Talk:Abnormal Development - Folic Acid and Neural Tube Defects

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2011

High intake of folic acid disrupts embryonic development in mice

Birth Defects Res A Clin Mol Teratol. 2011 Jan;91(1):8-19. doi: 10.1002/bdra.20754. Epub 2010 Dec 22.

Pickell L, Brown K, Li D, Wang XL, Deng L, Wu Q, Selhub J, Luo L, Jerome-Majewska L, Rozen R.

Department of Human Genetics, McGill University and Montreal Children's Hospital Research Institute, Montreal, Quebec, Canada.

Abstract

BACKGROUND: Folic acid fortification and supplementation has increased folate intake and blood folate concentrations and successfully reduced the incidence of neural tube defects. However, the developmental consequences of high folate intake are unknown. This study investigated the impact of high folate intake, alone or with methylenetetrahydrofolate reductase (MTHFR) deficiency, on embryonic and placental development in mice.

METHODS: Mthfr +/+ or +/- pregnant mice on a control diet (CD; recommended intake of folic acid for rodents) or folic acid-supplemented diet (FASD; 20-fold higher than the recommended intake) were examined for embryonic loss, delay, and defects at 10.5 and 14.5 days post coitum (dpc); 10.5-dpc placenta, and 14.5-dpc embryo hearts were studied histologically.

RESULTS: Total plasma folate was 10-fold higher in FASD compared to CD mice; plasma homocysteine levels were not affected by diet. At 10.5 dpc, the FASD was associated with embryonic delay and growth retardation, and may confer susceptibility to embryonic defects. The FASD did not adversely affect 10.5-dpc placental development. At 14.5 dpc, embryos from the FASD Mthfr +/+ group were delayed and the FASD was associated with thinner ventricular walls in embryonic hearts. There was a significant interaction between maternal MTHFR deficiency and a high folate diet for several developmental outcomes.

CONCLUSIONS: Our study suggests that high folate intake may have adverse effects on fetal mouse development and that maternal MTHFR deficiency may improve or rescue some of the adverse outcomes. These findings underscore the need for additional studies on the potential negative impact of high folate intake during pregnancy.

Copyright © 2010 Wiley-Liss, Inc. PMID: 21254354

2006

Eichholzer M, Tonz O, Zimmermann R. Folic acid: a public-health challenge. Lancet. 2006 Apr 22;367(9519):1352-61. "... In the USA, Canada, and Chile, mandatory fortification of flour substantially improved folate and homocysteine status, and neural tube defects rates fell by between 31% and 78%. Nevertheless, many countries do not choose mandatory folic acid fortification, in part because expected additional health benefits are not yet scientifically proven in clinical trials, in part because of feared health risks, and because of the issue of freedom of choice. Thus, additional creative public-health approaches need to be developed to prevent neural tube defects and improve the folate status of the general population."

Padmanabhan R. Etiology, pathogenesis and prevention of neural tube defects. Congenit Anom (Kyoto). 2006 Jun;46(2):55-67.

Tamura T, Picciano MF. Folate and human reproduction. Am J Clin Nutr. 2006 May;83(5):993-1016.

Wen SW, Walker M. An exploration of health effects of folic acid in pregnancy beyond reducing neural tube defects. J Obstet Gynaecol Can. 2005 Jan;27(1):13-9.

Gonzalez MJ, et al. [See Related Articles] Folate supplementation and neural tube defects: a review of a public health issue. P R Health Sci J. 1997 Dec;16(4):387-93. Review.

1995

Folate levels and neural tube defects. Implications for prevention

JAMA. 1995 Dec 6;274(21):1698-702.

Daly LE, Kirke PN, Molloy A, Weir DG, Scott JM. Source Department of Public Health Medicine and Epidemiology, University College Dublin, Ireland.

Abstract

Using data from a recent case-control study, a woman's risk of having a child with a neural tube defect (NTD) was found to be associated with early pregnancy red cell folate levels in a continuous dose-response relationship. These findings were used to calculate the reduction in NTD cases that would be expected under two different strategies to raise folate levels. Targeting high-risk individuals has a small effect on the population prevalence but can substantially change an individual's risk. Targeting the population produces a small change in individual risk but has a large effect on the population prevalence. Supplementation of high-risk women would be the most efficient method to implement the high-risk strategy, while food fortification would be preferable for the population approach. The current guidelines for the prevention of NTD are for an increased folic acid intake of 0.4 mg per day. This would result in a 48% reduction in NTDs, which may be near optimal. The two intervention strategies should be considered complementary in prevention of NTDs.

Comment in JAMA. 1995 Dec 6;274(21):1717-8. JAMA. 1996 Jun 5;275(21):1635-6.

PMID 7474275