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Methylation

Is Taking Folic Acid Dangerous? Breast Cancer Concerns

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The question of folic acid fortification an issue that has been growing in the medical literature as it relates to risk of colon and breast cancer.

Unfortunately, as with most problems dealing with physiology, the ones who will ultimately be making recommendations (mainstream medicine and the mainstream media) will likely not have the background to fully understand the issue.

Folic acid (as well as the vitamins B12, B6, SAM-e and betaine) play a role in a process called methylation.  Methylation does many things, one of which is adding a “tag” onto DNA to allow the right DNA to be expressed at the right time. In other words, this process makes sure that “liver” cells do not do “brain” stuff.

Sounds good, but there are certain genes that silence other genes (called tumor suppressor genes).  If you suppress the suppressor of tumor growth, you can create a problem!  Sound complicated?  Then factor in the MTHFR genetic factor, and not enough folic acid will cause DNA damage to occur!

Which brings us to this particular article.  In it, researchers looked at folic acid levels in the bloodstream and a woman’s risk of breast cancer based on estrogne receptor status.  They found that women with the higher levels of folate acid in their blood had a 267% higher risk of estrogen receptor beta negative ERβ−) breast cancer.

So is folic acid good or bad for us?

First, supplementation aside, we should NOT be getting or folic acid from fortified breads and cereals, because these are refined and very bad for us.  Second, a healthy overall lifestyle will avoid cancer growth regardless of folic acid status.  Third, we should all try to find out what our MTHFR gene is so we know whether more or less folic acid is good for us.  Most labs can now easily run this testing in a normal blood sample.

Induction of tumors in mice by genomic hypomethylation – (04-23-03)

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Induction of tumors in mice by genomic hypomethylation

If you wish to fully understand the folic acid cycle and its contribution to the methylation process and how this drastically impacts our current health and disease prevention and how this pathway is subject to multiple genetic variations then don’t ask me. I don’t remember all that biochemistry either. Just know that folic acid and SAM-e are essential players in the ability of our bodies to protect DNA through a process called methylation. I have actually added high dose folic acid supplementation to my recommended basic vitamin list.

Entrez-PubMed

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L-5-methyltetrahydrofolate vs folic acid on plasma homocysteine – (03-04-03)

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L-5-methyltetrahydrofolate vs folic acid on plasma homocysteine.

Oral folic acid needs to be converted by the enzyme MHTFR to 5-MTHF before it can be used by the body in the methylation pathways. As has been previously discussed in Updates, the enzyme MHTFR is a common site of genetic differences, with certain genotypes producing a very sluggish enzyme that does not readily activate the oral folic acid. The idea has been that, by giving 5-MHTF directly, you can bypass genetic defects. This study does not support this theory, but it was also done on normal patients without consideration of their genetic makeup.

AJCN — Abstracts: Venn et al. 77 (3): 658

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Constipation and the future risk of Parkinson’s disease – (08-23-01)

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Constipation and the future risk of Parkinson’s disease

Isn’t this interesting? At this point no one is sure whether constipation is a sign of PD or whether constipation is a risk factor. Knowing what we know about the GI tract, however, would lead me to believe that the latter will turn out to be true. Much evidence points to the idea that methylation disorders contribute strongly to PD and that high dose folic acid and B12 may affect the progress of the disease. However, as with many other chronic disease, I am very sure that there is an inflammatory component to PD, and the GI tract is notorious for upregulating the immune system. Throw food allergies into the mix (which have been linked to constipation as well as brain lesions…) and there may be multiple pathways by which constipation could contribute to PD.

Neurology — Abstracts: Abbott et al. 57 (3): 456

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Alteration of DNA methylation in gastrointestinal carcinogenesis – (10-08-01)

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Alteration of DNA methylation in gastrointestinal carcinogenesis

I know this sounds a little technical, but the take home message is that alterations in the body’s ability to methylate DNA may lead to cancer. Methylation helps to protect DNA from damage. Slow methylation can come from a variety of sources, with dietary alterations and genetic sluggishness at the top of the list. Combine the two and it’s not a pretty picture. Folic acid and Vit B12 are some of the most important players in this game. Making sure you eat lots of whole grains and fresh fruit will provide high levels of these nutrients. However, in patients with genetic sluggishness, high doses of folic acid may be needed in supplement form.

Synergy : Journal of Gastroenterology and Hepatology 16 (9), 960-968

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S-Adenosyl-L-methionine: its role in the treatment of liver disorders – (10-24-02)

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S-Adenosyl-L-methionine: its role in the treatment of liver disorders

When a nutrient seems to affect multiple conditions, we can assume two case scenarios. A. The nutrient is offered by a multi level marketing company and is reported to fix everything from diabetes to cancer to my bald spot. B. The nutrient affects a basic metabolic defect/deficiency that leads to many downstream conditions. SAM-e falls into the second category. SAM-e is a strong methyl donor, and methylation is an incredibly important process that is essential for many biological processes such as homocysteine conversion, protecting DNA from damage and, in this study, protecting the liver by assisting in the production of glutathione (the liver’s heavy hitter when it comes to detoxification). This would put SAM-e on the list along with milk thistle for any patients with liver problems.

AJCN — Abstracts: Lieber 76 (5): 1183S –

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Homocysteine Levels and the Risk of Osteoporotic Fracture – (06-10-04)

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Homocysteine Levels and the Risk of Osteoporotic Fracture

Now that homocysteine is a well established risk factor for heart disease, the research community is moving on to other things homocysteine may contribute to. Remember the homocysteine may just be a marker for altered methylation ability, which is a process aided by Vit B12, B6, riboflavin, SAM-e, betaine and folic acid that is integral to the proper cell division of every single cell and well as the protection of DNA and the production of some neurotransmitters.

So, defects in the homocysteine pathway (which are very susceptible to genetic uniqueness’s  can lead to a wide variety of downstream conditions. The bottom line–interventions designed to lower homocysteine levels would probably benefit most patients and be cheaper than checking blood levels.

NEJM — Homocysteine Levels and the Risk of Osteoporotic Fracture.

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Environmental toxins can have their negative effects by inhibiting the methylation of DNA – (04-08-04)

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Activation of methionine synthase by insulin-like growth factor-1 and dopamine: a target for neurodevelopmental toxins and thimerosal

For those of us that are not biochemists and our eyes glazed over at the title to this one–basically, environmental toxins can have their negative effects by inhibiting the methylation of DNA. Remember that methylation reactions are incredibly important and effect such a basic role in human physiology. Thus, problems with methylation can lead to problems in many organ systems.

In this study, the authors found that environmental toxins such as mercury-containing thimerosal inhibit DNA methylation. For the life of me, I cannot see how anyone in the pharmaceutical industry could have even considered the use of mercury as a preservative. I can see it now…”I need something to extend the shelf live of this vaccine so we can make a larger profit on vaccines given to infants. Hey–how about that potent neurotoxin mercury?”

Activation of methionine synthase by insulin-like growth factor-1 and dopamine: a target for neurodevelopmental toxins and thimerosal.

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