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Research has shown that homocysteine, a toxic amino acid, is associated with depression. About one-third of all depressed patients have low levels of Vitamin B-12 or folic acid.

Vitamin deficiencies are also associated with dementia. For example, about 16% of dementia patients have Vitamin B-12 deficiency. Not surprisingly, a Harvard study linked Alzheimer's disease to elevated homocysteine blood levels (hyperhomocysteinemia).

Dementia and heart disease are also more common in depressed people.

Stroke is a condition that occurs more often in people with elevated homocysteine blood levels. Supplementation with folate and methylcobalamin (coenzyme Vitamin B-12) has improved hyperhomocysteinemia.

Stroke is also associated with between a two- and fourfold increase in risk of subsequent hip fractures. In a controlled study by Sato et al., the risk of fractures were also reduced by 80% using methylcobalamin and folate supplementation.

Studies show folic acid supplementation reduces the risk of spina bifida and other neural tube defects. As a result, it has been used to fortify foods.

Folic acid supplementation, however, can mask Vitamin B-12 deficiency, thereby causing this common vitamin deficiency to go undetected.

Everyone should take supplemental Vitamin B-12 to avoid the damage to the brain, heart, bones, and immune system associated with Vitamin B-12 deficiency.

World-wide, one in five pregnant women has folic acid deficiency. In Guatemala, one in three children has deficient or marginal Vitamin B-12 levels. Most of these children also have problems with chronic infections and bacterial overgrowth, interfering with Vitamin B-12 absorption. Imagine if all children developed their full potential by receiving all essential nutrients.

Vegetarians, and people who eat very little meat, run the risk of developing Vitamin B-12 deficiency. Many vegetarians also have elevated homocysteine levels. Vitamin supplementation is essential for anyone in this category.

The body rids itself of homocysteine build-up with the aid of essential nutrients.

Coenzyme Vitamin B-12 (methylcobalamin) and folate (5-methyltetrahydrofolate) work together to change the toxic amino acid, homocysteine, into the beneficial amino acid, methionine.

Coenzyme Vitamin B-6 (pyridoxal-5-phosphate) helps convert it into cysteine.

Coenzymes are small organic molecules that are required by enzymes to power chemical reactions in the body.

Most coenzymes are derived from the vitamins found in food or supplements containing synthetic forms of vitamins. The production of coenzymes require the transformation of food-derived and synthetic vitamins by specific enzyme systems.

Non-coenzyme supplementation does not have the same robust effect on homocysteine nor does it reduce the risk of recurrent stroke. B-complex vitamin supplements have the largest impact on homocysteine levels, even though emphasis has been placed on the impact of single B-vitamins such as folate.

Methylcobalamin is the most common form of Vitamin B-12 found in the blood. Another coenzyme form of Vitamin B-12 (adenosylcobalamin) is found in the mitochondria (the cell's energy factories). It helps eliminate methylmalonic acid within the mitochondria.

Coenzyme and stabilized vitamins are more easily absorbed.

Calcium folinate, folinic acid and 5-methyl-tetrahydrofolate (as in the formulation found in Premium Brain Support™) are examples of stabilized folates. Dietary folates and folic acid found in most supplements will degrade more readily when exposed to light, air and stomach acid.

Supplement optimization, through the incorporation of coenzymes and stabilized vitamins, is an enormous advantage for people who have digestive problems.

Digestive problems are commonplace and can prevent your body from absorbing vitamins from food.

If you drink any alcohol, take certain medications, or have an infection, you may not be able to absorb or metabolize synthetic vitamins or the building blocks of vitamins found in food.

Many women take too much Vitamin B-6 in its non-coenzyme form, pyridoxine. The average daily intake is 120 mg., and above 200 mg. a day, people run a high risk of developing liver and peripheral nerve damage. These problems can slowly develop even at 120 mg a day, especially in smaller women, who are getting more Vitamin B-6 per pound than larger women.

Liver health also varies among people. Hepatitis and other liver diseases, or taking certain medications may cause problems metabolizing Vitamin B-6. Women taking oral contraceptives need supplemental Vitamin B-6.

The coenzyme form of Vitamin B-6 (pyridoxol-5-phosphate) is safer and easier to absorb than pyridoxine.*

REFERENCES

Bailey, L.B., and Gregory, J.F., III, Folate metabolism and requirements. J. Nutr., 129: 779-782, 1999.

Bottiglieri, T., Folate, vitamin B12 and neuropsychiatric disorders. Nutr. Rev., 54: 382-390, 1997.

Bottiglieri, T., et al., Cerebrospinal fluid S-adenosylmethionine in depression and dementia: effects of treatment with parenteral and oral S-adenosylmethionine. J. Neurol. Neurosurg. Psychiatry, 53: 1096-98, 1990.

Brinker, F., Herb Contraindications and Drug Interactions. Sandy, OR: Eclectic Medical Publications, 1998.

Brown, K.H., Diarrhea and malnutrition. J. Nutr., 133(suppl.): 328S-332S, 2003.

Carper, J., Your Miracle Brain. New York: Harper Row, 2000.

Caudill, M.A., et al., Folate status response to controlled folate intake in pregnant women. J. Nutr. 127: 2363-2370, 1997.

