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Vitamin B9 (folic acid) DNA health report

Follow the link of the selected polymorphism to read a brief description of how the selected polymorphism affects Vitamin B9 (folic acid) and see a list of existing studies.

SNP polymorphisms related to the topic Vitamin B9 (folic acid):

rs162036Disorders of intracellular metabolism of cobalamin. Positive effect on the efficacy of folic acid therapy in patients with hyperhomocysteinaemia.
rs651933May mean that folic acid cannot be transported into cells, and may indicate a need for more folic acid
rs1051266The protein encoded by the gene transports folic acid into the cell and thus plays a role in the intracellular regulation of folate concentration. In this genotype, folate absorption is worse. Folic acid requirement is higher. Alcohol consumption is more critical for the risk of vitamin B9 deficiency.
rs1801131Reduces the formation of the active form of folic acid, which is necessary for the remethylation of homocysteine and other DNA molecules. Administration of the active form of folic acid (5-MTHF or L-methyltetrahydrofolate) can significantly improve risk scores for the effects of mutations. Also a factor that moderately increases the need for vitamin B2.
rs1801133A gene fragment known as MTHFR C677T, which encodes an enzyme involved in folic acid metabolism. A break in this gene fragment results in high levels of homocysteine, low levels of B12 and folic acid. If your tests show high homocysteine levels, your doctor will likely advise you on an appropriate diet and supplementation regime. Taking varieties of the active form of B9 methylfolate (5-MTHF or L-methyltetrahydrofolate), the active form of vitamin B12, methylcobalamin, is recommended to reduce your risks.
rs1801394Polymorphism can lead to elevated homocysteine levels independent of folic acid, vitamin B12 or B6 levels. It is a risk factor for neural tube defects and Down syndrome in the setting of higher homocysteine levels.
rs1805087Moderate risk factor for hyperhomocysteinaemia. A factor that increases the body's need for folic acid and vitamin B12.
rs1979277Polymorphism of enzymes that metabolise folic acid.It is required to obtain sufficient vitamin B6 for optimal gene activity.
rs2236225Possible increased risk of fetal birth defects. A 1.5-fold higher risk for Caucasian mothers to give birth to children with DNT (neural tube defect). The association in children with this mutation with an increased risk of heart defects is greater if their mother did not get enough folic acid during pregnancy. The risk is reduced with adequate levels of folic acid and vitamin B6.
rs2287780Polymorphism in folic acid pathway genes causing B12 deficiency and increased homocysteine.
rs2295639Gene responsible for folate pathway abnormalities, increases likelihood of late-onset Alzheimer's disease.
rs4973216The breakage results in impaired ability of the protein to transport folate and thiamine into cells, resulting in reduced absorption of vitamin B1 from food. Thiamine-reactive encephalopathy, characterised by seizures responding to high doses of thiamine, may develop.
rs7925545May mean that folic acid cannot be transported into cells, and may indicate a need for more folic acid
rs10064631Methionine synthase deficiency, impairing the metabolism of folic acid B9 and cobalamin B12.
rs11754661Genetic alteration of the folate pathway affecting genomic methylation content.
rs12512471Breakdown can cause tetrahydrobiopterin (BH4) deficiency. Treatment for tetrahydrobiopterin problems usually involves some combination of supplementation with L-DOPA, 5-HTP, B4 and folic acid.
rs17349743Gene responsible for folate pathway abnormalities, increases likelihood of late-onset Alzheimer's disease.
rs144637717Deficiency of cerebral transport of folic acid.