Folate

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Folate (Vitamin B9) is involved in many different metabolic pathways, including the synthesis of nucleic acids. (the building blocks of RNA and DNA) It is especially important for the synthesis and maintenance of red blood cells. It is also critical for the One-Carbon Cycle, also referred to as the Methylation Cycle.

Folate goes through a number of chemical forms in the human body. The most important form is methylfolate, also known as methyltetrahydrofolate, MTHF, or levomefolic acid. This form, along with another of its active forms, tetrahydrofolate, (THF) is involved in nucleotide synthesis and both forms are important in pregnancy and infancy.

The form found in many supplements and fortified foods is folic acid. This is a synthetic form of folate that is not naturally found in the human diet and is not naturally used by the human body. The popularity of folic acid is partly due to its shelf-stable nature.

Deficiency[edit | edit source]

Deficiency of either folate or Vitamin B12 can lead to megaloblastic anemia.

Deficiency is associated with increased blood homocysteine and an increased risk of cardiovascular disease.

Folate is essential for brain development and function.

However, high doses of folic acid may cause long-term issues as it is not fully converted to the folate form naturally found in the human diet, and the unconverted amount may act as a competitive inhibitor of folate. (Methylfolate is more advisable as a supplement for long-term use.[1])

MTHFR mutation[edit | edit source]

The 5,10-methylenetetrahydrofolate reductase (MTHFR) gene codes for an enzyme that allows for the conversion of synthetic folic acid to natural folate. Mutations in this gene may impair a person's ability to convert the synthetic folic acid to natural folate, which may lead in some cases to a de facto folate deficiency.

ME/CFS[edit | edit source]

High homocysteine is found in the cerebral spinal fluid of ME/CFS patients and lowering it with vitamin B12/Folate may help cognitive symptoms.[2]

See also[edit | edit source]

Learn more[edit | edit source]


References[edit | edit source]