Talk:Abnormal Development - Folic Acid and Neural Tube Defects: Difference between revisions
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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 | |||
==Old Recent Findings== | ==Old Recent Findings== | ||
Revision as of 10:02, 27 February 2011
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Cite this page: Hill, M.A. (2024, April 18) Embryology Abnormal Development - Folic Acid and Neural Tube Defects. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Abnormal_Development_-_Folic_Acid_and_Neural_Tube_Defects |
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
Old Recent Findings
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.
