Special Issue "Folic Acid Fortification and Supplement Use: Unanticipated Benefits and Risks"

A special issue of Nutrients (ISSN 2072-6643).

Deadline for manuscript submissions: closed (30 November 2017).

Special Issue Editors

Professor Ralph Green
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Guest Editor
Department of Pathology and Laboratory MedicineUniversity of California, Davis 4400 V Street, PATH BuildingSacramento, CA 95817
Professor Joshua W. Miller
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Guest Editor
Dept. of Nutritional SciencesSchool of Environmental and Biological SciencesRutgers, The State University of New Jersey65 Dudley Road, Room 107New Brunswick, NJ 08901

Special Issue Information

Dear Colleagues,

Folate is an essential B vitamin for a broad range of biochemical reactions involving transfer of one-carbon groups, including purine and pyrimidine synthesis for RNA and DNA, amino acid interconversions, cell division, tissue growth and methylation. Deficiencies of folate or imbalance of its active and inactive forms and interactions with other B-vitamins, notably vitamin B12, may lead to perturbations that result in adverse health consequences. In addition, genetic polymorphisms and environmental factors can disturb the normal function of one-carbon metabolism with detrimental effects on human health. The successful introduction of widespread folic acid fortification of the diet to reduce the incidence of neural tube defects, as well as the widespread use of folic acid supplements has also been associated with several unanticipated consequences, some beneficial and some potentially detrimental. Although a vast volume of research has already been conducted in this area, there are still significant gaps in our knowledge that require further investigations. This Special Issue of Nutrients invites submission of manuscripts, original research or reviews of the scientific literature, focused on novel findings in relation to folic acid intake through fortification and supplement use that have had an effect on disease risk relating to the metabolic role of folate and its interaction with vitamin B12, as well as gene-nutrient interactions. These effects include fetal growth and programming; and risk of disease (e.g., birth defects and pregnancy related conditions, cancer, cardiovascular disease including hypertension, neuropsychiatric disease, allergic disorders and osteoporosis).

Prof. Dr. Ralph Green
Prof. Dr. Joshua W. Miller
Guest Editors

Manuscript Submission Information

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Keywords

  • folate
  • folic acid
  • supplementation
  • fortification
  • Vitamin B12
  • homocysteine
  • DNA
  • methylation
  • cancer
  • cardiovascular disease

Published Papers (3 papers)

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Research

Open AccessArticle
Association between Duration of Folic Acid Supplementation during Pregnancy and Risk of Postpartum Depression
Nutrients 2017, 9(11), 1206; https://doi.org/10.3390/nu9111206 - 02 Nov 2017
Cited by 9
Abstract
Postpartum depression (PPD), as a common complication of childbearing, could have adverse consequences on mothers, children, and families. This cohort study aimed to assess the association between duration of folic acid (FA) supplementation during pregnancy and the onset of PPD in Chinese women. [...] Read more.
Postpartum depression (PPD), as a common complication of childbearing, could have adverse consequences on mothers, children, and families. This cohort study aimed to assess the association between duration of folic acid (FA) supplementation during pregnancy and the onset of PPD in Chinese women. A total of 1592 participants were recruited, and data collected between July 2015 and March 2017 in Tianjin, China. Participants’ baseline data were collected regarding socio-demographic and lifestyle characteristics, obstetric history, and FA supplementation during pregnancy. The Chinese version of the self-rating depression scale was used to assess depressive symptoms at 6–12 weeks postpartum, and the prevalence of PPD in participants was 29.4%. Pregnant women who took FA supplements for >6 months had a lower prevalence of PPD, compared to those who took FA for ≤6 months. After using the 1:1 ratio propensity score matching, 601 FA-users ≤ 6 months and 601 FA-users > 6 months were included in the further analyses; this also yielded similar results (P < 0.05). Logistic regression analysis showed that FA intake for >6 months was an independent determinant of PPD (odds ratio = 0.76; 95% confidence interval: 0.59–0.98; P < 0.05). Thus, prolonged FA supplementation during pregnancy was associated with a decreased risk of PPD in Chinese women. Full article
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Open AccessArticle
A Cross-Sectional Study of Dietary and Genetic Predictors of Blood Folate Levels in Healthy Young Adults
Nutrients 2017, 9(9), 994; https://doi.org/10.3390/nu9090994 - 08 Sep 2017
Cited by 3
Abstract
Since 1998, the U.S. has mandated folic acid (FA) fortification of certain grain products to reduce the risk of neural tube defects. Folate intake and red blood cell (RBC) folate concentrations increased substantially post-intervention, although recent studies raise concerns about the level of [...] Read more.
Since 1998, the U.S. has mandated folic acid (FA) fortification of certain grain products to reduce the risk of neural tube defects. Folate intake and red blood cell (RBC) folate concentrations increased substantially post-intervention, although recent studies raise concerns about the level of ongoing benefit. This study investigated blood folate level determinants in healthy young adults, including intake of naturally occurring food folate, synthetic FA, and the interaction of naturally occurring food folate with a common missense variant in the FOLH1 gene thought to affect absorption. Participants (n = 265) completed the Diet History Questionnaire II, RBC folate testing, and were genotyped for the 484T>C FOLH1 variant. Men reported significantly greater intake of all folate sources except for supplemental FA, but RBC folate levels did not significantly differ by sex. Synthetic FA was a stronger predictor of RBC folate than naturally occurring food folate. In the largest racial group, synthetic FA and the interaction of FOLH1 genotype with naturally occurring food folate significantly predicted RBC folate, with the overall model accounting for 13.8% of the variance in RBC folate levels. Blood folate levels rely on a complex interaction of natural and synthetic folate intake as well as FOLH1 genotype. Full article
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Open AccessArticle
Maternal Prenatal Folic Acid Supplementation Programs Offspring Lipid Metabolism by Aberrant DNA Methylation in Hepatic ATGL and Adipose LPL in Rats
Nutrients 2017, 9(9), 935; https://doi.org/10.3390/nu9090935 - 26 Aug 2017
Cited by 4
Abstract
The effects of maternal prenatal folic acid supplementation (FAS) on offspring lipid metabolism in adulthood remains unclear, although prenatal FAS is compulsively suggested in many countries. Female Sprague-Dawley rats were fed with control (CON) or FAS diets before and during pregnancy. Male offspring [...] Read more.
The effects of maternal prenatal folic acid supplementation (FAS) on offspring lipid metabolism in adulthood remains unclear, although prenatal FAS is compulsively suggested in many countries. Female Sprague-Dawley rats were fed with control (CON) or FAS diets before and during pregnancy. Male offspring of CON and FAS dams were further divided into two groups at seven weeks for CON and high-fat (HF) diet interventions for eight weeks in adulthood (n = 10). The interactive effects of maternal prenatal FAS and offspring HF in adulthood on lipid metabolism and DNA methylation of genes involved in lipids metabolism were assessed. The male offspring of FAS dams had elevated serum and liver triglyceride level when fed with HF compared to the male offspring of CON dams. The mRNA and protein expression levels of hepatic ATGL and adipose LPL were significantly decreased in offspring of FAS dams than in offspring of CON dams. Furthermore, maternal prenatal FAS resulted in elevated DNA methylation levels in the promoter and first exon region of hepatic ATGL and adipose LPL in offspring. Maternal FAS exacerbated the adverse effects of HF on lipid metabolism in offspring through inducing aberrant DNA methylation levels of hepatic ATGL and adipose LPL. Full article
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