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Methylcobalamin (methyl B12) is the neurologically active, most bioavailable and best utilized form of vitamin B12. Methyl B12 is more effective than traditional forms of B12 for treating pernicious anemia (B12 deficiency) as there is no need for conversion by the body and is better retained by the liver and other tissues.
Clinical studies have documented the efficacy of methyl B12 in slowing down or even reversing the effects on nerve tissue. Methyl B12 also appears to play a role in balancing brain chemicals and synthesizing neurotransmitters, which are the chemical means of communication between nerve cells. Studies also demonstrate B12's ability to reduce high homocysteine serum levels, which have been linked to arterial injury.
Methyl B12 has exhibited beneficial effects against brain aging, irregular sleep patterns and reducing high homocysteine serum levels. It may also support immune function, and promote normal cell growth.
Methyl B12 represents one of the best values in nutritional products, given its comparably low cost and its wide range of potential benefits.
Of the six structurally related compounds generically termed vitamin B12, methyl B12 possesses numerous distinct advantages:
Methyl B12 has demonstrated beneficial effects on a variety of physiological states. Some of the highlights of the current research are: The ability of methyl B12 to protect brain cells against glutamate-induced cytotoxicity synergizes with L-dopa supporting regimens. Based on this same protective mechanism, clinical studies have also administered large amounts of methyl B12 to Alzheimer's patients as a nutritional aid. Patients exhibited better cognitive functions such as memory, elevated mood and improved communication with other people when their levels of methylated B12 were improved.
Easily absorbed
Jarrow Formulas Methyl B12 lozenges are dissolved under the tongue, where a small additional amount is absorbed directly into the bloodstream before swallowing to further advance absorption. 98% of vitamin B-12 deficiency is due to poor gut absorption.
Methycobalamin is also safer than cyanocobalamin, which contains trace amounts of cyanide.
100% Active Coenzyme
Methyl B12 is one of only two forms of vitamin B12 that is in an active, coenzymated state (the other being adenosylcobalamin). Most other cobalamin forms can be converted to coenzymes, but the process is inefficient. In fact, in order for ordinary vitamin B12 to be activated and ready for methyl donation, it must first be converted to methylcobalamin by S-Adenosylmethionine (aka SAMe), an important intermediate metabolite.
Efficiently Utilized
Human urinary excretion of methyl B12 is about one-third that of a similar dose of cyanocobalamin, indicating substantially greater tissue retention.
Neurologically Active
In nerve and brain tissue, only methyl B12 initiates methylation, a process by which methyl groups (from methyl B12) are donated to the myelin sheath that insulates nerve fibers, maintaining and regenerating neurons. Methyl B12 plays a role in the synthesis of the neurotransmitters serotonin, dopamine, and norepinephrine.
Lowers Homocysteine Level
Methyl B12 is a catalyst for the biochemical conversion of homocysteine (linked to arterial damage) to methionine, an essential amino acid.
Documented Effects of Methyl B12
Brain Aging
Methyl B12 has been shown to prevent cellular degradation in the brain due to glutamate-, aspartate-, and
nitroprusside-induced cytotoxicity. Such chemicals regularly circulate within the brain, but when present in excess can kill ageing brain cells.Nerve Function
Methy B12 improves nerve function by contributing to nerve myelination. It has also been shown to stimulate protein synthesis for repair and neural regeneration in motor neurons.
Irregular cell growth
Administration of methy B12 has been shown to facilitate normal cell growth in mice.Immune Function
A clinical study showed that methy B12 improved the activity of T-cells (cells involved in immune response).Sleep Patterns
Methyl B12 initiates better 24-hour sleep patterns by provoking the pineal gland to release melatonin ("the sleep hormone") earlier in the evening. At the end of the sleep cycle, it causes the circulating melatonin levels to decrease earlier, making morning wake-ups much more refreshing.Muscle Contraction
A double-blind controlled study showed that high doses of methyl B12 significantly increased averaged Compound Muscle Action Potential amplitudes (CMAPs). Extended clinical trials may be able to demonstrate methyl B12's potential usefulness in improving or slowing muscle wasting.
