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I'm more inclined to believe that deficiency would be related to autism than excess.
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Some of these links might be of interest:
http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
1: Clin Genet. 1999 Sep;56(3):216-20.Related Articles, Links
Fetal anticonvulsant syndrome and mutation in the maternal MTHFR gene.
Dean JC, Moore SJ, Osborne A, Howe J, Turnpenny PD.
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| Around 6% of infants born to mothers taking anticonvulsants have malformations, including neural tube defects, and a further proportion show developmental delay in later childhood. Three commonly used anticonvulsants, carbamazepine, phenytoin and sodium valproate, interfere with folic acid metabolism. |
A clinical study of 57 children with fetal anticonvulsant syndromes
http://www.jpands.org/vol9no4/boris.pdf.
Association of MTHFR Gene Variants with Autism
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| In the study group, there were 142 males (84.5%) and 26 females (15.5%). The distribution by gender was statistically similar for both autism and PDD. Among the 168 children, 149 were diagnosed with regressive autism, and 19 showed no evidence of regression. In a study by Ramaekers et al., low 5-methyltetrahydrofolate levels in the spinal fluid of children who had normal neurodevelopment until age 4 to 6 months was associated with subsequent neurological regression. Addition of folinic acid as a dietary supplement corrected the symptoms. The observed favorable response to folinic acid further supports a central role for methylation in at least some developmental disorders. Overall, the data show an increased risk of autism spectrum disorder (ASD) associated with common mutations affecting the folate/methylation cycle. These associations by themselves may provide a partial explanation for a subgroup of children genomically at risk for ASD disorders. Increased folinic acid during pregnancy and early development may offset the genomic risk factors, and this deserves further study. This study does not take into account the numerous potential influencing cofactors, which may be additive to the MTHFR observations, e.g. dietary folate, serum folate, dietary B vitamin intakes, amino acid deficiencies, environmental exposures, or heavy-metal exposure. It is likely some combination of these influences the phenotypic expression (ASD symptoms) of the genomic risk factors (MTHFR polymorphisms) |
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| Folic acid, from fruits and vegetables, plays a role by powerfully protecting against methanol (formaldehyde) toxicity. Many common drugs, such as aspirin, interfere with folic acid, as do some mutations in relevant enzymes. |
Effect of folic acid supplementation on aluminum accumulation in rats
2005, vol. 21, no3, pp. 406-410 [5 page(s) (article)] (25 ref.)
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| These results suggest that folate supplementation might be useful to decrease Al accumulation in its main target organs, i.e., bone, kidney, and brain. |
http://collegepharmacy.com/AMTrx/Ima...20Protocol.pdf.
FOLIC ACID
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| A large complex vitamin, folic acid has an almost obligatory infinity for formaldehyde. Perhaps it is this vitamin that is the ultimate protector of the human body. However, it is also known that too much folic acid is not good. By trapping all the formaldehyde (or methyl groups), proper building, repairing and healing cannot occur. |







