Folate – Vit B9 deficiency or MTHFR gene mutation

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Folate – Vit B9 or MTHFR deficiency has a frequency of 1 in 1.9 .

Those with potentially “severe” mutations should check homocysteine with their doctor. Folate deficiency: A deficiency in folic acid (folate) could be linked to MTHFR mutation and is worth checking out. Common symptoms include extreme fatigue, light-headedness, and forgetfulness.

Homocysteine is an amino acid and breakdown product of protein metabolism that, when present in high concentrations, has been linked to an increased risk of heart attacks and strokes. Elevated homocysteine levels are thought to contribute to plaque formation by damaging arterial walls.

Homocysteine is an amino acid thought to damage the lining of your arteries and other cells of the body. It is naturally formed in the body, but gets broken down (recycled) by 5-MTHF.  Elevated homocysteine levels in the blood is an independent risk factor for heart disease, stroke and other forms of cardiovascular disease.  It has also been linked with a wide range of other health problems including macular degeneration, Alzheimer’s disease, hearing loss, depression and cancer.

MTHFR mutation/gene variation can impact how well your body metabolizes folate and folic acid. Both are forms of vitamin B9, required for numerous critical bodily functions.  A fault in this metabolic cycle is linked to many serious health problems (neck pain,others).

MTHFR, short for Methylenetetrahydrofolate Reductase, is a very important enzyme in the body.  It’s necessary for Methylation to occur, a metabolic process that switches genes on and off, repairs DNA and many other important things.  Methylation is also essential to convert both folate and folic acid – each a form of Vitamin B9 – into its active, usable form called 5-MTHF.

One reader, a Rehab, Nutrition and Lifestyle Coach, Josh Rubin from California notes:

“…Folic acid def[initely] leads to catabolism of histadine. Low levels of histadine creates catabolism in the body and has been shown to be as a marker to arthritic and RA conditions.

“Low folate levels can lead to inhibition of DNA synthesis, impaired cell division, and alterations in protein synthesis.”

Histidine can even help protect tissues from damage caused by radiation or heavy metals. High histidine foods include beef, lamb, cheese, chicken, turkey, soy, fish, nuts, seeds, eggs, beans, and whole grains. The recommended daily intake for histidine is 10mg per kilogram of body weight, or 4.5mg per pound.

Diet

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Diet should include greens, whole foods, lemon, Vit B and Vit C rich whole foods, potassium and iron-rich foods) and vinegar (to aid in absorbtion of nutrients). Vit C and vinegar help in the absorption of nutrients from whole foods.

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What is folic acid/vitamin B9?

Vitamin B9, more commonly known as folate or folic acid, is a water-soluble vitamin that is part of the B vitamin family. B vitamins/folate help support adrenal function, help calm and maintain a healthy nervous system, and are necessary for key metabolic processes. Folate occurs naturally in foods, while folic acid is the synthetic form of folate.

Why is vitamin B9 necessary?

Vitamin B9 is essential for human growth and development, encourages normal nerve and proper brain functioning, and may help reduce blood-levels of the amino acid homocysteine (elevated homocysteine levels have been implicated in increased risk of heart disease and stroke). Folic acid or folate may also help protect against cancers of the lung, colon, and cervix, and may help slow memory decline associated with aging.

Pregnant women have an increased need for folic acid: it supports the growth of the placenta and fetus, and helps to prevent several types of birth defects, especially those of the brain and spine. Pregnant women and women of child-bearing age should take extra caution to get enough folic acid (see below for recommended amounts).

What are the signs of a folic acid deficiency?

Deficiency has been linked to birth defects, low birth weight, pregnancy loss, depression, memory loss, and cervical dysplasia. Alcoholics, pregnant women, and people living in institutional settings are at a higher risk of vitamin B9 or folate deficiency.


Folate and Depression

Many studies, going back to the 1960s, show an elevated incidence of folate deficiency in patients with depression.2 Studies vary depending on the criteria used to define folate deficiency, but often, about one-third of depression patients were deficient. Given that depression is often accompanied by decreased appetite and weight loss, the high incidence of folate deficiency in depression patients is not surprising. However, there is some evidence, though not conclusive, that folate deficiency may be involved in the etiology of depression in a minority of patients. Alternatively, depressed mood may decrease appetite, lower folate levels and thereby help to prevent recovery from depression. A recent review and metaanalysis looked at the results from the limited number of studies that investigated the effect of giving folate to depression patients and concluded that “there is some evidence that augmentation of antidepressant treatment with folate may improve patient outcome.”3 Whether the putative beneficial effect of folate is limited to those with folate deficiency is not clear.1,3

If folate deficiency can contribute to depressed mood and folate supplementation is beneficial in patients, a plausible mechanism implicates serotonin. In most,4–8 but not all,9,10 studies on patients with neuropsychiatric disorders, folate deficiency was associated with low levels of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the cerebrospinal fluid (CSF). In one study, supplementation with folate restored CSF 5-HIAA levels to normal.8

There is also a decrease in serotonin synthesis in patients with 5,10-methylenetetrahydrofolate reductase (MTHFR) deficiency, a disorder of folate metabolism.11,12

While the mechanism relating folate deficiency to low serotonin is not known, it may involve S-adenosylmethionine (SAMe). SAMe is a major methyl donor formed from methionine. Folate is involved in a cycle that regenerates methionine from homocysteine after SAMe is demethylated to S-adenosylhomocysteine, with subsequent conversion to homocysteine. Folate deficiency decreases SAMe in the rat brain.13 In humans, SAMe is an antidepressant14,15 and increases CSF 5-HIAA levels.16 Thus, there is some consistency in what is known about the interrelations of folate, SAMe and depression.

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