Read this letter on why DFH improved all its products to contain natural folate.
L-5-MTHF was designed for patients with demonstrated increased need for folate such as those with either the A1298C or C677T MTHFR mutation. It provides 1000 mcg per capsule of folate in the bioidentical, bioactive form, 5-MethylTetraHydroFolate. L-5-MTHF (the "L" signifying that it is the all-natural [6S] isomer) is the active circulating form of folate found in the body and one of the several forms found in food. In nature it is found only as this [6S] isomer, which is why DFH provides 5-MTHF as this natural isomer rather than the mixed (or racemic) form.
L-5-MTHF should be used when high doses of folate are needed.
Individuals who have tested homozygous with either the A1298C or C677T MTHFR mutation, or those with elevated homocysteine levels, should be using L-5-MTHF as the preferred form of folate supplementation. This will be more effective for them than other forms of folic acid or folates.
Others who may benefit from L-5-MTHF:
pregnant women and women wishing to become pregnant who have familial history of depression, high homocysteine levels, or genetic defect in MTHFR. Note: All pregnant women should takePrenatal Pro as their comprehensive multivitamin; can combine with L-5-MTHF if higher levels of folate are needed.
women with abnormal pap smears (precancerous)
those with very high homocysteine levels not responding quickly to Homocysteine Supreme(consider using them together)
dialysis patients
organic acid testing that reveals elevated FIGLU (marker used to identify folate deficiency)
patients with family history of dementia/vascular dementia
patients with depression
long-term alcoholism
long-term use of oral contraceptives, and persistent use of medications to lower folate levels, including high doses of NSAIDs such as aspirin or ibuprofen; anticonvulsants (phenytoin, phenobarbital, and primidone); trimethoprim (antibiotic), pyrimethamine (antimalarial), triamterene (blood pressure med.) and sulfasalazine (treatment for ulcerative colitis).
Do not take 5-MTHF simultaneously with the cholesterol-lowering agents cholestyramine or colestipol because they may decrease the absorption of folate.
*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.
Serving Size: 1 capsule Servings Per Container: 120
Active Ingredients:
Folate (as [6S]-5-Methyltetrahydrofolate) 1000 mcg
Inactive Ingredients: Microcrystalline cellulose, spinach juice powder, L-Leucine.
Recommended Dosage: As a dietary supplement, take one capsule daily or as directed by your health care practitioner.
This product does not contain: wheat, yeast, soy, gluten, eggs, dairy, corn, artificial colors, flavors, sugars, or preservatives.
NOTICE: Color, size or shape may appear different between lots.
STORE IN A COOL, DRY PLACE.
KEEP OUT OF REACH OF CHILDREN.
Read customer questions and answers about Folic acid on our blog.
Folate and Human Health Folate is one of the most essential nutrients needed during rapid cell division and growth. It is no surprise that pregnancy doubles the need for dietary folates. Folate coenzymes play a vital role in metabolism through two different pathways: the synthesis of DNA from its precursors (purines/thymidines) and the homocysteine (methionine) pathway. 5-MTHF is needed for the conversion of homocysteine to methionine which allows for the production of S-adenosylmethionine (known as SAMe). The importance of this is that SAMe is the universal methyl donor. Methyl-group donation is vital to proper cell replication and differentiation, and to many biochemical conversion processes, including the synthesis of serotonin, melatonin, and DNA.
Folate vs. Folic Acid While folates are naturally occurring in food, folic acid is a fully oxidized, synthetic compound (pteroylmonoglutamic acid) used in most dietary supplements and in food fortification, but is not found in nature. Designs for Health uses only natural folates found in food rather than folic acid. Due to enzyme defects or deficiencies, many people do not properly convert folic acid into natural folates including 5-MTHF. Although folic acid has been associated with several health benefits, such as reduction of neural tube defects and homocysteine, 5-MTHF supplementation would be a better way to reap these benefits since it is already activated and not associated with high levels of unmetabolized folic acid in the blood, as unmetabolized folic acid is implicated in an increase in the number of cancer deaths in the US. New research has emerged raising concern over the safety of chronic intake of high levels of folic acid from fortified foods, beverages and dietary supplements.
