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Folic acid (or folate) is vitamin B9, a water-soluble vitamin that plays a key role in DNA and RNA synthesis, red blood cell production, the metabolism of proteins, and healthy genetic expression. BioFolate contains L-5-methyltetrahydrofolate (L-5-MTHF), the active form of folate that is used in the body. Folate deficiency can cause a number of health problems, of which the most documented is neural tube defects in developing infants. Symptoms of folate deficiency include: weakness, fatigue, irritability, headaches, difficulties in cognitive function, mood imbalances, cramps, palpitations, shortness of breath, and can lead to more serious health problems.
Certain medical conditions can actually lead to secondary folate deficiencies through decreased absorption or an increase in the body’s demand for folate. These include alcoholism, Crohn’s disease, lymphoma or amyloidosis of the small intestine, diabetic enteropathy, gluten sensitivity, sickle cell disease, chronic exfoliative skin disorders and of course, pregnancy.
Additionally, a large percentage of the population has a certain gene mutation called MTHFR which renders them unable to convert dietary folate into the biologically active form, leading to folate deficiency. Taking folate in the form of L-5-MTHF ensures that even those with the MTHFR mutation are able to absorb the folate and avoid deficiency. BioFolate also contains a small amount of vitamin B12 in the active form of methylcobalamin, since folate supplementation can mask a vitamin B12 deficiency.
BioFolate contains the preferred, biologically active form of folate that is produced in the body. BioFolate helps the body to metabolize carbohydrates, fats, and proteins and form red blood cells.
|Serving Size: 1 Capsule||Amount||% Daily|
|Vitamin B12 (Methylcobalamin)||2.8 mcg|
microcrystalline cellulose, silicon dioxide, sodium stearyl fumarate. Capsule: hypromellose.
AOR™ guarantees that all ingredients have been declared on the label. Contains no wheat, gluten, corn, nuts, peanuts, sesame seeds, sulphites, mustard, soy, dairy, eggs, fish, shellfish or any animal byproducts.
Take 1 capsule daily with food, or as directed by a qualified health care practitioner.
Folate supplementation can mask a vitamin B12 deficiency. Consult a health care practitioner prior to use if you are uncertain whether or not you are taking adequate vitamin B12.
Neural tube defects
The information and product descriptions appearing on this website are for information purposes only, and are not intended to provide or replace medical advice to individuals from a qualified health care professional. Consult with your physician if you have any health concerns, and before initiating any new diet, exercise, supplement, or other lifestyle changes.
Folic acid (or folate) is a water-soluble vitamin that plays a key role in the biosynthesis of DNA and RNA, red blood cell production and the metabolization of proteins. Folic acid is also necessary for genome maintenance, the regulation of gene expression, and other functions. Natural folates are found in dark green leafy vegetables (spinach, kale, mustard greens, turnip greens) as well as oranges, broccoli, cauliflower, liver and brewer’s yeast. The absorption efficiency of natural folates is approximately 50% that of supplemental folic acid. This is because natural food folates are pteroylpolyglutamate derivatives. These require cleavage (by an enzyme called folate conjugase) to pteroylmonoglutamate forms prior to absorption from the small intestine.
Folic acid (in supplemental form) is already a pteroylmonoglutamate and therefore does not require this process, making it much more efficiently absorbed as a result. When most health practitioners and astute observers of preventative health and nutrition think of folic acid, they refer to the overwhelming amount of research supporting folic acid’s ability to prevent neural tube defects. So strong is this evidence, in fact, that even the highly reticent U.S. Food & Drug Administration began enforcing a regulation in 1998 that required all uncooked flour, grain and cereal products to be fortified with folic acid. It is safe to say that nutrient fortification is legislated on a highly reactionary, sporadic and admonitory basis, and for folic acid to achieve this kind of legislative recognition speaks volumes in and of itself.
Deficiency & Implications
A deficiency in dietary folate has wide-ranging implications over and above the risk of aforementioned neural tube defects among expectant and potential mothers. Such implications can include weakness, fatigue, irritability, headaches, difficulties in cognitive function, cramps, palpitations, shortness of breath and atrophic glossitis.
Studies have also revealed that low folate levels are linked to elevated serum homocysteine concentration, hypersegmentation of the neutrophils, and decreased hemogloblin and erythrocyte concentrations. Folate deficiencies have also been linked to increased risks of cardiovascular disease, abnormal cell growth, altered cognitive function and mood. A number of conditions can lead to folate deficiency. Chronic alcohol users can become deficient in the vitamin due in part to ethanol’s impairment of folate absorption and hepatobiliary metabolism, as well as to increased renal folate excretion caused by ethanol. Crohn’s disease, amyloidosis of the small intestine, diabetic enteropathy, and tropical and non-tropical sprue (gluten-sensitive enteropathy) can also result in folate deficiency. Some conditions or situations such as chronic hemolytic anemias (e.g., sickle cell disease), chronic hemodialysis, peritoneal dialysis, chronic exfoliative skin disorders and of course pregnancy, all cause an increased demand for folate.