Craig, S.A.S., Betaine in human nutrition. Am. J. Clin. Nutr., 80: 539-549, 2004. Crellin, R., Bottiglieri, T., and Reynolds, E.H., Folates and psychiatric disorders. Drugs, 45: 623-636, 1995.

Fava, M., et al., Folate, B12, and homocysteine in major depression." Am. J. Psychiatry, 154: 426-428, 1997.

Fairfield, K.M., and Fletcher, R.H., Vitamins for chronic disease prevention in adults. JAMA, 287: 3116-3126, 2002.

Haddad, E.H., et al., Dietary intake and biochemical, hematologic, and immune status of vegans compared with nonvegetarians. Am. J. Clin. Nutr., 70(suppl.): 586S-593S, 1999.

Herrmann, C., et al., Total homocysteine, vitamin B12, and total antioxidant status in vegetarians. Clin. Chem., 47: 1094-1101, 2001.

Institute of Medicine, Dietary reference intakes for thiamin, riboflavin, niacin, Vitamin B₆, folate, Vitamin B₁₂, pantothenic acid, biotin, and choline. Washington, D.C.: National Academy Press, 1998.

Klee, G.G., Cobalamin and folate evaluation: measurement of methylmalonic acid and homocysteine vs vitamin B-12 and folate. Clin. Chem., 46: 1277-1283, 2000.

Kuzminski, A.M., et al. Effective treatment of cobalamin deficiency with oral cobalamin. Blood, 92: 1191-1198, 1998.

Loehrer, F.M., et al., Low whole-blood S adenosylmethionine and correlation with 5-methyltetrahydrofolate and homocysteine in coronary artery disease. Arterioscler. Thrombosis Biol., 16: 727-733, 1996.

Ohta, T., et al., Treatment of persistent sleep-wake schedule disorder in adolescents with methylcobalamin. Sleep, 14: 414-418, 1991.

Okawa, M. et al., Vitamin B12 treatment for sleep-wake rhythm disorders. Sleep, 13: 15-23, 1990.

Ravaglia, G., et al., Homocysteine and cognitive function in healthy elderly community dwellers in Italy. Am. J. Clin. Nutr., 77: 668-673, 2003.

Refsum, H., et al., Facts and recommendations about total homocysteine determinations: An expert opinion. Clin. Chem., 50: 3-32, 2004.

Rogers, L.M., et al., Predictors of cobalamin deficiency in Guatemalan school children: diet, Heliocobacter pylori, or bacterial overgrowth? J. Pediatr. Gastroenterol. Nutr., 36: 27-36, 2003.

Rogers, L.M., et al., High prevalence of cobalamin deficiency in Guatemalan schoolchildren: association with low plasma holotranscobalamin II and elevated serum methylmalonic acid and plasma homocysteine concentrations. Am. J. Clin. Nutr., 77: 433-440, 2003.

Rosenberg, L.E., Disorders of propionate and methylmalonate metabolism, in The Metabolic Basis of Inherited Disease. Stansbury, J.B., et al., eds. New York: McGraw-Hill, 474-497, 1983.

Rowe, P.B., Inherited disorders of folate metabolism, in The Metabolic Basis of Inherited Disease. Stansbury, J.B., et al., eds. New York: McGraw-Hill, 498-521, 1983.

Sato, Y., et al., Effects of folate and mecobalamin on hip fractures in patients with stroke. A randomized controlled trial. JAMA, 293: 1082-1088, 2005.

Sakane, T., et al., Effects of methyl B12 on in vitro immune functions of human T lymphocytes. Experientia, 48: 716-720, 1982.

Sesdradri, A., et al., Plasma homocysteine as a risk factor for dementia and Alzheimer's disease. N. Eng. J. Med., 346: 476-483, 2002.

Segasothy, M., and Phillips, P.A., Vegetarian diet: panacea for modern lifestyle diseases? QJM, 92: 531-544, 1999.

Tatro, D.S., ed., Drug Interaction Facts. St. Louis, MO: Facts and Comparisons, 2001.

Toole, J.F., et al., Lowering homocysteine in patients with ischemic stroke to prevent recurrent stroke, myocardial infarction, and death: The vitamin intervention for stroke prevention (VISP) randomized controlled trial. JAMA, 291: 565-575, 2004.

Venn, B.J., Green, T.J., Moser, R., and Mann, J.I., Comparison of the effects of low dose supplements with L-5-methyltetrahydrofolate or folic acid on plasma homocysteine: a randomized placebo-controlled study. Am. J. Clin. Nutr., 77: 658-662, 2003.

Wilson, J.D. Vitamin deficiencies and excess, in Harrison's Priniciples of Internal Medicine, Vol. I. Fauci, A.S., et al., eds. New York: McGraw-Hill, 480-489, 1998.

*These statements have not been evaluated by the Food and Drug Administration. Our products are not intended to diagnose, treat, cure or prevent any disease. All references made for the use of our products are intended for nutritional support to improve normal physiological states and conditions. Any impression made that our products are to be used to treat a disease state or condition should be considered inadvertent and coincidental. Our products are intended to supplement balanced diets.

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