Supplements upon Supplements – MTHFR edition

This is a big lifestyle change: pill popping.  When I fell pregnant with Nash, I was caught with my pants down, so to speak!  The only thing I was taking at the time was copious amounts of wine and coffee.  DH and I were off of red meat, and that left plenty of room for more wine.

I had to rush out and buy prenatals and folic acid.  I took A LOT of folic acid – to the tune of an additional 800ug (micrograms) per day on top of the recommended 400ug already found in the prenatals I was taking.  Little did I know, as a heterozygous carrier of MTHFR C677T folic acid is toxic to me.  There is some debate as to how much folic an MTHFRer can process, certain sources say a hetero carrier can absorb 60% of folic acid (in the synthetic form, not from natural foods, natural foods are easiest to absorb), others say 35-40%, and this Dr. Ben guy says zero.

In fact, this simple gene polymorphism is found in almost 50% of the American population, but we only just “discovered” it in 1998.  Since 1998, folic acid fortification has been mandatory in our foods.  Good luck finding ANYTHING in the grocery store made with wheat flour that is not fortified. I’ve spent a small fortune at Whole Foods doing my best to avoid folic acid fortification.  I do however take L-5-Methylfolate (see below), and that is how I get the much needed folate, which is the natural form of “folic acid” – which, let me repeat, is SYNTHETIC folate.

{…could this be the source of the rise in gluten intolerance that was not seen in prior to recent years? … most wheat products have folic fortification AND gluten…}

Thanks to the March of Dimes, we know that folic acid supplementation in women of child bearing age helps limit gestational developmental problems like neural tube defects.  What has NOT been widely disseminated are these other interesting items: MTHFR polymorphisms (those carriers who have synthetic folic acid to folate conversion dysfunction) have been linked to autism spectrum disorders, psychiatric disorders, congenital heart defects (like Nash), pulmonary hypertension with heart defects/disease, and on and on.  With regard to ASDs, I would suspect that infants who developed in utero with highly enriched, folinated environments who then are born and either do not get breast milk or when they are weaned from enriched breast milk (from mom who is still taking folic/folate), then the lack of supplementation might cause a disruption.  There is a lot of research happening around this right now.  This is just a small sampling:

The point is: we are still learning about MTHFR, folate metabolism and how it effects our fertility and other functions.  I will say, in late February of this year I switched from a B-100 complex with folic acid to a 5-MTHF methylfolate and my energy went through the roof.  I had been heavily supplementing with something that was super toxic to my system.

MTHFR folks do tend to have elevated homocysteine and that in turn raises the risk for blood clots.  Pregnant women are also more prone to blood clots, which is a greater risk when you have elevated homocysteine levels.  But MTHFR researcher, Dr. Ben Lynch, says it isn’t enough to look at homocysteine levels when dealing with pregnancy complications and loss. My homocysteine levels are perfect – and here I sit with a very thick medical record jacket and a very complicated obstetrical history.

Andrea, at MTHFRLiving, writes the following:

It is important to remember that MTHFR gene mutations are inherited. Therefore, depending on what mutations are present in the mother and father, the fetus is likely to inherit MTHFR in some form. The baby can inherit problems in its own DNA, which present symptoms, and can also suffer from the nutritional deficiencies of the mother that are caused by her gene mutations. The most common problem is the risk of neural tube defects because of the mother’s inability to convert folic acid into l-methylfolate. Before I was aware of MTHFR, I was ingesting copious amounts of folic acid. This just blocks a person with MTHFR’s ability to absorb and assimilate natural folate and methylfolate. It is a major failing of current widespread prenatal advice that more women are not aware of the problems of folic acid for so many members of the population. A lack of folate and/or B12 can cause everything from spina bifida to anencephaly to Down’s Syndrome. Elevated homocysteine can cause low birth weight and premature birth.

There are also additional risks once the baby is born, which makes testing for methylation gene defects important. MTHFR has been linked to congenital heart disease, autism, ADD/ADHD and a host of other illnesses. As Dr. Kendal Stewart reminds us, it’s possible to use epigenetics to bypass the harmful effects of these mutations in your child, but only if you know which mutations he has. Ensuring proper methylation in a baby will prevent impaired immunity and virus and heavy metal accumulation from birth. This is an essential component to preventing autism and other serious health conditions.

I take 4mg – that’s right, FOUR MILLIGRAMS – of 5-MTHF-methylfolate with 5000ug of active B12 containing methylcobalamin and adenosylcobalamin for better absorption.  Folgard, which is commonly and mistakenly prescribed to MTHFR gals, has 2.2mg of folic acid, and I am essentially doubling that intake.  I may cut my dose in half and see how I do.  Since we are not TTC-ing this month I do not see any harm in it, AND I have been on 4mg for at least 2 miscarriages, so this clearly is not the key to my infertility.

Lovenox becomes a natural part of this discussion, but is beyond the scope of this post.  I will discuss it in future posts, so if you are interested just click on the *lovenox* tag to the right and you should see all associated posts as I publish more.

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