The MTHF Reductase enzyme, or MTHFR, plays a prominent role in the homocysteine pathway, a chemical reaction involving folates. One of this enzymes functions is to process homocysteine, changing it to methionine which is then used to make SAMe, the most important methyl donor in the body. To be more specific, reduction of 5,10-methylenetetrahydrofolate (methyleneTHF) to 5-methyltetrahydrofolate (methylTHF), the primary methyl donor for methionine synthesis, is catalyzed by the MTHFR enzyme.
Having a mutation in the MTHFR gene impacts how well the MTHFR enzyme performs. A MTHFR deficiency may lead to hyperhomocysteinemia. There are several MTHFR gene mutations which result in a mild to severe impairment of the activity of the MTHFR enzyme, the most characterized mutation being C677T (C677T MTHFR mutation).
This gene mutation makes a patient more susceptible to:
coronary heart disease
stroke
preeclampsia (high blood pressure in pregnant women)
birth defects including neural tube defects
sub-optimal methylation issues
Methylation issues caused by this gene mutation are due to a decrease in SAMe production, again the bodys primary methyl donor. Research studies have correlated this with demyelination of the brain and spinal cord.
References:
Homocysteine and folate metabolism in depression. Bottiglieri T. Prog 1. Neuropsychopharmacol Biol Psychiatry. 2005;29:1103-12.
An open trial of methyltetrahydrofolate in elderly depressed patients. Guaraldi GP, Fava 2. M, Mazzi F, la Greca P. Ann Clin Psychiatry. 1993 Jun;5(2):101-5.
Oral 5-methyltetrahydrofolic acid in senile organic mental disorders with depression: 3. results of a double-blind multi-center study. Passeri M, Cucinotta D, Abate G, Senin U, Ventura A, Stramba Badiale M. Aging.1993 Feb;5(1):63-71.
Is methylfolate effective in relieving major depression in chronic alcoholics? A hypothesis 4. of treatment. C. Di Palma, R. Urani, R. Agricola, V. Giorgetti and G. Dalla Verde. Current Therapeutic Research. Volume 55, Issue 5, May 1994, Pages 559-568.
A candidate genetic risk factor for vascular disease: a common mutation in methylenetet5. rahydrofolate reductase. Frosst P, Blom HJ, Milos R, Goyette P, Sheppard CA, Matthews RG, Boers GJ, den Heijer M, Kluijtmans LA, van den Heuvel LP. et al. Nat Genet. 1995 May;10(1):111-3
Effects of common polymorphisms on the properties of recombinant human methyle6. netetrahydrofolate reductase. Yamada K, Chen Z, Rozen R, Matthews RG. Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):14853-8. Epub 2001 Dec 11
Folic acid fortification and supplementation--good for some but not so good for others. 7. Kim YI. Nutr Rev. 2007 Nov;65(11):504-11.
Folic acid supplements and fortification affect the risk for neural tube defects, vascular 8. disease and cancer: evolving science. Bailey LB, Rampersaud GC, Kauwell GP. J Nutr. 2003 Jun;133(6):1961S-1968S.
Methyltetrahydrofolate: The superior alternative to folic acid. In: Kramer K, Hoppe PP, 9. Packer L, editors. Scott J. Nutraceuticals in health and disease prevention. New York: Marcer Decker; 2001. p. 75-90.
Compartmentation of folate-mediated one-carbon metabolism in eukaryotes. Appling 10. DR. FASEB J. 1991 Sep;5(12):2645-51.
Antiepileptic drugs as independent predictors of plasma total homocysteine levels. 11. Apeland T, Mansoor MA, Strandjord RE. Epilepsy Res. 2001 Nov;47(1-2):27-35.
Folate, homocysteine and neural tube defects: an overview. van der Put NM, van Straaten 12. HW, Trijbels FJ, Blom HJ. Exp Biol Med (Maywood). 2001 Apr;226(4):243-70.
Demyelination and decreased S-adenosylmethionine in 5,10-methylenetetrahydrofolate 13. reductase deficiency. Hyland K, Smith I Bottiglieri T, Perry J, Wendel U, Clayton PT, Leonard JV. Neurology. 1988 Mar;38(3):459-62.
[6S]-5-methyltetrahydrofolate increases plasma folate more effectively than folic acid 14. in women with the homozygous or wild-type 677C-->T polymorphism of methylenetetrahydrofolate reductase. Prinz-Langenohl R, et al., Br J Pharmacol. 2009 Dec;158(8):2014-21.