Advancing age, medication, and diet are the primary (but not the only) risk factors for vitamin B12 deficiency. It is recommended that individuals over fifty years of age get most of their intake from supplements or vitamin B12-fortified foods. This recommendation is based on estimates that up to 40 percent of older individuals may (with or without their knowledge) suffer from reduced gastric hydrochloric acid (atrophic gastritis), a condition that impairs absorption of protein-bound vitamin B12 in food. Medications for stomach ulcers, heartburn, or gastro-esophageal reflux inhibit gastric secretions, also impairing vitamin B12 absorption. Of course, any individual with disorders of the digestive tract (regardless of age) may be at risk for malabsorption and deficiency of various nutrients including vitamin B12.
Diet is another risk factor for vitamin B12 deficiency. The best sources of B12 are animal products such as meat. eggs, and fish. Strict vegetarians (those who eat no animal products), therefore, are at greater risk of B12 deficiency.
Jarrow Formulas' Methylcobalamin B12 is used as a dietary supplement. The RDI for adolescents and adults is 6 mcg per day. Clinical trials have used up to 6,000 mcg daily. Lozenges can be
dissolved under the tongue with meals, or as directed by your
qualified health consultant.
These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.
Selected References
1. Groff, J.L., Gropper, S.S. & Hunt, S.M. (1995) Advanced nutrition and human metabolism (2nd edition). St. Paul, MN: West Publishing Company
2. Freeman, A.G. (1992). Cyanocobalamin - a case for withdrawal: Discussion paper. J R Soc Med 85, 868-687.
3. Berlin, R. et al. (1978). Vitamin B12 body stores during oral and parenteral treatment of pernicious anemia. Acta Med Scand 204 (1-2), 81-84.
4. Kuzminski, A.M., et al. (1998). Effective treat. of cobalamin deficiency with oral cobalamin. Blood 92, 1191-1198.
5. Okuda, K., Yashima, K., Kitazaki, T. & Takara, I. (1973). Intestinal absorption and concurrent chemical changes of methylcobalamin. J Lab Clin Med 81, 557-567.
6. Nishizawa, Y., et al. (1997). Effects of methylcobalamin on the proliferation of androgen-sensitive or estrogen-sensitive malignant cells in culture and in vivo. Int J Vitam Nutr Res 67 (3), 164-170.
7. Akaike, A. Tamura, Y., Sato, Y, Yokota, T. (1993), Protective effects of a vitamin B12 analog, methylcobalamin, against glutamate cytotoxicity in cultured cortical neurons. Eur J Pharmacol 241 (1), 1-6.
8. Mayeda, T. et al..(1997). L-dopa neurotoxicity is mediated by glutamate release in cultured rat striatal neurons. Brain Research 771,(1), 159-162.
9. Ikeda, T. et al. (1993). Treatment of Alzheimer-type dementia with intravenous mecobalamin. Clinical Therapeutics 14 (3), 426-437.
10. Watanaabe, T., Kaji, R., Oka, N., Bara, W., Kimura, J. (1994). Ultra high dose methylcobalamin promotes nerve regeneration in experimental acrylamide neuropathy. J Neurol Sci 122 (2), 140-143.
11. Shimizu, N. et al. (1987). Experimental study of antitumor effect of methyl B12. Oncology 44 (3), 169-173.
12. Sakane, T. et al.. (1982). Effects of methyl B12 on in vitro immune functions of human T lymphocytes. Experientia 48 (8), 716-720.
13. Kamgar-Parsi, B. et al. (1983). Successful treatment of human non-24-hour sleep-wake syndrome. Sleep 6, 257-264.
14. Mayer, G. et al. (1996). Effects of vitamin B12 on performance and circadian rhythm in normal subjects. Neurpsychophar 15, 456-464.
15. Kaju, R. et al.. (1998). Effect of ultra high dose methylcobalamin on compound muscle action potentials in amyotrophic lateral sclerosis: a double-blind controlled study. Muscle Nerve 21, 1775-1778.
16. Tucker, K.L.. et al.. (2000). Plasma vitamin B12 concentrations relate to intake source in the Framingham Offspring Study. Am J Clin Nutr 71, 514-522.
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