Years ago it was determined that increased intake of folic acid significantly reduced the risk of birth defects like spina bifida by reducing homocysteine levels. The problem was, we had yet to understand how folic acid reduced these levels. A new study that pinpoints this process may lead to a reduction in not only birth defects, but in heart attacks and strokes as well.
Researchers from the University of Michigan have unraveled the mystery behind folic acid’s effectiveness by studying an enzyme called methylenetetrahydrofolate reductase, thankfully given the acronym MTHFR.
MTHFR converts homocysteine in the body to an essential amino acid called methionine. Within the MTHFR molecule is a vitamin derived molecule called flavin adenine dinucleotide or FAD. When a fairly-common genetic mutation occurs in MTHFR, it encourages the loss of FAD from the enzyme. When the levels of FAD decrease, MTHFR cannot do its job and homocysteine cannot be converted to methionine. This leaves the homocysteine to build up in blood plasma.
This is where folic acid comes in.
“Increased levels of folates help bind FAD more tightly to MTHFR—protecting the enzyme against heat inactivation and allowing the homocysteine-to-methionine conversion pathway to proceed normally,” said Martha L. Ludwig, Ph.D., one of the researchers. She went on to say that folic acid supplementation would reduce homocysteine levels for humans with normal and mutated MTHFR. MTHFR mutation is present in approximately 10 percent of the population.
As mentioned, homocysteine levels have been linked to not only birth defects, but also to heart attacks and strokes. More research is necessary to determine whether or not folic acid can aid in the treatment and prevention of heart attack and stroke, but a better understanding of controlling the homocysteine associated with these diseases may be a good start.