Folic acid fortification prevents much more than neural tube defects

March 09, 2004
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Folic acid fortification prevents much more than neural tube defects





Homocysteine Reduction


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Folic acid and vitamin B12 capsules


Life Extension Magazine March 2004 issue



B vitamins lower dangerous homocysteine levels

Life Extension Update Exclusive

Folic acid fortification prevents much more than neural tube defects
The American Heart Association's 44th annual Conference on Cardiovascular Disease Epidemiology and Prevention was the site of a presentation by medical epidemiologist Lorenzo D. Botto, MD, with the Centers for Disease Control and Prevention's National Center on Birth Defects and Developmental Disabilities in Atlanta, announcing his research team's findings that the folic acid fortification of food begun in the previous decade has been followed by a reduction in the death rates for ischemic heart disease and stroke. An estimated 17,000 deaths associated with ischemic heart disease and 31,000 stroke-related deaths may have been prevented every year since fortification with the B vitamin was initiated in the U.S. in 1996 to help prevent neural tube birth defects.

The CDC team, led by Quanhe Yang, PhD, studied national death certificate data to determine changes in mortality trends following the implementation of folic acid fortification. They found the improvement in death rates due to ischemic heart disease and stroke were not explained by changes in other major risk factors, such as smoking and hypertension, many of which did not improve during the period examined.

The researchers suggest that folic acid may be helping to lower serum homocysteine in the U.S. population, thereby reducing fatalities from cardiovascular disease and stroke. Dr Botto explained, “Many studies have shown that folic acid can lower serum homocysteine levels, and that people with higher than average homocysteine levels are at higher risk for stroke and heart disease. We think high homocysteine somehow causes an insult on the vascular wall, weakening the vessel and making it more prone to damage. “

"We found evidence of a three-fold acceleration in the decline of stroke-associated mortality that is temporally related to fortification of flour with folic acid,” Dr Botto summarized. “If folic acid fortification is responsible for the improvement in stroke-associated mortality, the public health benefits are substantial . . . Importantly, the decline in mortality associated with stroke showed a consistent pattern that ran across all genders and racial groups, with improvements for both men and women, whites and blacks.”


Homocysteine Reduction
The medical establishment woke up to the dangers of homocysteine when the New England Journal of Medicine (April 9, 1998) and the Journal of the American Medical Association (JAMA, Dec. 18, 1996) published articles suggesting that vitamin supplements be used to lower homocysteine levels. This same message was published by the Life Extension Foundation 18 years earlier (Anti-Aging News, Nov. 1981, 85-86).

Elevated homocysteine can be reduced (or detoxified) in two ways. The most common pathway is via the remethylation process, where methyl groups are donated to homocysteine to transform it into methionine and S-adenosylmethionine (SAMe).

A potent remethylation agent is TMG, which stands for trimethylglycine. The tri means there are three methyl groups on each glycine molecule that can be transferred to homocysteine to transform (remethylate) it into methionine and SAMe. The remethylation (or detoxification) of homocysteine requires the following minimum factors: (1) folic acid, (2) vitamin B12, (3) zinc, and (4) TMG.

Choline is another "methyl donor" that helps to lower elevated homocysteine levels, and this conversion doesn't require cofactors. However, choline only enhances remethylation in the liver and kidney, which is why it is so important to take adequate amounts of remethylating factors such as folic acid and vitamin B12 to protect the brain and the heart. The published literature emphasizes that folic acid and vitamin B12 are critical nutrients in the remethylation (detoxification) pathway of homocysteine.

The other pathway in which elevated homocysteine is reduced is via its conversion into cysteine and eventually glutathione via the trans-sulfuration pathway. This pathway is dependent on vitamin B6. The amount of vitamin B6 required to lower homocysteine has considerable individual variability. Methionine is the only amino acid that creates homocysteine. People who eat foods that are high in methionine (such as red meat and chicken) may need more vitamin B6. Elevated homocysteine can occur when there are insufficient vitamin cofactors (such as folate and vitamin B6) to detoxify the amount of methionine being ingested in the diet.

Featured Product of the Week

Folic Acid with Vitamin B12 capsules

B vitamins are used in the body individually or in combination with enzymes to help release energy from carbohydrates, fat, and protein. Vitamin B coenzymes are crucial to the metabolic pathways that generate the energy needed by every cell in the body. Because they are co-dependent in their metabolic activities, a deficiency of one B vitamin can affect optimal functioning of organ systems throughout the body.

Folic acid (folate) is a member of the B-complex family. It is found in abundance in leafy green vegetables, but is often deficient in the standard American diet. Folic acid participates in a coenzyme reaction that synthesizes DNA needed for cell growth and new cell formation and helps convert vitamin B12 to one of its coenzyme forms.

Life Extension Magazine March 2004 issue

Homocysteine Reduction
Researchers at Germany 's University of Hanover evaluated the dietary intake and blood status of 178 German women aged 60 to 70 years old.* The study participants completed a three-day diet record that assessed their energy and nutrient intakes. This was compared to the corresponding recommended dietary allowance (RDA) for older women. Blood samples were drawn after an overnight fast and used to measure the levels of thiamine (B1), riboflavin (B2), pyridoxine (B6), cobalamin (B12), folate, and homocysteine.

Riboflavin intake was sufficient for the most part, with only 2% of the study participants below the RDA. By contrast, more than 82% of the women had a folate intake below the RDA. Blood levels of cobalamin, thiamine, and pyridoxine were below the respective RDAs for these vitamins in 42%, 29%, and 17% of the women, respectively. Plasma homocysteine was dramatically elevated in 17% of the study participants. Because the subjects had above-average levels of education, the researchers speculated that poor B-vitamin status might be even more prevalent in the general population.

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For longer life,

Dayna Dye
Editor, Life Extension Update
954 766 8433 extension 7716
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