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Folic acid during pregnancy
Gynecologists prescribe folic acid to every pregnant woman. It helps prevent defects in the neural tube, from which the brain and spinal cord form.
The official recommendations disregard the genetics of 40% of the population with the MTHFR gene mutation. Under such conditions, folic acid will be poorly absorbed, and it will also build up and become toxic by itself. In addition, homocysteine will rise, harming the vessels. Is this why there are so many problems with blood vessels in pregnant women?
For general understanding, the methylation process in our bodies is in charge of neutralizing and expelling various toxic compounds from the body.
MTHFR is an enzyme known as the main methylation gene that is responsible for converting dietary folate to methyl folate.
This mechanism is more heavily involved during pregnancy to support the growth of the embryo and placenta. Also, the genes connected with MTHFR regulate the baby’s health while it is still in the womb. Depending on the percentage of this gene breakdown, various types of “garbage” build up, and as a result, the baby develops a wide range of neurological problems and problems with detox.
The optimal functioning of the MTHFR gene contributes to maintaining adequate levels of folate and homocysteine in blood. As a result, when MTHFR is defective, homocysteine cannot be re-converted, SAMe declines (along with the SAMe-SAH ratio), and a methyl cycle malfunction follows. This abnormality causes birth defects and autism in children.1
The polymorphisms that have received the greatest attention are C677T (rs1801133) and A1298C, which are crucial for evaluating the MTHFR’s performance (rs1801131).
The C677 mutation affects the body’s ability to convert homocysteine into methionine.
The enzyme is at least 70% damaged if your genetic response is MTHFR (A/A) rs 1801133, which prevents it from efficiently converting folic acid to 5-methyfolate.
If the genotype is A/G (or +/-), then the activity of the enzyme is reduced by 40%.
In both cases, correction requires a form of 5-MTHF to bypass the genetic block and restore the biochemistry. In this case, consuming synthetic folic acid will be dangerous and will lead to an increased level of unmetabolized folic acid in the blood.
Unlike C677, a defect in the A1298 (rs1801131) does not lead to an increase in homocysteine unless observed in combination with an MTHFR C677 mutation in a homozygous or heterozygous state (i.e., C677 A/A or A/G).
To correct MTHFR (rs1801131), it will be correct to use B12 in the form of hydroxycobalamin and folinic acid. People with this defect will be more at risk of depression. MTHFR (G/G) rs 1801131 carriers need extra liver support, BH4, immune system support, and neurotransmitters.
Food products are also enriched with synthetic folic acid. In excess, folic acid may raise the chance of cancer2, increasing the risk of children with allergic diseases, insulin resistance, and excessive blood lipids.
When folic acid enters the body, it has to undergo several transformations in the liver. It first turns into dihydrofolate (DHF), and then DHF transforms into tetrahydrofolate (TGF), and finally, TGF enters the folate cycle with the aid of the enzyme dihydrofolate reductase (DHFR).
While folinic acid may enter into a biochemical reaction without the use of DHFR.
If you don’t know if you have MTHFR, then folic acid in the form of 5-methyl folate is recommended, as it can easily enter the folate cycle without using the enzyme.
Those with regular MTHFR enzyme activity will benefit from taking supplements of L-methyl folate (5-MTHF), as it will support the enzyme’s optimal function.
MTHFR also needs magnesium and the energy of ATP to do its work.
Focusing only on correcting MTHFR can have negative consequences. In any case, preparation for pregnancy should be comprehensive. You can order the transcript of the methylation process, which will help your doctor or nutritionist draw up your personal health plan.
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