lipogenesis and reduced cholesterol catabolism into bile. We suggest that high folic acid consumption reduces MTHFR protein and activity levels, creating a pseudo-MTHFR deficiency. This deficiency results in hepatocyte degeneration, suggesting a 2-hit mechanism whereby mutant hepatocytes cannot accommodate the lipid disturbances and altered membrane integrity arising from changes in phospholipid/lipid metabolism. These preliminary findings may have clinical implications for individuals consuming high-dose folic acid supplements, particularly those who are MTHFR deficient.American Journal of Clinical Nutrition 03/2015; 101(3). DOI:10.3945/ajcn.114.086603 · 6.92 Impact Factor
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ABSTRACT: Vitamin deficiencies are common in inflammatory bowel disease. Here we present 5 year follow up data of 61 patients. No folate or vitamin B12 deficiency was identified throughout the study. A daily multivitamin supplement was sufficient to replete 100 % of vitamin A and E deficient patients. 52% of vitamin D deficient patients corrected, but 15% who had normal vitamin D levels at diagnosis developed deficiency. 63% of zinc deficient patients normalized zinc status, but 15% developed zinc deficiency at follow up despite supplementation.Journal of Pediatric Gastroenterology and Nutrition 07/2014; 59(4). DOI:10.1097/MPG.0000000000000477 · 2.87 Impact Factor