Homocysteine & Heart Health
Folic acid’s critical role in converting homocysteine back to methionine gives it the potential to address many of the myriad of health conditions that are initiated by high homocysteine levels. One meta-analysis determined that folate supplementation reduced plasma homocysteine levels in a dose-dependent fashion. Based upon findings from this meta-analysis, it has been estimated that for every 50 microgram daily increase in average folic acid intake, 4,000 to 18,000 deaths due to cardiovascular disease could be prevented annually in the U.S. alone. It has also been demonstrated in a prospective, randomized, placebo-controlled trial that high-dose folic acid supplementation (10 mg daily for two weeks) can help prevent some of the deleterious effects of triglyceride-rich lipoproteins on endothelium-dependent vasodilation in healthy volunteers challenged with an acute oral fat load. In another study, this one among 45 subjects with established cardiovascular disease, folic acid intake was significantly inversely associated with multiple indices of oxidized LDL-cholesterol. This correlation remained significant even when adjusted for potential confounding variables, including consumption of other vitamins and nutrients.
Folate (or folic acid) is known as the main supplement during pregnancy to prevent neural tube defects in the fetus.
It is also now known that about 20% of the population has a genetic mutation that makes their bodies unable to convert dietary folate to its active form, L-5-MTHF (methyl-tetra-hydro-folate), making supplementation with the active form very important for this sub-group of people.
AOR’s Biofolate provides a high dose of the active form of folate combined with a minimal amount of active B12, because folate supplementation can mask a B12 deficiency.
5-methyltetrahydrofolate. Monograph. Altern Med Rev. 2006 Dec;11(4):330-7. Review.
Ulrich CM, Potter JD. Folate and cancer–timing is everything. JAMA 2007 Jun 6;297(21):2408-9.
The folic acid metabolite L-5-methyltetrahydrofolate effectively reduces total serum homocysteine level in orthotopic liver transplant recipients: a double-blind placebo-controlled study.
Eur J Clin Nutr. 2008 Jun;62(6):796-801.
Akoglu B, Schrott M, Bolouri H, Jaffari A, Kutschera E, Caspary WF, Faust D.
Objective: Hyperhomocysteinemia is a described risk factor of cardiovascular diseases. The aim of this study was the treatment of hyperhomocysteinemia in liver transplant recipients with L-5-methyltetrahydrofolate (L-5-MTHF; 1 mg) vs folic acid (1 mg) vs placebo in a double-blind placebo-controlled study and to compare the relative responsiveness of these patients to L-5-MTHF and folic acid.
Subjects/Methods: Patients were recruited from Hepatology-Transplantation-Unit at Johann Wolfgang Goethe-University, Frankfurt. Sixty patients were included in this study and 12 patients dropped out for different reasons. The patients were treated over 8 weeks with supplemental L-5-MTHF or folic acid or placebo. Serum homocysteine (HCY) was analyzed with high-performance liquid chromatography (HPLC) beside routine lab tests.
Results: We observed only a significant decrease of total serum HCY in the L-5-MTHF group during the study period (at week 0: 15 /-7.7 mu M; after 8 weeks treatment: 9.41 /-2.6 mu M, P
Conclusion: The effects of L-5-MTHF are significantly more potent than folic acid itself. Therefore, lowering serum HCY in liver transplant recipients is effective with L-5-MTHF.
Reduction of the genomic damage level in haemodialysis patients by folic acid and vitamin B12 supplementation.
Nephrol Dial Transplant. 2008 May 9.
Stopper H, Treutlein AT, Bahner U, Schupp N, Schmid U, Brink A, Perna A, Heidland A.
Background and objective: genomic damage of peripheral lymphocytes are elevated in patients with end-stage renal failure. Among other uraemic toxins, homocysteine (Hcy) levels are increased in most of these patients. In healthy individuals, plasma Hcy correlates with the degree of genomic damage observed in peripheral blood lymphocytes (PBL). The accumulation of Hcy can be reduced by supplementation with folic acid and vitamin B12. The aim of this study was to analyse whether this supplementation can also lower the genomic damage in PBL of haemodialysis patients…..
Design, participants and methods: In a prospective study with 27 patients, we analysed the genomic damage in dialysis patients before and at different time points after the initiation of folate/vitamin B12 supplementation. Genomic damage was measured by the frequency of micronuclei, a subset of chromosomal aberrations, in PBL.
RESULTS: Supplementation with folic acid and vitamin B12 (more markedly with both) reduced the micronucleus frequency in PBL of dialysis patients. This was not mediated by altered lymphocyte proliferation capacity or changes in DNA cytosine-methylation. Plasma-Hcy was lowered more efficiently by the combined folic acid/vitamin B12 supplementation, and lymphocyte DNA of this group exhibited a nonsignificant trend for a reduction of 1,N(6)-etheno-2′-deoxyadenosine, a marker for oxidative stress.
CONCLUSIONS: A reduction of the genomic damage in PBL can be achieved in dialysis patients by supplementation with folic acid and vitamin B12. This may be mediated by Hcy reduction.
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