Can you be tested to see whether you have a genetic variation that prevents you from absorbing folate from your food, possibly resulting in hearing loss as you age? Senior citizens worried about hearing loss should know it's a combination of genes, exposure to loud noises, and possibly a deficiency of folate in your blood. But some people have a gene variant that prevents them from absorbing folate unless it's eaten in the active form. Check out the study, "Not Enough Folate May Quicken Hearing Loss."
You can check out a new study published in the Journal of Nutrition where researchers in Australia found that a deficiency of folate in the blood may considerably increase the risk of developing age-related hearing loss.The study recruited nearly 3,000 people age 50 and older. According to the September 23, 2010 Lee Swanson research report, in another recent study, researchers found that it’s very important for a mother to have healthy levels of vitamin D in her body when she becomes pregnant.
Basically, if you take folate, or vitamin B 12, you first have to find out from a genetic test whether or not you have the gene that prevents absorption of folate unless you take it in the bioactive form. Perhaps you need to take any vitamins in the bioactive form.
According to the website on BioActive folate, medical studies have proven that the conversion of folic acid into active folate is frequently disrupted by genetic factors, age-related problems and metabolic obstacles. Check out the study "Unmetabolized folic acid in serum: acute studies in subjects consuming fortified food and supplements."
- Up to 40% of adults are affected by genetic flaws that limit the amount of folic acid converted to the active folate that neutralizes homocysteine.3-10
- Transformation of folic acid into active folate falls off after ingesting 200 mcg, and is saturated at doses in the region of 400 mcg. Higher doses result in unabsorbed folic acid circulating in the blood, and we do not know the long term biological effects of a lifetime of exposure to unmodified synthetic folate.1,10
- Studies show transformation of folic acid into active folate falls off after ingesting 200 mcg, and is saturated at doses in the region of 400 mcg. And when folic acid fails to be converted to active folate it remains in the bloodstream for days, even weeks at a time.1,10
- Medical researchers are now investigating whether "unused" folic acid in the bloodstream actually blocks the absorption of folate from natural sources such as green leafy vegetables.
- If testing your blood and cell tissue to confirm your active folate status doesn't thrill you, here's an intelligent alternative: Let your body bypass the four-step conversion of folic acid by giving your body the exact form of folate it prefers and can immediately absorb, by getting your folate in the bioactive form. For more information, see the homocysteine fighters website, and check out the references to medical articles listed on the site.
Compared to the ingredients commonly found in multivitamins or B-complex formulas, the high-absorption bioactive forms (also known as coenzymes) of Folate and B12:
- Bypass genetic, age-related and metabolic obstacles
- Require fewer steps to be absorbed and utilized by the body
- Are the body's preferred form for neutralizing homocysteine
- Significantly reduces excretion of unabsorbed nutrients
Medical Journal Studies on Absorption of Folic Acid
1 Kelly P, McPartlin J, Goggins M, Weir DG, Soctt JM.Unmetabolized folic acid in serum: acute studies in subjects consuming fortified food and supplements. Am J Clin Nutr. 1997;65:1790-5>
2 Morita H, Taguchi J, Kurihara H, Kitaoka M, Kaneda H, Kurihara Y, Maemura K, Shindo T, Minamino T, Ohno M, Yamaoki K, Ogasawara K, Aizawa T, Suzuki S, Yakazi Y. Genetic polymorphism of 5,10-methylenetetrahydrofolate reductase (MTHFR) as a risk factor of coronary artery disease. Circulation 95:2032-2036, 1997.
3 Goyette P, Christensen B, Rosenblatt DS, Rozen R. Severe and mild mutations in cis for the methylenetetrahydrofolate reductase (MTHFR0 gene, and description of 5 novel mutations in MTHFR. Am. J. Hum. Genet. 59:1268-1275, 1996.
4 Bailey LB,Gregory JF. Polymorphisms of methylenetetrahydrofolate reductase and other enzymes: metabolic significance, risks and impact on folate requirement. J Nutr 1999;129(5):919-22.
5 Deloughery TG, Evans A, Sadeghi A, et al. Common mutation in methylenetetrahydrofolate reductase. Correlation with homocysteine metabolism and late-onset vascular disease. Circulation 1996;94(12):3074-78.
6 Kim YI. Methylenetetrahydrofolate reductase polymorphisms, folate, and cancer risk: a paradigm of gene-nutrient interactions in carcinogenesis. Nutr Rev 2000;58:205-17.
7 Choi S-W, Mason JB. Folate and carcinogenesis: an integrated scheme. J Nutr 2000;130:129-32.
8 Ma J, Stampfer MJ, Hennekens CH, et al. Methylenetetrahydrofolate reductase polymorphism, plasma folate, homocysteine, and risk of myocardial infarction in US physicians. Circulation 1996;94(10):2410-16.
9 Miyao M, Morita H, Hosoi T, et al. Association of methylenetetrahydrofolate reductase(MTHFR) polymorphism with bone mineral density in postmenopausal Japanese women. Calcif Tissue Int 2000;66:190-94.
10 Lucock MD, Wild J, Smithells R, Hartley R. Invivo characterization of the absorption and biotransformation of pteroylglutamic acid in man: a model for future studies. Biochem Med Metaab Biol 1989;42:30-42.