Low Vitamin D results in Spina Bifida in children
Supplementing mice with Vitamin D reduced NTD by 500%
Folate supplementation reduces Spina Bifida by 40%
Low 25-hydroxy vitamin D levels in Children with Spina Bifida
South Med J. 2016 Jan;109(1):31-5. doi: 10.14423/SMJ.0000000000000397.
Lynnette J. Mazur, MD, MPH lynnette.j.mazur at uth.tmc.edu : The University of Texas Health Science Center, Houston, Texas
Lisa D. Wilsford, MPH, MS, PA-C: Shriners Hospital for Children, Houston, Texas
Laura Rosas:University of Notre Dame, Notre Dame, Indiana Elroy Sullivan PhD: Shriners Hospital for Children, Houston, Texas
Aim: To determine vitamin D status in children with spina bifida (SB).
Methods: Charts of all patients with SB at the Shriners Hospital for Children - Houston seen between July 2011 and June 2013 were retrospectively reviewed. Daily intake of milk, vitamins, amount of screen time and time spent outdoors were recorded along with height, weight, BMI and serum vitamin D levels.
Results: Thirty eight patient were identified. The mean level of vitamin D was 58.8 nmoles/L (23.5 ng/dl);
- 30(81%)had insufficient levels, 50 to 75 nmoles/L (20 to 30 ng/ml) or deficient levels, <50nmoles/L (<20ng/ml).
- African American and Hispanic descent correlated with decreased levels, p=0.017.
Daily vitamin D supplementation correlated with increased levels, p=0.046.
Conclusion: Many children with SB have suboptimal vitamin D levels. Healthcare providers should consider the routine measurement of vitamin D levels and advise supplementation with insufficient/deficient levels in this population.
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Spina Bifida decreased 40% by folic acid fortification (of bread, etc)
"estimates of spina bifida were lower in regions with mandatory folic acid fortification (33.86 per 100,000 live births) compared to those without such policies (48.35 per 100,000 live births)"
5X reduction in Neural Tube defects by 5X (like Spina Bifida) by Vitamin D supplementation of mice - May 2015
Supplementation With Vitamin D3 During Pregnancy Protects Against Lipopolysaccharide-Induced Neural Tube Defects Through Improving Placental Folate Transportation
Toxicol Sci. 2015 May; 145(1): 90–97. doi: 10.1093/toxsci/kfv036
Yuan-Hua Chen,*†‡,1 Zhen Yu,*†,1 Lin Fu,* Mi-Zhen Xia,§ Mei Zhao,† Hua Wang,*† Cheng Zhang,* Yong-Fang Hu,* Fang-Biao Tao,†,2 and De-Xiang Xu*†,2
Several reports demonstrated that maternal lipopolysaccharide (LPS) exposure at middle gestational stage caused neural tube defects (NTDs). This study investigated the effects of supplementation with vitamin D3 (VitD3) during pregnancy on LPS-induced NTDs. Pregnant mice except controls were ip injected with LPS (25 μg/kg) daily from gestational day (GD)8 to GD12. In LPS+VitD3 group, pregnant mice were orally administered with VitD3 (25 μg/kg) before LPS injection. As expected, a 5-day LPS injection resulted in 62.5% (10/16) of dams and 20.3% of fetuses with NTDs. Additional experiment showed that a 5-day LPS injection downregulated placental proton-coupled folate transporter (pcft) and reduced folate carrier 1 (rfc1), 2 major folate transporters in placentas. Consistent with downregulation of placental folate transporters, folate transport from maternal circulation into embryos was disturbed in LPS-treated mice.
Interestingly, VitD3 not only inhibited placental inflammation but also attenuated LPS-induced downregulation of placental folate transporters.
Correspondingly, VitD3 markedly improved folate transport from maternal circulation into the embryos. Importantly, supplementation with VitD3 during pregnancy protected mice from LPS-induced NTDs.
Taken together, these results suggest that supplementation with VitD3 during pregnancy prevents LPS-induced NTDs through inhibiting placental inflammation and improving folate transport from maternal circulation into the embryos.
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